Slow Viruses: The Original Sin Against the Laws of Virology
This is a great article showing how real the whole issue of viruses
is and how baseless the issue of vaccines for so-called viral illnesses are.
Sheri
BIO for author Peter Duesberg at the end..........(On the basis of
his experience with retroviruses, Duesberg has challenged the
virus-AIDS hypothesis)
http://www.mercola.com/2000/dec/31/slow_virus.htm
Dr. Joseph Mercola
Slow Viruses: The Original Sin Against the Laws of Virology
By Peter H. Duesberg and Bryan J. Ellison
from "INVENTING THE AIDS VIRUS", Regnery publishing, 1996
Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto
From the discovery of tobacco mosaic virus through the polio
epidemic, scientists have found and legitimately blamed many viruses
for a variety of diseases, each having passed the acid test of Koch's
postulates. But for every truly dangerous virus, many more perfectly
harmless passenger viruses can be found in humans and animals.
NIH-sponsored polio research during the late 1950s proved the point.
Researchers trying to isolate new strains of poliovirus accidentally
found numerous closely related passenger viruses -- such as Coxsackie
and echoviruses - that, like polio, infected the digestive system.
Scientists classified some of these viruses as "orphans" - viruses
without corresponding diseases.
The virus hunters could not bring themselves to believe microbes
could exist without being harmful and expected even these "orphan"
viruses would someday find appropriate sicknesses.
When trying to blame a passenger virus for a disease, how-ever, one
nagging problem haunts the virus hunter: The laws of virology dictate
that the illness will strike the victim soon after infection. When
microbes infect a new host, they cause sickness within days or weeks
at most. In order to cause disease, viruses need to grow into
sufficient numbers to take over the body; otherwise, the host's
immune defenses will neutralize the invader and prevent disease altogether.
The rate-determining step of such fast, exponential growth is the
generation time of the virus. Since the generation time of all human
viruses is between eight and forty-eight hours, and since the
infected cell produces one hundred to one thousand viruses per day,
viruses multiply exponentially, increasing in numbers hundred- to
thousand-fold per day. Within a week or two, one hundred trillion
(1014) cells can be produced-one for each of the one hundred trillion
cells in the human body.
Therefore, if scientists wish to convict an innocent virus, they must
invent a new property for it that allows the virus to violate the
laws of virology.
For example, they can hypothesize a "latent period" of months or
years between the time the virus invades the body and the appearance
of symptoms - hence, a "slow" virus.
However, the slow virus concept has never been reconciled with the
short generation time of viruses and the immune system. Once the
virus lies totally dormant, an intact immune system will never allow
any virus to be reactivated to multiply into numbers that would
threaten the host.
For a virus to be reactivated, the immune system first must be
destroyed by something else - the real cause of a disease. A
reactivated virus would just contribute an opportunistic infection.
Thus, there are no slow viruses, only slow virologists.
A conventional virus could, however, be slow acting in a defective
immune system.
Indeed, some exceptional victims suffer pre-existing health problems
that prevent their immune systems from reacting decisively against
the virus, allowing it to continue growing and damaging the host for
a long period of time. This can happen with virtually any type of
virus, but it is extremely rare. When such a chronic infection does
occur, as with a small percentage of hepatitis cases whose immune
system is damaged by alcoholism or intravenous drug addiction, the
virus keeps growing abundantly in the body and can easily be found by
experimental tests.
Other germs, like herpes viruses, can hide out in some recess of the
body, breaking out periodically to strike again when the immune
system passes a seasonal low.In both examples, only the weakened
immune system of the host allows the infection to smolder or
occasionally reappear from hibernation.
By contrast, a slow virus is an invention credited with the natural
ability to cause disease only years after infection - termed the
"latent period" - in previously healthy persons, regardless of the
state of their immunity. Such a concept allows scientists to blame a
long-neutralized virus for any disease that appears decades after
infection. The slow virus is the original sin against the laws of virology.
The slow-virus or latent-period concept, now used to connect HIV with
AIDS, can be traced back to the days of the war on polio. The
researcher who popularized this modern myth is today an authority for
AIDS researchers and one whose career epitomizes the evolution of the
virus hunters over the past three decades.
Dr. Carleton Gajdusek is a pediatrician who has worked as a
virologist at the NIH for decades. Having spent a great deal of time
studying contagious childhood diseases around the world, Gajdusek was
sponsored by the NFIP and sent to New Guinea in 1957.
There, a doctor with the local health department introduced him to a
disease called kuru, a mysterious ailment that attacked the brain,
rendering the victim increasingly spasmodic or paralyzed until death
within months. The syndrome existed only among the thirty-five
thousand tribal villagers in one set of valleys, mostly the Fore tribe.
Before Gajdusek's arrival, no outsider had ever described kuru,
although the Fore tribesmen told him the condition had begun
appearing a few decades earlier.
Gajdusek's initial study assumed the disease to be infectious. He
reported that the natives routinely cannibalized the brains of
relatives for ritual purposes, a practice that they told him had
begun around the same time as the arrival of kuru.
Gajdusek later explained to one interviewer that cannibalism
"expressed love for their dead relatives," and that it also "provided
a good source of protein for a meat-starved community."
Gajdusek decided that kuru was transmitted by the eating of deceased
victims' brains. Yet when he searched for a virus, he ran into a
baffling absence of evidence. None of the typical signs of infection
could be found in the patients. Their bodies showed no inflammation
and no fever, no changes were registered in their supposedly infected
spinal fluid, their immune systems failed to react as if any microbe
had invaded the body, and those people with suppressed immune
defenses had no greater risk of catching the disease.
Another scientific group soon arrived from Australia and concluded
that kuru might be genetically inherited.
Upon arriving back in the United States, Gajdusek was hired by the
NIH to work at its institute for studying neurological disease. While
continuing to monitor kuru incidence, he devoted his time to
laboratory study of the condition.
Word of his discovery of kuru meanwhile made its way to England,
where another virus hunter was investigating a sheep disease known as
scrapie, which involved symptoms of brain degeneration. The English
researcher suggested to Gajdusek that kuru might be caused by a slow
virus, one with a long latent period.
Gajdusek was immediately hooked by the revolutionary idea, despite
his own "misgivings" that genes, toxins, or nutritional deficiencies
might be the cause of kuru.
Again determined to find an elusive virus, he tried to transmit kuru
from victims to chimpanzees. But none of the animals became sick when
injected with blood, urine, or other bodily fluids from kuru
patients, nor from the cerebrospinal fluid that surrounds the brain,
which should have been full of the alleged brain-destroying virus.
Indeed, the monkeys contracted no disease even from eating
kuru-affected brains - the authentic animal model of cannibalism.
Only one bizarre experiment did work, in which the brains of kuru
patients were ground into a fine mush and injected directly into the
brains of live monkeys through holes drilled in their skulls.
Ultimately, some of the experimental monkeys suffered coordination
and movement problems.
Surprisingly, though, even this extreme method could not transfer
kuru to dozens of other animal species. And no virus could be seen in
the brain tissue, even using the best electron microscopes.
At this point, one might expect Gajdusek would have suspected
something was seriously wrong with his virus hypothesis. If evidence
for the invisible virus could not be found anywhere but in unpurified
brain tissue, if it did not elicit any defensive reactions by the
body, and if it could not be transmitted in pure form to animals,
then probably no virus existed at all. The homogenized brain tissue
of dead kuru patients - full of every imaginable protein and other
compounds-should in itself be toxic when inoculated into monkeys' brains.
Nevertheless, the sick monkeys convinced Gajdusek and his colleagues
he had found a virus. Since he could not isolate it apart from the
brain tissue, he decided to study the virus and its structure with a
standard experiment.
He would define which chemical and physical treatments would destroy
the microbe, thereby gathering clues about its nature. But to his
astonishment, almost nothing seemed to harm the mystery germ.
Powerful chemicals, acids and bases, boiling temperatures,
ultraviolet and ionizing radiation, ultrasound-no matter how he
treated the brain tissue, it still caused "kuru" in his lab monkeys.
Further tests also proved that no foreign genetic material, which all
viruses require for their existence, could be found anywhere in
kuru-affected brains.
Employing the strongest virus-destroying treatments, Gajdusek had
failed to render the kuru brain tissue harmless in his experiments.
His results lent themselves to one obvious interpretation: No virus
existed in the first place, so it could not possibly be destroyed.
But Gajdusek clung to his virus hypothesis. Despite his disappointing
experiments, he turned the results upside down and argued that the
"kuru virus" was actually a new type of super-microbe or, as he put
it, an "unconventional virus." This new virus also needed to act as a
slow virus, since long periods of time elapsed between an act of
cannibalism and the onset of kuru; he liberally suggested latent
periods extending into years or even decades.
At an earlier time, and in another context, Gajdusek probably would
have been ignored by orthodox scientists. But he offered this
hypothesis to a generation of scientists dominated and impressed by
virus hunters.
The year was 1965, polio had largely disappeared, and the burgeoning
ranks of NIH-funded virologists welcomed any new research direction
on which to use their skills. Thus, they embraced Gajdusek's slow
virus hypothesis enthusiastically.
They listened uncritically when he claimed a similar unconventional
virus caused Creutzfeld-Jakob disease, a rare brain disorder that
seems to strike mostly Westerners having undergone previous brain
surgery (obviously such medical operations might well be suspected as
the real cause).
Gajdusek proposed slow or even unconventional viruses as the causes
of a huge laundry list of nerve and brain disorders, ranging from
scrapie in sheep to multiple sclerosis and Alzheimer's disease in
humans, and he was taken seriously even though he offered no
proof.Entranced, his peers awarded him the 1976 Nobel Prize for
medicine, specifically for the kuru and Creutzfeld-Jakob viruses he
has yet to find. And the NIH promoted him to head its Laboratory of
Central Nervous System Studies.
In the meantime another crucial, if embarrassing, bit of information
has emerged as a challenge to Gajdusek's virus-kuru hypothesis. The
published transcript of his Nobel acceptance speech, in a 1977 issue
of Science magazine, included a photo ostensibly showing New Guinea
natives eating their cannibalistic meal. The photo is not very clear.
When colleagues asked Gajdusek if the photo truly showed cannibalism,
he admitted the meal was merely roast pork. According to Science, "He
never publishes actual pictures of cannibalism, he says, because they
are 'too offensive.'" Unconvinced, anthropologist Lyle Steadman of
Arizona State University has investigated and directly challenged
Gajdusek, claiming "there is no evidence of cannibalism in New Guinea."
Steadman, who spent two years doing fieldwork in New Guinea, noted
that he often heard tales of cannibalism but when he probed, "the
evidence evaporated."
Gajdusek, angered by the hint of malfeasance, has insisted that "he
has actual photographs of cannibalism, but he would never publish
them because they 'so offend the relatives of the people who used to
do it.'" This statement contradicts his earlier claims that the
tribesman proudly ate their dead relatives out of respect, quitting
the practice only in deference to outside pressure from government
authorities.
For evidence of cannibalism, Gajdusek also cited Australian arrests
of tribesmen for the alleged crime - which, as it turned out, were
based on hearsay accusations. So perhaps New Guinea natives stand
falsely accused of ritual cannibalism.
In addition, few people outside of Gajdusek's original research team
have ever personally witnessed kuru victims. This means we also
depend on his own descriptions and statistics for our knowledge of
the disease itself, particularly since he claims cannibalism and kuru
both ceased to exist within a few years after his 1957 trip. Phantom
viruses, transmitted through phantom cannibalism, cause phantom disease.
Yet Gajdusek has reshaped the thinking of an entire generation of
biologists, his seductive message of slow viruses having landed on
eager ears. He and the virus hunters inspired by him have built
careers chasing viruses and attributing them to latent periods in
order to connect them to noninfectious diseases.
SMON, the nerve-destroying disease that struck Japan during the
1960s, became one unfortunate example. Japanese virologists, greatly
impressed with Gajdusek's accomplishments, spent years searching for
slow viruses they presumed would cause the disease and thereby
delayed finding the true cause - a prescribed medication.
Another example of a pointless virus hunt involved diabetes.
Beginning in the early 1960s, some scientists tried to blame this
noncontagious syndrome on the virus that also causes mumps. The
evidence has been pathetically sparse, forcing virologists to point
to occasional children who become diabetic after they have also
suffered mumps or, if they really stretch their case, to argue that
both mumps and diabetes become most common during the same annual
season in one county of New York.
Having become soldiers without a war, veteran polio virologists
invaded the diabetes field as well, proposing since the early 1970s
that Coxsackie viruses may cause the disease. Antibodies against
several strains of these harmless viruses, first discovered as
by-products of polio research, have been found in a few diabetic children.
But between 20 percent and 70 percent of young diabetics have never
been infected, and the remainder have already neutralized the virus
with their immune systems long before the onset of diabetes.
Apparently, an equal percentage of non-diabetic children have also
been infected with these Coxsackie viruses. Needless to say, none of
the above viruses meets Koch's postulates for causing diabetes.
Hilary Koprowski, like Gajdusek, typifies the modern virus hunter.
Although Koprowski's virology career began earlier, Gajdusek's work
helped rescue Koprowski from the obsolescence that threatened polio
researchers after the war on polio. Like so many of his colleagues,
he found his newest calling in the war on AIDS.
Koprowski's work on viruses started at the Rockefeller Institute in
New York. By the late 1940s he moved across town to the Lederle
pharmaceutical company, where he worked feverishly to develop a polio
vaccine. By 1954 he had invented one, but Jonas Salk was announcing
the field trials for another vaccine, and Koprowski's already-tested
product was shunted aside by Salk's public acclaim.
Koprowski left Lederle in I957 to take a position as director of the
privately endowed Wistar Institute of Pennsylvania, where he began
tests on humans and stepped up the campaign to get approval for his
vaccine. By now Albert Sabin had tested his own polio immunization on
millions of people in foreign countries, completely overshadowing
Koprowski's equally successful but less-promoted vaccine.
Nevertheless, Koprowski's day did arrive. His vaccine became the
standard used by the World Health Organization in America during the
late 1950s and 1960s.
In the meantime he spent several years studying the rabies virus and
creating a vaccine against that virus, which attacks the brain and
nervous system. But because rabies is relatively rare, Koprowski's
vaccine never achieved the stardom of other immunizations. More
important, however, his rabies research placed him squarely in the
field of neurological diseases just in time to meet up with
Gajdusek's kuru work.
The news of slow viruses enticed Koprowski with visions of
groundbreaking science. He quickly realized that the notion of slow
viruses could become a useful tool, allowing him to source slow,
noninfectious diseases to viruses, so long believed to be fast-acting
agents. He participated as a "program advisor" in Gajdusek's first
major conference on slow and unconventional viruses held in 1964 at
the NIH head-quarters in Bethesda, Maryland. From that point forward,
Hilary Koprowski joined the new virus-hunting trend from which he
would never turn back.
His first big opportunity to take a crack at slow viruses came at the
end of the 1960s. Subacute sclerosing panencephalitis (SSPE), a
mouthful of a name for such a rare condition, attacks a small number
of schoolchildren and teenagers each year, causing dementia, learning
disabilities, and finally death.
Doctors first recognized SSPE in the 1930s, and by the 1960s the
virus hunters were searching for an SSPE germ. At that time, the most
fashionable viruses for research belonged to the myxovirus family,
which included the viruses that caused influenza, measles, and mumps.
Animal virologists therefore started by probing for signs of myxoviruses.
Excitement mounted after trace quantities of measles virus were
detected in the brains of SSPE patients, and in 1967 most of the
victims were found to have antibodies against measles. The facts that
SSPE affected only one of every million measles -- infected people
and that this rare condition appeared from one to ten years after
infection by measles were no longer a problem: Researchers simply
hypothesized a one- to ten-year latency period. Little wonder they
could also easily rationalize that one virus could cause two totally
different diseases.
Koprowski's foray into SSPE research began in the early 1970s. He
began isolating the measles virus from dying SSPE victims, a nearly
impossible task because their immune systems had long before
completely neutralized the virus (some SSPE cases, more-over had
never had measles, merely the measles vaccine). His characteristic
patience nonetheless paid off, yielding a tiny handful of virus
particles from some patients that could be coaxed to begin growing
again, if only in laboratory cell culture.
In other patients only defective viruses that were unable to grow had
remained so many years after the original measles infection.
Rather than concluding the measles virus had nothing to do with SSPE,
he employed the new logic of virus hunting to argue that a defective
measles virus caused SSPE!
Koprowski continued this line of SSPE research for several more
years. But in 1985 Gajdusek himself entered the SSPE fray, publishing
a paper with leading AIDS researcher Robert Gallo in which they
proposed that HIV, the supposed AIDS virus, caused SSPE while
remaining latent. With hardly a blink, several leading virologists
jettisoned the old measles-SSPE hypothesis in favor of a newly
popular, but equally innocent, virus.
Multiple sclerosis (MS), the notorious disease that also attacks the
nervous system and ultimately kills, has provided yet another
opportunity for the virus hunters.
First, they blamed the measles virus starting in the 1960s, since
many MS patients had antibodies against the virus. Ten years later
others suggested the mumps virus, which is similar to measles. The
early I980s brought the coronavirus hypothesis of MS, the category of
virus better known for causing some colds. In 1985, with Gajdusek
stealing his thunder for SSPE, Koprowski also published a scientific
paper that year in Nature with Robert Gallo, in this case arguing
that some virus similar to HIV now caused MS. Unfortunately for
Koprowski, even this hypothesis was abandoned within just a few years.
Phantom Viruses and Big Bucks
Most virus hunters prefer chasing real, if arguably harmless, viruses
as their deadly enemies. But Gajdusek's "unconventional" viruses -
the ones neither he nor anyone else have ever found - have been
making a comeback in recent years. Given the abundance of research
dollars being poured into biomedical science by the NIH and other
agencies, opportunistic virus hunters have been finding creative ways
to cash in. One increasingly successful method utilizes modern
biotechnology to isolate viruses that may not even exist.
Hepatitis, or liver disease, has yielded profitable virus-hunting
opportunities in recent years. Hepatitis can be a truly painful
affliction, starting like a flu but progressing to more severe
symptoms, including high fevers and yellow skin. At least three
varieties seem to exist.
Hepatitis A is infectious, spread through unsanitary conditions, and
is caused by a conventional virus.
Hepatitis B also results from a virus (discovered in the 1960s) and
is transmitted mostly between heroin addicts sharing needles, among
sexually active and promiscuous people, or in the Third World from
mothers to their children around the time of birth.
A third type of hepatitis was found in the 1970s, again restricted to
heroin addicts, alcoholics, and patients who have received blood transfusions.
Most scientists assumed these cases were either hepatitis A or B,
until widespread testing revealed neither virus in the victims.
Roughly thirty-five thousand Americans die each year of any type of
the disease, a fraction of those from this "non-A, non-B hepatitis,"
as it was known for years.
Today it is called hepatitis C. This form of hepatitis does not
behave as an infectious disease, for it rigidly confines itself to
people in well- defined risk groups rather than spreading to larger
populations or even to the doctors treating hepatitis patients. Yet
virologists have been eyeing the disease from the beginning, hoping
one day to find a virus causing it.
That day arrived in 1987. The laboratory for the job was no less than
the research facility of the Chiron Corporation, a biotechnology
company located directly across the bay from San Francisco. Equipped
with the most advanced techniques, a research team started its search
in 1982 by injecting blood from patients into chimpanzees. None of
monkeys contracted hepatitis, although subtle signs vaguely
resembling infection or reddening did appear.
For the next step, the scientists probed liver tissue for a virus.
None could be found. Growing desperate, the team fished even for the
smallest print of a virus, finally coming across and greatly
amplifying a small piece of genetic information, encoded in a
molecule known as ribonucleic acid (RNA), that did not seem to belong
in the host's genetic code.
This fragment of presumably foreign RNA, the researchers assumed,
must be the genetic information of some undetected virus. Whatever it
was, liver tissue contains it only in barely detectable amounts. Only
about half of all hepatitis C patients contain the rare foreign RNA.
And in those who contain it, there is only one RNA molecule for every
ten liver cells - hardly a plausible cause for disease.
The Chiron team used newly available technology to reconstruct pieces
of the mystery virus. Now they could test patients for antibodies
against this hypothetical virus and soon discovered that only a
slight majority of hepatitis C patients had any evidence ofthese
antibodies in their blood.
1. Koch's first postulate, of course, demands that a truly harmful
virus be found in huge quantities in every single patient.
2. His second postulate requires that the virus particles be
isolated and grown, although this supposed hepatitis virus has never
been found intact.
3. And the third postulate insists that newly infected animals, such
as chimpanzees, should get the disease when injected with the virus.
This hypothetical microbe fails all three tests. But Koch's standards
were the furthest thing from the minds of the Chiron scientists when
they announced in 1987 that they had finally found the "hepatitis C" virus.
Now more paradoxes are confronting the viral hypothesis. Huge numbers
of people testing positive for the hypothetical hepatitis C virus
never develop any symptoms of the disease, even though the "virus" is
no less active in their bodies than in hepatitis patients.
And according to a recent large-scale study of people watched for
eighteen years, those with signs of "infection" live just as long as
those without. Despite these facts, scientists defend their
still-elusive virus by giving it an undefined latent period extending
into decades.
Paradoxes like these no longer faze the virus-hunting research
establishment. Indeed, rewards are generally showered upon any new
virus hypothesis, no matter how bizarre. Chiron did not spend five
years creating its own virus for nothing. Having patented the test
for the virus, the company put it into production and began a
publicity campaign to win powerful allies.
The first step was a paper published in Science, the world's most
prestigious science magazine, edited by Dan Koshland, Jr., professor
of molecular and cell biology at the University of California at Berkeley.
Edward Penhoet, chief executive officer for Chiron, also holds a
position as professor of molecular and cell biology at the University
of California at Berkeley. The NIH-supported virology establishment
soon lent the full weight of its credibility to the hepatitis C virus
camp. As Chiron's CEO boasted, "We have a blockbuster product."
A regulatory order from the Food and Drug Administration (FDA) to
test the blood supply would reap enormous sales for Chiron.
Their big chance presented itself in late 1988 as a special request
from Japanese Emperor Hirohito's doctors. The monarch was dying and
constantly needed blood transfusions; could Chiron provide a test to
make sure he received no blood tainted with hepatitis C? The biotech
company jumped at the opportunity, making for itself such a name in
Japan that the Tokyo government gave the product its approval within one year.
The emperor died in the meantime, but excitement over Chiron's test
was fueled when the Japanese government placed hepatitis C high on
its medical priority list. Chiron's test kit now earns some $60
million annually in that country alone.
By the middle of 1990, the United States followed suit.
The FDA not only approved the test, but even recommended the
universal testing of donated blood.
The American Association of Blood Banks followed suit by mandating
the $5 test for all 12 million blood donations made each year in this
country - raking in another $60 million annually for Chiron while
raising the nation's medical costs that much more.
And all this testing is being done for a virus that has never been isolated.
Profits from the test kit have generated another all-too-common part
of virus hunting. With Chiron's new income from the hepatitis C test,
Penhoet's company bought out Cetus, another biotech company, founded
by Donald Glaser, who, like Penhoet, also holds a position as
professor of molecular and cell biology at the University of
California at Berkeley. And Chiron made an unrestricted donation of
about 12 million to the Department of Molecular and Cell Biology at
the University of California at Berkeley that generates $100,000 in
interest each year.
Unfortunately for Peter Duesberg, who belongs to the same department,
his supervisor is yet another professor who consults for Chiron
Corporation - and displays little sympathy for Duesberg for
challenging modern virus hunting by restricting his academic duties
to undergraduate student teaching and by not appointing him to
decision-making committees.
Such conflicts of interest have become standard fixtures in
university biology departments.
The modern biomedical research establishment differs radically from
any previous scientific program in history. Driven by vast infusions
of federal and commercial money, it has grown into an enormous and
powerful bureaucracy that greatly amplifies its successes, all the
while stifling dissent.
Such a process can no longer be called science, which by definition
depends on self-correction by internal challenge and debate.
Despite their popularity among scientists and their companies,
"latent," "slow," and "defective" viruses have achieved only little
prominence as hypothetical causes of degenerative diseases before the
AIDS era. Their hypothetical role in degenerative diseases, which
result from the loss of large numbers of cells, remained confined to
rare, exclusive illnesses like kuru and hepatitis C.
However, because latent, slow, and defective viruses cannot kill
cells, such "viruses" eventually achieved prominence as hypothetical
causes of cancer and thus entered the courts of health care and
medical research. The next chapter describes the terms under which
these viruses were promoted as causes of cancer and how some of these
terms were eventually used to promote latent, slow, and defective
viruses as causes of degenerative diseases including, above all, AIDS.
Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto
*****
http://www.duesberg.com/
Peter H. Duesberg, Ph.D. is a professor of Molecular and Cell Biology
at the University of California, Berkeley. Biographical Sketch
http://www.duesberg.com/about/pdbio.html
He isolated the first cancer gene through his work on
retroviruses in 1970, and mapped the genetic structure of these
viruses. This, and his subsequent work in the same field, resulted in
his election to the National Academy of Sciences in 1986. He is also
the recipient of a seven-year Outstanding Investigator Grant from the
National Institutes of Health.
On the basis of his experience with retroviruses, Duesberg has
challenged the virus-AIDS hypothesis in the pages of such journals as
Cancer Research, Lancet, Proceedings of the National Academy of
Sciences, Science, Nature, Journal of AIDS, AIDS Forschung,
Biomedicine and Pharmacotherapeutics, New England Journal of Medicine
and Research in Immunology. He has instead proposed the hypothesis
that the various American/European AIDS diseases are brought on by
the long-term consumption of recreational drugs and/or AZT itself,
which is prescribed to prevent or treat AIDS. See The AIDS Dilemma:
Drug diseases blamed on a passenger virus.
For a detailed discussion of American/European AIDS as opposed
to African AIDS, see The African AIDS Epidemic: New and Contagious or
Old Under a New Name.
This is Duesberg's official site, containing his written works
on the subject, as well as other scientists that support his views
such as Kary B. Mullis. Kary Mullis won the 1993 Nobel Prize in
Chemistry for his invention of the polymerase chain reaction
technique for detecting DNA. This is the technique used to search for
fragments of HIV in AIDS patients.
Prof. Duesberg's findings have been a thorn in the side of the
medical establishment and drug companies since 1987. Instead of
engaging in scientific debate, however, the only response has been to
cut-off funding to further test Professor's Duesberg's hypothesis.
You can show your support by contributing a tax deductible
donation to help support Prof. Duesberg's lab at the University of
California Berkeley.
Sheri Nakken, former R.N., MA, Hahnemannian Homeopath
http://www.wellwithin1.com/homeo.htm & http://www.wellwihtin1.com/vaccine.htm
ONLINE/Email classes in Homeopathy; Vaccine Dangers; Childhood Diseases
Slow Viruses: The Original Sin Against the Laws of Virology
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Sheri Nakken
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Sheri Nakken
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Re: Slow Viruses: The Original Sin Against the Laws of Virology
-Slow Viruses: The Original Sin Against the Laws of Virology
This is a great article showing how real the whole issue of viruses
is and how baseless the issue of vaccines for so-called viral illnesses are.
Sheri
BIO for author Peter Duesberg at the end..........(On the basis of
his experience with retroviruses, Duesberg has challenged the
virus-AIDS hypothesis)
http://www.mercola.com/2000/dec/31/slow_virus.htm
Dr. Joseph Mercola
Slow Viruses: The Original Sin Against the Laws of Virology
By Peter H. Duesberg and Bryan J. Ellison
from "INVENTING THE AIDS VIRUS", Regnery publishing, 1996
Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto
From the discovery of tobacco mosaic virus through the polio
epidemic, scientists have found and legitimately blamed many viruses
for a variety of diseases, each having passed the acid test of Koch's
postulates. But for every truly dangerous virus, many more perfectly
harmless passenger viruses can be found in humans and animals.
NIH-sponsored polio research during the late 1950s proved the point.
Researchers trying to isolate new strains of poliovirus accidentally
found numerous closely related passenger viruses -- such as Coxsackie
and echoviruses - that, like polio, infected the digestive system.
Scientists classified some of these viruses as "orphans" - viruses
without corresponding diseases.
The virus hunters could not bring themselves to believe microbes
could exist without being harmful and expected even these "orphan"
viruses would someday find appropriate sicknesses.
When trying to blame a passenger virus for a disease, how-ever, one
nagging problem haunts the virus hunter: The laws of virology dictate
that the illness will strike the victim soon after infection. When
microbes infect a new host, they cause sickness within days or weeks
at most. In order to cause disease, viruses need to grow into
sufficient numbers to take over the body; otherwise, the host's
immune defenses will neutralize the invader and prevent disease altogether.
The rate-determining step of such fast, exponential growth is the
generation time of the virus. Since the generation time of all human
viruses is between eight and forty-eight hours, and since the
infected cell produces one hundred to one thousand viruses per day,
viruses multiply exponentially, increasing in numbers hundred- to
thousand-fold per day. Within a week or two, one hundred trillion
(1014) cells can be produced-one for each of the one hundred trillion
cells in the human body.
Therefore, if scientists wish to convict an innocent virus, they must
invent a new property for it that allows the virus to violate the
laws of virology.
For example, they can hypothesize a "latent period" of months or
years between the time the virus invades the body and the appearance
of symptoms - hence, a "slow" virus.
However, the slow virus concept has never been reconciled with the
short generation time of viruses and the immune system. Once the
virus lies totally dormant, an intact immune system will never allow
any virus to be reactivated to multiply into numbers that would
threaten the host.
For a virus to be reactivated, the immune system first must be
destroyed by something else - the real cause of a disease. A
reactivated virus would just contribute an opportunistic infection.
Thus, there are no slow viruses, only slow virologists.
A conventional virus could, however, be slow acting in a defective
immune system.
Indeed, some exceptional victims suffer pre-existing health problems
that prevent their immune systems from reacting decisively against
the virus, allowing it to continue growing and damaging the host for
a long period of time. This can happen with virtually any type of
virus, but it is extremely rare. When such a chronic infection does
occur, as with a small percentage of hepatitis cases whose immune
system is damaged by alcoholism or intravenous drug addiction, the
virus keeps growing abundantly in the body and can easily be found by
experimental tests.
Other germs, like herpes viruses, can hide out in some recess of the
body, breaking out periodically to strike again when the immune
system passes a seasonal low.In both examples, only the weakened
immune system of the host allows the infection to smolder or
occasionally reappear from hibernation.
By contrast, a slow virus is an invention credited with the natural
ability to cause disease only years after infection - termed the
"latent period" - in previously healthy persons, regardless of the
state of their immunity. Such a concept allows scientists to blame a
long-neutralized virus for any disease that appears decades after
infection. The slow virus is the original sin against the laws of virology.
The slow-virus or latent-period concept, now used to connect HIV with
AIDS, can be traced back to the days of the war on polio. The
researcher who popularized this modern myth is today an authority for
AIDS researchers and one whose career epitomizes the evolution of the
virus hunters over the past three decades.
Dr. Carleton Gajdusek is a pediatrician who has worked as a
virologist at the NIH for decades. Having spent a great deal of time
studying contagious childhood diseases around the world, Gajdusek was
sponsored by the NFIP and sent to New Guinea in 1957.
There, a doctor with the local health department introduced him to a
disease called kuru, a mysterious ailment that attacked the brain,
rendering the victim increasingly spasmodic or paralyzed until death
within months. The syndrome existed only among the thirty-five
thousand tribal villagers in one set of valleys, mostly the Fore tribe.
Before Gajdusek's arrival, no outsider had ever described kuru,
although the Fore tribesmen told him the condition had begun
appearing a few decades earlier.
Gajdusek's initial study assumed the disease to be infectious. He
reported that the natives routinely cannibalized the brains of
relatives for ritual purposes, a practice that they told him had
begun around the same time as the arrival of kuru.
Gajdusek later explained to one interviewer that cannibalism
"expressed love for their dead relatives," and that it also "provided
a good source of protein for a meat-starved community."
Gajdusek decided that kuru was transmitted by the eating of deceased
victims' brains. Yet when he searched for a virus, he ran into a
baffling absence of evidence. None of the typical signs of infection
could be found in the patients. Their bodies showed no inflammation
and no fever, no changes were registered in their supposedly infected
spinal fluid, their immune systems failed to react as if any microbe
had invaded the body, and those people with suppressed immune
defenses had no greater risk of catching the disease.
Another scientific group soon arrived from Australia and concluded
that kuru might be genetically inherited.
Upon arriving back in the United States, Gajdusek was hired by the
NIH to work at its institute for studying neurological disease. While
continuing to monitor kuru incidence, he devoted his time to
laboratory study of the condition.
Word of his discovery of kuru meanwhile made its way to England,
where another virus hunter was investigating a sheep disease known as
scrapie, which involved symptoms of brain degeneration. The English
researcher suggested to Gajdusek that kuru might be caused by a slow
virus, one with a long latent period.
Gajdusek was immediately hooked by the revolutionary idea, despite
his own "misgivings" that genes, toxins, or nutritional deficiencies
might be the cause of kuru.
Again determined to find an elusive virus, he tried to transmit kuru
from victims to chimpanzees. But none of the animals became sick when
injected with blood, urine, or other bodily fluids from kuru
patients, nor from the cerebrospinal fluid that surrounds the brain,
which should have been full of the alleged brain-destroying virus.
Indeed, the monkeys contracted no disease even from eating
kuru-affected brains - the authentic animal model of cannibalism.
Only one bizarre experiment did work, in which the brains of kuru
patients were ground into a fine mush and injected directly into the
brains of live monkeys through holes drilled in their skulls.
Ultimately, some of the experimental monkeys suffered coordination
and movement problems.
Surprisingly, though, even this extreme method could not transfer
kuru to dozens of other animal species. And no virus could be seen in
the brain tissue, even using the best electron microscopes.
At this point, one might expect Gajdusek would have suspected
something was seriously wrong with his virus hypothesis. If evidence
for the invisible virus could not be found anywhere but in unpurified
brain tissue, if it did not elicit any defensive reactions by the
body, and if it could not be transmitted in pure form to animals,
then probably no virus existed at all. The homogenized brain tissue
of dead kuru patients - full of every imaginable protein and other
compounds-should in itself be toxic when inoculated into monkeys' brains.
Nevertheless, the sick monkeys convinced Gajdusek and his colleagues
he had found a virus. Since he could not isolate it apart from the
brain tissue, he decided to study the virus and its structure with a
standard experiment.
He would define which chemical and physical treatments would destroy
the microbe, thereby gathering clues about its nature. But to his
astonishment, almost nothing seemed to harm the mystery germ.
Powerful chemicals, acids and bases, boiling temperatures,
ultraviolet and ionizing radiation, ultrasound-no matter how he
treated the brain tissue, it still caused "kuru" in his lab monkeys.
Further tests also proved that no foreign genetic material, which all
viruses require for their existence, could be found anywhere in
kuru-affected brains.
Employing the strongest virus-destroying treatments, Gajdusek had
failed to render the kuru brain tissue harmless in his experiments.
His results lent themselves to one obvious interpretation: No virus
existed in the first place, so it could not possibly be destroyed.
But Gajdusek clung to his virus hypothesis. Despite his disappointing
experiments, he turned the results upside down and argued that the
"kuru virus" was actually a new type of super-microbe or, as he put
it, an "unconventional virus." This new virus also needed to act as a
slow virus, since long periods of time elapsed between an act of
cannibalism and the onset of kuru; he liberally suggested latent
periods extending into years or even decades.
At an earlier time, and in another context, Gajdusek probably would
have been ignored by orthodox scientists. But he offered this
hypothesis to a generation of scientists dominated and impressed by
virus hunters.
The year was 1965, polio had largely disappeared, and the burgeoning
ranks of NIH-funded virologists welcomed any new research direction
on which to use their skills. Thus, they embraced Gajdusek's slow
virus hypothesis enthusiastically.
They listened uncritically when he claimed a similar unconventional
virus caused Creutzfeld-Jakob disease, a rare brain disorder that
seems to strike mostly Westerners having undergone previous brain
surgery (obviously such medical operations might well be suspected as
the real cause).
Gajdusek proposed slow or even unconventional viruses as the causes
of a huge laundry list of nerve and brain disorders, ranging from
scrapie in sheep to multiple sclerosis and Alzheimer's disease in
humans, and he was taken seriously even though he offered no
proof.Entranced, his peers awarded him the 1976 Nobel Prize for
medicine, specifically for the kuru and Creutzfeld-Jakob viruses he
has yet to find. And the NIH promoted him to head its Laboratory of
Central Nervous System Studies.
In the meantime another crucial, if embarrassing, bit of information
has emerged as a challenge to Gajdusek's virus-kuru hypothesis. The
published transcript of his Nobel acceptance speech, in a 1977 issue
of Science magazine, included a photo ostensibly showing New Guinea
natives eating their cannibalistic meal. The photo is not very clear.
When colleagues asked Gajdusek if the photo truly showed cannibalism,
he admitted the meal was merely roast pork. According to Science, "He
never publishes actual pictures of cannibalism, he says, because they
are 'too offensive.'" Unconvinced, anthropologist Lyle Steadman of
Arizona State University has investigated and directly challenged
Gajdusek, claiming "there is no evidence of cannibalism in New Guinea."
Steadman, who spent two years doing fieldwork in New Guinea, noted
that he often heard tales of cannibalism but when he probed, "the
evidence evaporated."
Gajdusek, angered by the hint of malfeasance, has insisted that "he
has actual photographs of cannibalism, but he would never publish
them because they 'so offend the relatives of the people who used to
do it.'" This statement contradicts his earlier claims that the
tribesman proudly ate their dead relatives out of respect, quitting
the practice only in deference to outside pressure from government
authorities.
For evidence of cannibalism, Gajdusek also cited Australian arrests
of tribesmen for the alleged crime - which, as it turned out, were
based on hearsay accusations. So perhaps New Guinea natives stand
falsely accused of ritual cannibalism.
In addition, few people outside of Gajdusek's original research team
have ever personally witnessed kuru victims. This means we also
depend on his own descriptions and statistics for our knowledge of
the disease itself, particularly since he claims cannibalism and kuru
both ceased to exist within a few years after his 1957 trip. Phantom
viruses, transmitted through phantom cannibalism, cause phantom disease.
Yet Gajdusek has reshaped the thinking of an entire generation of
biologists, his seductive message of slow viruses having landed on
eager ears. He and the virus hunters inspired by him have built
careers chasing viruses and attributing them to latent periods in
order to connect them to noninfectious diseases.
SMON, the nerve-destroying disease that struck Japan during the
1960s, became one unfortunate example. Japanese virologists, greatly
impressed with Gajdusek's accomplishments, spent years searching for
slow viruses they presumed would cause the disease and thereby
delayed finding the true cause - a prescribed medication.
Another example of a pointless virus hunt involved diabetes.
Beginning in the early 1960s, some scientists tried to blame this
noncontagious syndrome on the virus that also causes mumps. The
evidence has been pathetically sparse, forcing virologists to point
to occasional children who become diabetic after they have also
suffered mumps or, if they really stretch their case, to argue that
both mumps and diabetes become most common during the same annual
season in one county of New York.
Having become soldiers without a war, veteran polio virologists
invaded the diabetes field as well, proposing since the early 1970s
that Coxsackie viruses may cause the disease. Antibodies against
several strains of these harmless viruses, first discovered as
by-products of polio research, have been found in a few diabetic children.
But between 20 percent and 70 percent of young diabetics have never
been infected, and the remainder have already neutralized the virus
with their immune systems long before the onset of diabetes.
Apparently, an equal percentage of non-diabetic children have also
been infected with these Coxsackie viruses. Needless to say, none of
the above viruses meets Koch's postulates for causing diabetes.
Hilary Koprowski, like Gajdusek, typifies the modern virus hunter.
Although Koprowski's virology career began earlier, Gajdusek's work
helped rescue Koprowski from the obsolescence that threatened polio
researchers after the war on polio. Like so many of his colleagues,
he found his newest calling in the war on AIDS.
Koprowski's work on viruses started at the Rockefeller Institute in
New York. By the late 1940s he moved across town to the Lederle
pharmaceutical company, where he worked feverishly to develop a polio
vaccine. By 1954 he had invented one, but Jonas Salk was announcing
the field trials for another vaccine, and Koprowski's already-tested
product was shunted aside by Salk's public acclaim.
Koprowski left Lederle in I957 to take a position as director of the
privately endowed Wistar Institute of Pennsylvania, where he began
tests on humans and stepped up the campaign to get approval for his
vaccine. By now Albert Sabin had tested his own polio immunization on
millions of people in foreign countries, completely overshadowing
Koprowski's equally successful but less-promoted vaccine.
Nevertheless, Koprowski's day did arrive. His vaccine became the
standard used by the World Health Organization in America during the
late 1950s and 1960s.
In the meantime he spent several years studying the rabies virus and
creating a vaccine against that virus, which attacks the brain and
nervous system. But because rabies is relatively rare, Koprowski's
vaccine never achieved the stardom of other immunizations. More
important, however, his rabies research placed him squarely in the
field of neurological diseases just in time to meet up with
Gajdusek's kuru work.
The news of slow viruses enticed Koprowski with visions of
groundbreaking science. He quickly realized that the notion of slow
viruses could become a useful tool, allowing him to source slow,
noninfectious diseases to viruses, so long believed to be fast-acting
agents. He participated as a "program advisor" in Gajdusek's first
major conference on slow and unconventional viruses held in 1964 at
the NIH head-quarters in Bethesda, Maryland. From that point forward,
Hilary Koprowski joined the new virus-hunting trend from which he
would never turn back.
His first big opportunity to take a crack at slow viruses came at the
end of the 1960s. Subacute sclerosing panencephalitis (SSPE), a
mouthful of a name for such a rare condition, attacks a small number
of schoolchildren and teenagers each year, causing dementia, learning
disabilities, and finally death.
Doctors first recognized SSPE in the 1930s, and by the 1960s the
virus hunters were searching for an SSPE germ. At that time, the most
fashionable viruses for research belonged to the myxovirus family,
which included the viruses that caused influenza, measles, and mumps.
Animal virologists therefore started by probing for signs of myxoviruses.
Excitement mounted after trace quantities of measles virus were
detected in the brains of SSPE patients, and in 1967 most of the
victims were found to have antibodies against measles. The facts that
SSPE affected only one of every million measles -- infected people
and that this rare condition appeared from one to ten years after
infection by measles were no longer a problem: Researchers simply
hypothesized a one- to ten-year latency period. Little wonder they
could also easily rationalize that one virus could cause two totally
different diseases.
Koprowski's foray into SSPE research began in the early 1970s. He
began isolating the measles virus from dying SSPE victims, a nearly
impossible task because their immune systems had long before
completely neutralized the virus (some SSPE cases, more-over had
never had measles, merely the measles vaccine). His characteristic
patience nonetheless paid off, yielding a tiny handful of virus
particles from some patients that could be coaxed to begin growing
again, if only in laboratory cell culture.
In other patients only defective viruses that were unable to grow had
remained so many years after the original measles infection.
Rather than concluding the measles virus had nothing to do with SSPE,
he employed the new logic of virus hunting to argue that a defective
measles virus caused SSPE!
Koprowski continued this line of SSPE research for several more
years. But in 1985 Gajdusek himself entered the SSPE fray, publishing
a paper with leading AIDS researcher Robert Gallo in which they
proposed that HIV, the supposed AIDS virus, caused SSPE while
remaining latent. With hardly a blink, several leading virologists
jettisoned the old measles-SSPE hypothesis in favor of a newly
popular, but equally innocent, virus.
Multiple sclerosis (MS), the notorious disease that also attacks the
nervous system and ultimately kills, has provided yet another
opportunity for the virus hunters.
First, they blamed the measles virus starting in the 1960s, since
many MS patients had antibodies against the virus. Ten years later
others suggested the mumps virus, which is similar to measles. The
early I980s brought the coronavirus hypothesis of MS, the category of
virus better known for causing some colds. In 1985, with Gajdusek
stealing his thunder for SSPE, Koprowski also published a scientific
paper that year in Nature with Robert Gallo, in this case arguing
that some virus similar to HIV now caused MS. Unfortunately for
Koprowski, even this hypothesis was abandoned within just a few years.
Phantom Viruses and Big Bucks
Most virus hunters prefer chasing real, if arguably harmless, viruses
as their deadly enemies. But Gajdusek's "unconventional" viruses -
the ones neither he nor anyone else have ever found - have been
making a comeback in recent years. Given the abundance of research
dollars being poured into biomedical science by the NIH and other
agencies, opportunistic virus hunters have been finding creative ways
to cash in. One increasingly successful method utilizes modern
biotechnology to isolate viruses that may not even exist.
Hepatitis, or liver disease, has yielded profitable virus-hunting
opportunities in recent years. Hepatitis can be a truly painful
affliction, starting like a flu but progressing to more severe
symptoms, including high fevers and yellow skin. At least three
varieties seem to exist.
Hepatitis A is infectious, spread through unsanitary conditions, and
is caused by a conventional virus.
Hepatitis B also results from a virus (discovered in the 1960s) and
is transmitted mostly between heroin addicts sharing needles, among
sexually active and promiscuous people, or in the Third World from
mothers to their children around the time of birth.
A third type of hepatitis was found in the 1970s, again restricted to
heroin addicts, alcoholics, and patients who have received blood transfusions.
Most scientists assumed these cases were either hepatitis A or B,
until widespread testing revealed neither virus in the victims.
Roughly thirty-five thousand Americans die each year of any type of
the disease, a fraction of those from this "non-A, non-B hepatitis,"
as it was known for years.
Today it is called hepatitis C. This form of hepatitis does not
behave as an infectious disease, for it rigidly confines itself to
people in well- defined risk groups rather than spreading to larger
populations or even to the doctors treating hepatitis patients. Yet
virologists have been eyeing the disease from the beginning, hoping
one day to find a virus causing it.
That day arrived in 1987. The laboratory for the job was no less than
the research facility of the Chiron Corporation, a biotechnology
company located directly across the bay from San Francisco. Equipped
with the most advanced techniques, a research team started its search
in 1982 by injecting blood from patients into chimpanzees. None of
monkeys contracted hepatitis, although subtle signs vaguely
resembling infection or reddening did appear.
For the next step, the scientists probed liver tissue for a virus.
None could be found. Growing desperate, the team fished even for the
smallest print of a virus, finally coming across and greatly
amplifying a small piece of genetic information, encoded in a
molecule known as ribonucleic acid (RNA), that did not seem to belong
in the host's genetic code.
This fragment of presumably foreign RNA, the researchers assumed,
must be the genetic information of some undetected virus. Whatever it
was, liver tissue contains it only in barely detectable amounts. Only
about half of all hepatitis C patients contain the rare foreign RNA.
And in those who contain it, there is only one RNA molecule for every
ten liver cells - hardly a plausible cause for disease.
The Chiron team used newly available technology to reconstruct pieces
of the mystery virus. Now they could test patients for antibodies
against this hypothetical virus and soon discovered that only a
slight majority of hepatitis C patients had any evidence ofthese
antibodies in their blood.
1. Koch's first postulate, of course, demands that a truly harmful
virus be found in huge quantities in every single patient.
2. His second postulate requires that the virus particles be
isolated and grown, although this supposed hepatitis virus has never
been found intact.
3. And the third postulate insists that newly infected animals, such
as chimpanzees, should get the disease when injected with the virus.
This hypothetical microbe fails all three tests. But Koch's standards
were the furthest thing from the minds of the Chiron scientists when
they announced in 1987 that they had finally found the "hepatitis C" virus.
Now more paradoxes are confronting the viral hypothesis. Huge numbers
of people testing positive for the hypothetical hepatitis C virus
never develop any symptoms of the disease, even though the "virus" is
no less active in their bodies than in hepatitis patients.
And according to a recent large-scale study of people watched for
eighteen years, those with signs of "infection" live just as long as
those without. Despite these facts, scientists defend their
still-elusive virus by giving it an undefined latent period extending
into decades.
Paradoxes like these no longer faze the virus-hunting research
establishment. Indeed, rewards are generally showered upon any new
virus hypothesis, no matter how bizarre. Chiron did not spend five
years creating its own virus for nothing. Having patented the test
for the virus, the company put it into production and began a
publicity campaign to win powerful allies.
The first step was a paper published in Science, the world's most
prestigious science magazine, edited by Dan Koshland, Jr., professor
of molecular and cell biology at the University of California at Berkeley.
Edward Penhoet, chief executive officer for Chiron, also holds a
position as professor of molecular and cell biology at the University
of California at Berkeley. The NIH-supported virology establishment
soon lent the full weight of its credibility to the hepatitis C virus
camp. As Chiron's CEO boasted, "We have a blockbuster product."
A regulatory order from the Food and Drug Administration (FDA) to
test the blood supply would reap enormous sales for Chiron.
Their big chance presented itself in late 1988 as a special request
from Japanese Emperor Hirohito's doctors. The monarch was dying and
constantly needed blood transfusions; could Chiron provide a test to
make sure he received no blood tainted with hepatitis C? The biotech
company jumped at the opportunity, making for itself such a name in
Japan that the Tokyo government gave the product its approval within one year.
The emperor died in the meantime, but excitement over Chiron's test
was fueled when the Japanese government placed hepatitis C high on
its medical priority list. Chiron's test kit now earns some $60
million annually in that country alone.
By the middle of 1990, the United States followed suit.
The FDA not only approved the test, but even recommended the
universal testing of donated blood.
The American Association of Blood Banks followed suit by mandating
the $5 test for all 12 million blood donations made each year in this
country - raking in another $60 million annually for Chiron while
raising the nation's medical costs that much more.
And all this testing is being done for a virus that has never been isolated.
Profits from the test kit have generated another all-too-common part
of virus hunting. With Chiron's new income from the hepatitis C test,
Penhoet's company bought out Cetus, another biotech company, founded
by Donald Glaser, who, like Penhoet, also holds a position as
professor of molecular and cell biology at the University of
California at Berkeley. And Chiron made an unrestricted donation of
about 12 million to the Department of Molecular and Cell Biology at
the University of California at Berkeley that generates $100,000 in
interest each year.
Unfortunately for Peter Duesberg, who belongs to the same department,
his supervisor is yet another professor who consults for Chiron
Corporation - and displays little sympathy for Duesberg for
challenging modern virus hunting by restricting his academic duties
to undergraduate student teaching and by not appointing him to
decision-making committees.
Such conflicts of interest have become standard fixtures in
university biology departments.
The modern biomedical research establishment differs radically from
any previous scientific program in history. Driven by vast infusions
of federal and commercial money, it has grown into an enormous and
powerful bureaucracy that greatly amplifies its successes, all the
while stifling dissent.
Such a process can no longer be called science, which by definition
depends on self-correction by internal challenge and debate.
Despite their popularity among scientists and their companies,
"latent," "slow," and "defective" viruses have achieved only little
prominence as hypothetical causes of degenerative diseases before the
AIDS era. Their hypothetical role in degenerative diseases, which
result from the loss of large numbers of cells, remained confined to
rare, exclusive illnesses like kuru and hepatitis C.
However, because latent, slow, and defective viruses cannot kill
cells, such "viruses" eventually achieved prominence as hypothetical
causes of cancer and thus entered the courts of health care and
medical research. The next chapter describes the terms under which
these viruses were promoted as causes of cancer and how some of these
terms were eventually used to promote latent, slow, and defective
viruses as causes of degenerative diseases including, above all, AIDS.
Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto
*****
http://www.duesberg.com/
Peter H. Duesberg, Ph.D. is a professor of Molecular and Cell Biology
at the University of California, Berkeley. Biographical Sketch
http://www.duesberg.com/about/pdbio.html
He isolated the first cancer gene through his work on
retroviruses in 1970, and mapped the genetic structure of these
viruses. This, and his subsequent work in the same field, resulted in
his election to the National Academy of Sciences in 1986. He is also
the recipient of a seven-year Outstanding Investigator Grant from the
National Institutes of Health.
On the basis of his experience with retroviruses, Duesberg has
challenged the virus-AIDS hypothesis in the pages of such journals as
Cancer Research, Lancet, Proceedings of the National Academy of
Sciences, Science, Nature, Journal of AIDS, AIDS Forschung,
Biomedicine and Pharmacotherapeutics, New England Journal of Medicine
and Research in Immunology. He has instead proposed the hypothesis
that the various American/European AIDS diseases are brought on by
the long-term consumption of recreational drugs and/or AZT itself,
which is prescribed to prevent or treat AIDS. See The AIDS Dilemma:
Drug diseases blamed on a passenger virus.
For a detailed discussion of American/European AIDS as opposed
to African AIDS, see The African AIDS Epidemic: New and Contagious or
Old Under a New Name.
This is Duesberg's official site, containing his written works
on the subject, as well as other scientists that support his views
such as Kary B. Mullis. Kary Mullis won the 1993 Nobel Prize in
Chemistry for his invention of the polymerase chain reaction
technique for detecting DNA. This is the technique used to search for
fragments of HIV in AIDS patients.
Prof. Duesberg's findings have been a thorn in the side of the
medical establishment and drug companies since 1987. Instead of
engaging in scientific debate, however, the only response has been to
cut-off funding to further test Professor's Duesberg's hypothesis.
You can show your support by contributing a tax deductible
donation to help support Prof. Duesberg's lab at the University of
California Berkeley.
Sheri Nakken, R.N., MA, Hahnemannian Homeopath
http://homeopathycures.wordpress.com/ &
http://vaccinationdangers.wordpress.com/
ONLINE/Email classes in Homeopathy; Vaccine Dangers; Childhood Diseases
Next classes start May 26
This is a great article showing how real the whole issue of viruses
is and how baseless the issue of vaccines for so-called viral illnesses are.
Sheri
BIO for author Peter Duesberg at the end..........(On the basis of
his experience with retroviruses, Duesberg has challenged the
virus-AIDS hypothesis)
http://www.mercola.com/2000/dec/31/slow_virus.htm
Dr. Joseph Mercola
Slow Viruses: The Original Sin Against the Laws of Virology
By Peter H. Duesberg and Bryan J. Ellison
from "INVENTING THE AIDS VIRUS", Regnery publishing, 1996
Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto
From the discovery of tobacco mosaic virus through the polio
epidemic, scientists have found and legitimately blamed many viruses
for a variety of diseases, each having passed the acid test of Koch's
postulates. But for every truly dangerous virus, many more perfectly
harmless passenger viruses can be found in humans and animals.
NIH-sponsored polio research during the late 1950s proved the point.
Researchers trying to isolate new strains of poliovirus accidentally
found numerous closely related passenger viruses -- such as Coxsackie
and echoviruses - that, like polio, infected the digestive system.
Scientists classified some of these viruses as "orphans" - viruses
without corresponding diseases.
The virus hunters could not bring themselves to believe microbes
could exist without being harmful and expected even these "orphan"
viruses would someday find appropriate sicknesses.
When trying to blame a passenger virus for a disease, how-ever, one
nagging problem haunts the virus hunter: The laws of virology dictate
that the illness will strike the victim soon after infection. When
microbes infect a new host, they cause sickness within days or weeks
at most. In order to cause disease, viruses need to grow into
sufficient numbers to take over the body; otherwise, the host's
immune defenses will neutralize the invader and prevent disease altogether.
The rate-determining step of such fast, exponential growth is the
generation time of the virus. Since the generation time of all human
viruses is between eight and forty-eight hours, and since the
infected cell produces one hundred to one thousand viruses per day,
viruses multiply exponentially, increasing in numbers hundred- to
thousand-fold per day. Within a week or two, one hundred trillion
(1014) cells can be produced-one for each of the one hundred trillion
cells in the human body.
Therefore, if scientists wish to convict an innocent virus, they must
invent a new property for it that allows the virus to violate the
laws of virology.
For example, they can hypothesize a "latent period" of months or
years between the time the virus invades the body and the appearance
of symptoms - hence, a "slow" virus.
However, the slow virus concept has never been reconciled with the
short generation time of viruses and the immune system. Once the
virus lies totally dormant, an intact immune system will never allow
any virus to be reactivated to multiply into numbers that would
threaten the host.
For a virus to be reactivated, the immune system first must be
destroyed by something else - the real cause of a disease. A
reactivated virus would just contribute an opportunistic infection.
Thus, there are no slow viruses, only slow virologists.
A conventional virus could, however, be slow acting in a defective
immune system.
Indeed, some exceptional victims suffer pre-existing health problems
that prevent their immune systems from reacting decisively against
the virus, allowing it to continue growing and damaging the host for
a long period of time. This can happen with virtually any type of
virus, but it is extremely rare. When such a chronic infection does
occur, as with a small percentage of hepatitis cases whose immune
system is damaged by alcoholism or intravenous drug addiction, the
virus keeps growing abundantly in the body and can easily be found by
experimental tests.
Other germs, like herpes viruses, can hide out in some recess of the
body, breaking out periodically to strike again when the immune
system passes a seasonal low.In both examples, only the weakened
immune system of the host allows the infection to smolder or
occasionally reappear from hibernation.
By contrast, a slow virus is an invention credited with the natural
ability to cause disease only years after infection - termed the
"latent period" - in previously healthy persons, regardless of the
state of their immunity. Such a concept allows scientists to blame a
long-neutralized virus for any disease that appears decades after
infection. The slow virus is the original sin against the laws of virology.
The slow-virus or latent-period concept, now used to connect HIV with
AIDS, can be traced back to the days of the war on polio. The
researcher who popularized this modern myth is today an authority for
AIDS researchers and one whose career epitomizes the evolution of the
virus hunters over the past three decades.
Dr. Carleton Gajdusek is a pediatrician who has worked as a
virologist at the NIH for decades. Having spent a great deal of time
studying contagious childhood diseases around the world, Gajdusek was
sponsored by the NFIP and sent to New Guinea in 1957.
There, a doctor with the local health department introduced him to a
disease called kuru, a mysterious ailment that attacked the brain,
rendering the victim increasingly spasmodic or paralyzed until death
within months. The syndrome existed only among the thirty-five
thousand tribal villagers in one set of valleys, mostly the Fore tribe.
Before Gajdusek's arrival, no outsider had ever described kuru,
although the Fore tribesmen told him the condition had begun
appearing a few decades earlier.
Gajdusek's initial study assumed the disease to be infectious. He
reported that the natives routinely cannibalized the brains of
relatives for ritual purposes, a practice that they told him had
begun around the same time as the arrival of kuru.
Gajdusek later explained to one interviewer that cannibalism
"expressed love for their dead relatives," and that it also "provided
a good source of protein for a meat-starved community."
Gajdusek decided that kuru was transmitted by the eating of deceased
victims' brains. Yet when he searched for a virus, he ran into a
baffling absence of evidence. None of the typical signs of infection
could be found in the patients. Their bodies showed no inflammation
and no fever, no changes were registered in their supposedly infected
spinal fluid, their immune systems failed to react as if any microbe
had invaded the body, and those people with suppressed immune
defenses had no greater risk of catching the disease.
Another scientific group soon arrived from Australia and concluded
that kuru might be genetically inherited.
Upon arriving back in the United States, Gajdusek was hired by the
NIH to work at its institute for studying neurological disease. While
continuing to monitor kuru incidence, he devoted his time to
laboratory study of the condition.
Word of his discovery of kuru meanwhile made its way to England,
where another virus hunter was investigating a sheep disease known as
scrapie, which involved symptoms of brain degeneration. The English
researcher suggested to Gajdusek that kuru might be caused by a slow
virus, one with a long latent period.
Gajdusek was immediately hooked by the revolutionary idea, despite
his own "misgivings" that genes, toxins, or nutritional deficiencies
might be the cause of kuru.
Again determined to find an elusive virus, he tried to transmit kuru
from victims to chimpanzees. But none of the animals became sick when
injected with blood, urine, or other bodily fluids from kuru
patients, nor from the cerebrospinal fluid that surrounds the brain,
which should have been full of the alleged brain-destroying virus.
Indeed, the monkeys contracted no disease even from eating
kuru-affected brains - the authentic animal model of cannibalism.
Only one bizarre experiment did work, in which the brains of kuru
patients were ground into a fine mush and injected directly into the
brains of live monkeys through holes drilled in their skulls.
Ultimately, some of the experimental monkeys suffered coordination
and movement problems.
Surprisingly, though, even this extreme method could not transfer
kuru to dozens of other animal species. And no virus could be seen in
the brain tissue, even using the best electron microscopes.
At this point, one might expect Gajdusek would have suspected
something was seriously wrong with his virus hypothesis. If evidence
for the invisible virus could not be found anywhere but in unpurified
brain tissue, if it did not elicit any defensive reactions by the
body, and if it could not be transmitted in pure form to animals,
then probably no virus existed at all. The homogenized brain tissue
of dead kuru patients - full of every imaginable protein and other
compounds-should in itself be toxic when inoculated into monkeys' brains.
Nevertheless, the sick monkeys convinced Gajdusek and his colleagues
he had found a virus. Since he could not isolate it apart from the
brain tissue, he decided to study the virus and its structure with a
standard experiment.
He would define which chemical and physical treatments would destroy
the microbe, thereby gathering clues about its nature. But to his
astonishment, almost nothing seemed to harm the mystery germ.
Powerful chemicals, acids and bases, boiling temperatures,
ultraviolet and ionizing radiation, ultrasound-no matter how he
treated the brain tissue, it still caused "kuru" in his lab monkeys.
Further tests also proved that no foreign genetic material, which all
viruses require for their existence, could be found anywhere in
kuru-affected brains.
Employing the strongest virus-destroying treatments, Gajdusek had
failed to render the kuru brain tissue harmless in his experiments.
His results lent themselves to one obvious interpretation: No virus
existed in the first place, so it could not possibly be destroyed.
But Gajdusek clung to his virus hypothesis. Despite his disappointing
experiments, he turned the results upside down and argued that the
"kuru virus" was actually a new type of super-microbe or, as he put
it, an "unconventional virus." This new virus also needed to act as a
slow virus, since long periods of time elapsed between an act of
cannibalism and the onset of kuru; he liberally suggested latent
periods extending into years or even decades.
At an earlier time, and in another context, Gajdusek probably would
have been ignored by orthodox scientists. But he offered this
hypothesis to a generation of scientists dominated and impressed by
virus hunters.
The year was 1965, polio had largely disappeared, and the burgeoning
ranks of NIH-funded virologists welcomed any new research direction
on which to use their skills. Thus, they embraced Gajdusek's slow
virus hypothesis enthusiastically.
They listened uncritically when he claimed a similar unconventional
virus caused Creutzfeld-Jakob disease, a rare brain disorder that
seems to strike mostly Westerners having undergone previous brain
surgery (obviously such medical operations might well be suspected as
the real cause).
Gajdusek proposed slow or even unconventional viruses as the causes
of a huge laundry list of nerve and brain disorders, ranging from
scrapie in sheep to multiple sclerosis and Alzheimer's disease in
humans, and he was taken seriously even though he offered no
proof.Entranced, his peers awarded him the 1976 Nobel Prize for
medicine, specifically for the kuru and Creutzfeld-Jakob viruses he
has yet to find. And the NIH promoted him to head its Laboratory of
Central Nervous System Studies.
In the meantime another crucial, if embarrassing, bit of information
has emerged as a challenge to Gajdusek's virus-kuru hypothesis. The
published transcript of his Nobel acceptance speech, in a 1977 issue
of Science magazine, included a photo ostensibly showing New Guinea
natives eating their cannibalistic meal. The photo is not very clear.
When colleagues asked Gajdusek if the photo truly showed cannibalism,
he admitted the meal was merely roast pork. According to Science, "He
never publishes actual pictures of cannibalism, he says, because they
are 'too offensive.'" Unconvinced, anthropologist Lyle Steadman of
Arizona State University has investigated and directly challenged
Gajdusek, claiming "there is no evidence of cannibalism in New Guinea."
Steadman, who spent two years doing fieldwork in New Guinea, noted
that he often heard tales of cannibalism but when he probed, "the
evidence evaporated."
Gajdusek, angered by the hint of malfeasance, has insisted that "he
has actual photographs of cannibalism, but he would never publish
them because they 'so offend the relatives of the people who used to
do it.'" This statement contradicts his earlier claims that the
tribesman proudly ate their dead relatives out of respect, quitting
the practice only in deference to outside pressure from government
authorities.
For evidence of cannibalism, Gajdusek also cited Australian arrests
of tribesmen for the alleged crime - which, as it turned out, were
based on hearsay accusations. So perhaps New Guinea natives stand
falsely accused of ritual cannibalism.
In addition, few people outside of Gajdusek's original research team
have ever personally witnessed kuru victims. This means we also
depend on his own descriptions and statistics for our knowledge of
the disease itself, particularly since he claims cannibalism and kuru
both ceased to exist within a few years after his 1957 trip. Phantom
viruses, transmitted through phantom cannibalism, cause phantom disease.
Yet Gajdusek has reshaped the thinking of an entire generation of
biologists, his seductive message of slow viruses having landed on
eager ears. He and the virus hunters inspired by him have built
careers chasing viruses and attributing them to latent periods in
order to connect them to noninfectious diseases.
SMON, the nerve-destroying disease that struck Japan during the
1960s, became one unfortunate example. Japanese virologists, greatly
impressed with Gajdusek's accomplishments, spent years searching for
slow viruses they presumed would cause the disease and thereby
delayed finding the true cause - a prescribed medication.
Another example of a pointless virus hunt involved diabetes.
Beginning in the early 1960s, some scientists tried to blame this
noncontagious syndrome on the virus that also causes mumps. The
evidence has been pathetically sparse, forcing virologists to point
to occasional children who become diabetic after they have also
suffered mumps or, if they really stretch their case, to argue that
both mumps and diabetes become most common during the same annual
season in one county of New York.
Having become soldiers without a war, veteran polio virologists
invaded the diabetes field as well, proposing since the early 1970s
that Coxsackie viruses may cause the disease. Antibodies against
several strains of these harmless viruses, first discovered as
by-products of polio research, have been found in a few diabetic children.
But between 20 percent and 70 percent of young diabetics have never
been infected, and the remainder have already neutralized the virus
with their immune systems long before the onset of diabetes.
Apparently, an equal percentage of non-diabetic children have also
been infected with these Coxsackie viruses. Needless to say, none of
the above viruses meets Koch's postulates for causing diabetes.
Hilary Koprowski, like Gajdusek, typifies the modern virus hunter.
Although Koprowski's virology career began earlier, Gajdusek's work
helped rescue Koprowski from the obsolescence that threatened polio
researchers after the war on polio. Like so many of his colleagues,
he found his newest calling in the war on AIDS.
Koprowski's work on viruses started at the Rockefeller Institute in
New York. By the late 1940s he moved across town to the Lederle
pharmaceutical company, where he worked feverishly to develop a polio
vaccine. By 1954 he had invented one, but Jonas Salk was announcing
the field trials for another vaccine, and Koprowski's already-tested
product was shunted aside by Salk's public acclaim.
Koprowski left Lederle in I957 to take a position as director of the
privately endowed Wistar Institute of Pennsylvania, where he began
tests on humans and stepped up the campaign to get approval for his
vaccine. By now Albert Sabin had tested his own polio immunization on
millions of people in foreign countries, completely overshadowing
Koprowski's equally successful but less-promoted vaccine.
Nevertheless, Koprowski's day did arrive. His vaccine became the
standard used by the World Health Organization in America during the
late 1950s and 1960s.
In the meantime he spent several years studying the rabies virus and
creating a vaccine against that virus, which attacks the brain and
nervous system. But because rabies is relatively rare, Koprowski's
vaccine never achieved the stardom of other immunizations. More
important, however, his rabies research placed him squarely in the
field of neurological diseases just in time to meet up with
Gajdusek's kuru work.
The news of slow viruses enticed Koprowski with visions of
groundbreaking science. He quickly realized that the notion of slow
viruses could become a useful tool, allowing him to source slow,
noninfectious diseases to viruses, so long believed to be fast-acting
agents. He participated as a "program advisor" in Gajdusek's first
major conference on slow and unconventional viruses held in 1964 at
the NIH head-quarters in Bethesda, Maryland. From that point forward,
Hilary Koprowski joined the new virus-hunting trend from which he
would never turn back.
His first big opportunity to take a crack at slow viruses came at the
end of the 1960s. Subacute sclerosing panencephalitis (SSPE), a
mouthful of a name for such a rare condition, attacks a small number
of schoolchildren and teenagers each year, causing dementia, learning
disabilities, and finally death.
Doctors first recognized SSPE in the 1930s, and by the 1960s the
virus hunters were searching for an SSPE germ. At that time, the most
fashionable viruses for research belonged to the myxovirus family,
which included the viruses that caused influenza, measles, and mumps.
Animal virologists therefore started by probing for signs of myxoviruses.
Excitement mounted after trace quantities of measles virus were
detected in the brains of SSPE patients, and in 1967 most of the
victims were found to have antibodies against measles. The facts that
SSPE affected only one of every million measles -- infected people
and that this rare condition appeared from one to ten years after
infection by measles were no longer a problem: Researchers simply
hypothesized a one- to ten-year latency period. Little wonder they
could also easily rationalize that one virus could cause two totally
different diseases.
Koprowski's foray into SSPE research began in the early 1970s. He
began isolating the measles virus from dying SSPE victims, a nearly
impossible task because their immune systems had long before
completely neutralized the virus (some SSPE cases, more-over had
never had measles, merely the measles vaccine). His characteristic
patience nonetheless paid off, yielding a tiny handful of virus
particles from some patients that could be coaxed to begin growing
again, if only in laboratory cell culture.
In other patients only defective viruses that were unable to grow had
remained so many years after the original measles infection.
Rather than concluding the measles virus had nothing to do with SSPE,
he employed the new logic of virus hunting to argue that a defective
measles virus caused SSPE!
Koprowski continued this line of SSPE research for several more
years. But in 1985 Gajdusek himself entered the SSPE fray, publishing
a paper with leading AIDS researcher Robert Gallo in which they
proposed that HIV, the supposed AIDS virus, caused SSPE while
remaining latent. With hardly a blink, several leading virologists
jettisoned the old measles-SSPE hypothesis in favor of a newly
popular, but equally innocent, virus.
Multiple sclerosis (MS), the notorious disease that also attacks the
nervous system and ultimately kills, has provided yet another
opportunity for the virus hunters.
First, they blamed the measles virus starting in the 1960s, since
many MS patients had antibodies against the virus. Ten years later
others suggested the mumps virus, which is similar to measles. The
early I980s brought the coronavirus hypothesis of MS, the category of
virus better known for causing some colds. In 1985, with Gajdusek
stealing his thunder for SSPE, Koprowski also published a scientific
paper that year in Nature with Robert Gallo, in this case arguing
that some virus similar to HIV now caused MS. Unfortunately for
Koprowski, even this hypothesis was abandoned within just a few years.
Phantom Viruses and Big Bucks
Most virus hunters prefer chasing real, if arguably harmless, viruses
as their deadly enemies. But Gajdusek's "unconventional" viruses -
the ones neither he nor anyone else have ever found - have been
making a comeback in recent years. Given the abundance of research
dollars being poured into biomedical science by the NIH and other
agencies, opportunistic virus hunters have been finding creative ways
to cash in. One increasingly successful method utilizes modern
biotechnology to isolate viruses that may not even exist.
Hepatitis, or liver disease, has yielded profitable virus-hunting
opportunities in recent years. Hepatitis can be a truly painful
affliction, starting like a flu but progressing to more severe
symptoms, including high fevers and yellow skin. At least three
varieties seem to exist.
Hepatitis A is infectious, spread through unsanitary conditions, and
is caused by a conventional virus.
Hepatitis B also results from a virus (discovered in the 1960s) and
is transmitted mostly between heroin addicts sharing needles, among
sexually active and promiscuous people, or in the Third World from
mothers to their children around the time of birth.
A third type of hepatitis was found in the 1970s, again restricted to
heroin addicts, alcoholics, and patients who have received blood transfusions.
Most scientists assumed these cases were either hepatitis A or B,
until widespread testing revealed neither virus in the victims.
Roughly thirty-five thousand Americans die each year of any type of
the disease, a fraction of those from this "non-A, non-B hepatitis,"
as it was known for years.
Today it is called hepatitis C. This form of hepatitis does not
behave as an infectious disease, for it rigidly confines itself to
people in well- defined risk groups rather than spreading to larger
populations or even to the doctors treating hepatitis patients. Yet
virologists have been eyeing the disease from the beginning, hoping
one day to find a virus causing it.
That day arrived in 1987. The laboratory for the job was no less than
the research facility of the Chiron Corporation, a biotechnology
company located directly across the bay from San Francisco. Equipped
with the most advanced techniques, a research team started its search
in 1982 by injecting blood from patients into chimpanzees. None of
monkeys contracted hepatitis, although subtle signs vaguely
resembling infection or reddening did appear.
For the next step, the scientists probed liver tissue for a virus.
None could be found. Growing desperate, the team fished even for the
smallest print of a virus, finally coming across and greatly
amplifying a small piece of genetic information, encoded in a
molecule known as ribonucleic acid (RNA), that did not seem to belong
in the host's genetic code.
This fragment of presumably foreign RNA, the researchers assumed,
must be the genetic information of some undetected virus. Whatever it
was, liver tissue contains it only in barely detectable amounts. Only
about half of all hepatitis C patients contain the rare foreign RNA.
And in those who contain it, there is only one RNA molecule for every
ten liver cells - hardly a plausible cause for disease.
The Chiron team used newly available technology to reconstruct pieces
of the mystery virus. Now they could test patients for antibodies
against this hypothetical virus and soon discovered that only a
slight majority of hepatitis C patients had any evidence ofthese
antibodies in their blood.
1. Koch's first postulate, of course, demands that a truly harmful
virus be found in huge quantities in every single patient.
2. His second postulate requires that the virus particles be
isolated and grown, although this supposed hepatitis virus has never
been found intact.
3. And the third postulate insists that newly infected animals, such
as chimpanzees, should get the disease when injected with the virus.
This hypothetical microbe fails all three tests. But Koch's standards
were the furthest thing from the minds of the Chiron scientists when
they announced in 1987 that they had finally found the "hepatitis C" virus.
Now more paradoxes are confronting the viral hypothesis. Huge numbers
of people testing positive for the hypothetical hepatitis C virus
never develop any symptoms of the disease, even though the "virus" is
no less active in their bodies than in hepatitis patients.
And according to a recent large-scale study of people watched for
eighteen years, those with signs of "infection" live just as long as
those without. Despite these facts, scientists defend their
still-elusive virus by giving it an undefined latent period extending
into decades.
Paradoxes like these no longer faze the virus-hunting research
establishment. Indeed, rewards are generally showered upon any new
virus hypothesis, no matter how bizarre. Chiron did not spend five
years creating its own virus for nothing. Having patented the test
for the virus, the company put it into production and began a
publicity campaign to win powerful allies.
The first step was a paper published in Science, the world's most
prestigious science magazine, edited by Dan Koshland, Jr., professor
of molecular and cell biology at the University of California at Berkeley.
Edward Penhoet, chief executive officer for Chiron, also holds a
position as professor of molecular and cell biology at the University
of California at Berkeley. The NIH-supported virology establishment
soon lent the full weight of its credibility to the hepatitis C virus
camp. As Chiron's CEO boasted, "We have a blockbuster product."
A regulatory order from the Food and Drug Administration (FDA) to
test the blood supply would reap enormous sales for Chiron.
Their big chance presented itself in late 1988 as a special request
from Japanese Emperor Hirohito's doctors. The monarch was dying and
constantly needed blood transfusions; could Chiron provide a test to
make sure he received no blood tainted with hepatitis C? The biotech
company jumped at the opportunity, making for itself such a name in
Japan that the Tokyo government gave the product its approval within one year.
The emperor died in the meantime, but excitement over Chiron's test
was fueled when the Japanese government placed hepatitis C high on
its medical priority list. Chiron's test kit now earns some $60
million annually in that country alone.
By the middle of 1990, the United States followed suit.
The FDA not only approved the test, but even recommended the
universal testing of donated blood.
The American Association of Blood Banks followed suit by mandating
the $5 test for all 12 million blood donations made each year in this
country - raking in another $60 million annually for Chiron while
raising the nation's medical costs that much more.
And all this testing is being done for a virus that has never been isolated.
Profits from the test kit have generated another all-too-common part
of virus hunting. With Chiron's new income from the hepatitis C test,
Penhoet's company bought out Cetus, another biotech company, founded
by Donald Glaser, who, like Penhoet, also holds a position as
professor of molecular and cell biology at the University of
California at Berkeley. And Chiron made an unrestricted donation of
about 12 million to the Department of Molecular and Cell Biology at
the University of California at Berkeley that generates $100,000 in
interest each year.
Unfortunately for Peter Duesberg, who belongs to the same department,
his supervisor is yet another professor who consults for Chiron
Corporation - and displays little sympathy for Duesberg for
challenging modern virus hunting by restricting his academic duties
to undergraduate student teaching and by not appointing him to
decision-making committees.
Such conflicts of interest have become standard fixtures in
university biology departments.
The modern biomedical research establishment differs radically from
any previous scientific program in history. Driven by vast infusions
of federal and commercial money, it has grown into an enormous and
powerful bureaucracy that greatly amplifies its successes, all the
while stifling dissent.
Such a process can no longer be called science, which by definition
depends on self-correction by internal challenge and debate.
Despite their popularity among scientists and their companies,
"latent," "slow," and "defective" viruses have achieved only little
prominence as hypothetical causes of degenerative diseases before the
AIDS era. Their hypothetical role in degenerative diseases, which
result from the loss of large numbers of cells, remained confined to
rare, exclusive illnesses like kuru and hepatitis C.
However, because latent, slow, and defective viruses cannot kill
cells, such "viruses" eventually achieved prominence as hypothetical
causes of cancer and thus entered the courts of health care and
medical research. The next chapter describes the terms under which
these viruses were promoted as causes of cancer and how some of these
terms were eventually used to promote latent, slow, and defective
viruses as causes of degenerative diseases including, above all, AIDS.
Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto
*****
http://www.duesberg.com/
Peter H. Duesberg, Ph.D. is a professor of Molecular and Cell Biology
at the University of California, Berkeley. Biographical Sketch
http://www.duesberg.com/about/pdbio.html
He isolated the first cancer gene through his work on
retroviruses in 1970, and mapped the genetic structure of these
viruses. This, and his subsequent work in the same field, resulted in
his election to the National Academy of Sciences in 1986. He is also
the recipient of a seven-year Outstanding Investigator Grant from the
National Institutes of Health.
On the basis of his experience with retroviruses, Duesberg has
challenged the virus-AIDS hypothesis in the pages of such journals as
Cancer Research, Lancet, Proceedings of the National Academy of
Sciences, Science, Nature, Journal of AIDS, AIDS Forschung,
Biomedicine and Pharmacotherapeutics, New England Journal of Medicine
and Research in Immunology. He has instead proposed the hypothesis
that the various American/European AIDS diseases are brought on by
the long-term consumption of recreational drugs and/or AZT itself,
which is prescribed to prevent or treat AIDS. See The AIDS Dilemma:
Drug diseases blamed on a passenger virus.
For a detailed discussion of American/European AIDS as opposed
to African AIDS, see The African AIDS Epidemic: New and Contagious or
Old Under a New Name.
This is Duesberg's official site, containing his written works
on the subject, as well as other scientists that support his views
such as Kary B. Mullis. Kary Mullis won the 1993 Nobel Prize in
Chemistry for his invention of the polymerase chain reaction
technique for detecting DNA. This is the technique used to search for
fragments of HIV in AIDS patients.
Prof. Duesberg's findings have been a thorn in the side of the
medical establishment and drug companies since 1987. Instead of
engaging in scientific debate, however, the only response has been to
cut-off funding to further test Professor's Duesberg's hypothesis.
You can show your support by contributing a tax deductible
donation to help support Prof. Duesberg's lab at the University of
California Berkeley.
Sheri Nakken, R.N., MA, Hahnemannian Homeopath
http://homeopathycures.wordpress.com/ &
http://vaccinationdangers.wordpress.com/
ONLINE/Email classes in Homeopathy; Vaccine Dangers; Childhood Diseases
Next classes start May 26
-
Sheri Nakken
- Posts: 3999
- Joined: Wed Apr 01, 2020 10:00 pm
Re: Slow Viruses: The Original Sin Against the Laws of Virology
-Slow Viruses: The Original Sin Against the Laws of Virology
This is a great article showing how real the whole issue of viruses
is (not) and how baseless the issue of vaccines for so-called viral
illnesses are.
And what a scam and lie 'slow' viruses are.
Don't be quick to buy into this lie.
Long article but excellent
http://www.healtoronto.com/slowvirus.html
Slow Viruses: The Original Sin Against the Laws of Virology
By Peter H. Duesberg and Bryan J. Ellison
from "INVENTING THE AIDS VIRUS", Regnery publishing, 1996
Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto
From the discovery of tobacco mosaic virus through the polio
epidemic, scientists have found and legitimately blamed many viruses
for a variety of diseases, each having passed the acid test of Koch's
postulates. But for every truly dangerous virus, many more perfectly
harmless passenger viruses can be found in humans and animals.
NIH-sponsored polio research during the late 1950s proved the point.
Researchers trying to isolate new strains of poliovirus accidentally
found numerous closely related passenger viruses -- such as Coxsackie
and echoviruses - that, like polio, infected the digestive system.
Scientists classified some of these viruses as "orphans" - viruses
without corresponding diseases.
The virus hunters could not bring themselves to believe microbes
could exist without being harmful and expected even these "orphan"
viruses would someday find appropriate sicknesses.
When trying to blame a passenger virus for a disease, how-ever, one
nagging problem haunts the virus hunter: The laws of virology dictate
that the illness will strike the victim soon after infection. When
microbes infect a new host, they cause sickness within days or weeks
at most. In order to cause disease, viruses need to grow into
sufficient numbers to take over the body; otherwise, the host's
immune defenses will neutralize the invader and prevent disease altogether.
The rate-determining step of such fast, exponential growth is the
generation time of the virus. Since the generation time of all human
viruses is between eight and forty-eight hours, and since the
infected cell produces one hundred to one thousand viruses per day,
viruses multiply exponentially, increasing in numbers hundred- to
thousand-fold per day. Within a week or two, one hundred trillion
(1014) cells can be produced-one for each of the one hundred trillion
cells in the human body.
Therefore, if scientists wish to convict an innocent virus, they must
invent a new property for it that allows the virus to violate the
laws of virology.
For example, they can hypothesize a "latent period" of months or
years between the time the virus invades the body and the appearance
of symptoms - hence, a "slow" virus.
However, the slow virus concept has never been reconciled with the
short generation time of viruses and the immune system. Once the
virus lies totally dormant, an intact immune system will never allow
any virus to be reactivated to multiply into numbers that would
threaten the host.
For a virus to be reactivated, the immune system first must be
destroyed by something else - the real cause of a disease. A
reactivated virus would just contribute an opportunistic infection.
Thus, there are no slow viruses, only slow virologists.
A conventional virus could, however, be slow acting in a defective
immune system.
Indeed, some exceptional victims suffer pre-existing health problems
that prevent their immune systems from reacting decisively against
the virus, allowing it to continue growing and damaging the host for
a long period of time. This can happen with virtually any type of
virus, but it is extremely rare. When such a chronic infection does
occur, as with a small percentage of hepatitis cases whose immune
system is damaged by alcoholism or intravenous drug addiction, the
virus keeps growing abundantly in the body and can easily be found by
experimental tests.
Other germs, like herpes viruses, can hide out in some recess of the
body, breaking out periodically to strike again when the immune
system passes a seasonal low.In both examples, only the weakened
immune system of the host allows the infection to smolder or
occasionally reappear from hibernation.
By contrast, a slow virus is an invention credited with the natural
ability to cause disease only years after infection - termed the
"latent period" - in previously healthy persons, regardless of the
state of their immunity. Such a concept allows scientists to blame a
long-neutralized virus for any disease that appears decades after
infection. The slow virus is the original sin against the laws of virology.
The slow-virus or latent-period concept, now used to connect HIV with
AIDS, can be traced back to the days of the war on polio. The
researcher who popularized this modern myth is today an authority for
AIDS researchers and one whose career epitomizes the evolution of the
virus hunters over the past three decades.
Dr. Carleton Gajdusek is a pediatrician who has worked as a
virologist at the NIH for decades. Having spent a great deal of time
studying contagious childhood diseases around the world, Gajdusek was
sponsored by the NFIP and sent to New Guinea in 1957.
There, a doctor with the local health department introduced him to a
disease called kuru, a mysterious ailment that attacked the brain,
rendering the victim increasingly spasmodic or paralyzed until death
within months. The syndrome existed only among the thirty-five
thousand tribal villagers in one set of valleys, mostly the Fore tribe.
Before Gajdusek's arrival, no outsider had ever described kuru,
although the Fore tribesmen told him the condition had begun
appearing a few decades earlier.
Gajdusek's initial study assumed the disease to be infectious. He
reported that the natives routinely cannibalized the brains of
relatives for ritual purposes, a practice that they told him had
begun around the same time as the arrival of kuru.
Gajdusek later explained to one interviewer that cannibalism
"expressed love for their dead relatives," and that it also "provided
a good source of protein for a meat-starved community."
Gajdusek decided that kuru was transmitted by the eating of deceased
victims' brains. Yet when he searched for a virus, he ran into a
baffling absence of evidence. None of the typical signs of infection
could be found in the patients. Their bodies showed no inflammation
and no fever, no changes were registered in their supposedly infected
spinal fluid, their immune systems failed to react as if any microbe
had invaded the body, and those people with suppressed immune
defenses had no greater risk of catching the disease.
Another scientific group soon arrived from Australia and concluded
that kuru might be genetically inherited.
Upon arriving back in the United States, Gajdusek was hired by the
NIH to work at its institute for studying neurological disease. While
continuing to monitor kuru incidence, he devoted his time to
laboratory study of the condition.
Word of his discovery of kuru meanwhile made its way to England,
where another virus hunter was investigating a sheep disease known as
scrapie, which involved symptoms of brain degeneration. The English
researcher suggested to Gajdusek that kuru might be caused by a slow
virus, one with a long latent period.
Gajdusek was immediately hooked by the revolutionary idea, despite
his own "misgivings" that genes, toxins, or nutritional deficiencies
might be the cause of kuru.
Again determined to find an elusive virus, he tried to transmit kuru
from victims to chimpanzees. But none of the animals became sick when
injected with blood, urine, or other bodily fluids from kuru
patients, nor from the cerebrospinal fluid that surrounds the brain,
which should have been full of the alleged brain-destroying virus.
Indeed, the monkeys contracted no disease even from eating
kuru-affected brains - the authentic animal model of cannibalism.
Only one bizarre experiment did work, in which the brains of kuru
patients were ground into a fine mush and injected directly into the
brains of live monkeys through holes drilled in their skulls.
Ultimately, some of the experimental monkeys suffered coordination
and movement problems.
Surprisingly, though, even this extreme method could not transfer
kuru to dozens of other animal species. And no virus could be seen in
the brain tissue, even using the best electron microscopes.
At this point, one might expect Gajdusek would have suspected
something was seriously wrong with his virus hypothesis. If evidence
for the invisible virus could not be found anywhere but in unpurified
brain tissue, if it did not elicit any defensive reactions by the
body, and if it could not be transmitted in pure form to animals,
then probably no virus existed at all. The homogenized brain tissue
of dead kuru patients - full of every imaginable protein and other
compounds-should in itself be toxic when inoculated into monkeys' brains.
Nevertheless, the sick monkeys convinced Gajdusek and his colleagues
he had found a virus. Since he could not isolate it apart from the
brain tissue, he decided to study the virus and its structure with a
standard experiment.
He would define which chemical and physical treatments would destroy
the microbe, thereby gathering clues about its nature. But to his
astonishment, almost nothing seemed to harm the mystery germ.
Powerful chemicals, acids and bases, boiling temperatures,
ultraviolet and ionizing radiation, ultrasound-no matter how he
treated the brain tissue, it still caused "kuru" in his lab monkeys.
Further tests also proved that no foreign genetic material, which all
viruses require for their existence, could be found anywhere in
kuru-affected brains.
Employing the strongest virus-destroying treatments, Gajdusek had
failed to render the kuru brain tissue harmless in his experiments.
His results lent themselves to one obvious interpretation: No virus
existed in the first place, so it could not possibly be destroyed.
But Gajdusek clung to his virus hypothesis. Despite his disappointing
experiments, he turned the results upside down and argued that the
"kuru virus" was actually a new type of super-microbe or, as he put
it, an "unconventional virus." This new virus also needed to act as a
slow virus, since long periods of time elapsed between an act of
cannibalism and the onset of kuru; he liberally suggested latent
periods extending into years or even decades.
At an earlier time, and in another context, Gajdusek probably would
have been ignored by orthodox scientists. But he offered this
hypothesis to a generation of scientists dominated and impressed by
virus hunters.
The year was 1965, polio had largely disappeared, and the burgeoning
ranks of NIH-funded virologists welcomed any new research direction
on which to use their skills. Thus, they embraced Gajdusek's slow
virus hypothesis enthusiastically.
They listened uncritically when he claimed a similar unconventional
virus caused Creutzfeld-Jakob disease, a rare brain disorder that
seems to strike mostly Westerners having undergone previous brain
surgery (obviously such medical operations might well be suspected as
the real cause).
Gajdusek proposed slow or even unconventional viruses as the causes
of a huge laundry list of nerve and brain disorders, ranging from
scrapie in sheep to multiple sclerosis and Alzheimer's disease in
humans, and he was taken seriously even though he offered no
proof.Entranced, his peers awarded him the 1976 Nobel Prize for
medicine, specifically for the kuru and Creutzfeld-Jakob viruses he
has yet to find. And the NIH promoted him to head its Laboratory of
Central Nervous System Studies.
In the meantime another crucial, if embarrassing, bit of information
has emerged as a challenge to Gajdusek's virus-kuru hypothesis. The
published transcript of his Nobel acceptance speech, in a 1977 issue
of Science magazine, included a photo ostensibly showing New Guinea
natives eating their cannibalistic meal. The photo is not very clear.
When colleagues asked Gajdusek if the photo truly showed cannibalism,
he admitted the meal was merely roast pork. According to Science, "He
never publishes actual pictures of cannibalism, he says, because they
are 'too offensive.'" Unconvinced, anthropologist Lyle Steadman of
Arizona State University has investigated and directly challenged
Gajdusek, claiming "there is no evidence of cannibalism in New Guinea."
Steadman, who spent two years doing fieldwork in New Guinea, noted
that he often heard tales of cannibalism but when he probed, "the
evidence evaporated."
Gajdusek, angered by the hint of malfeasance, has insisted that "he
has actual photographs of cannibalism, but he would never publish
them because they 'so offend the relatives of the people who used to
do it.'" This statement contradicts his earlier claims that the
tribesman proudly ate their dead relatives out of respect, quitting
the practice only in deference to outside pressure from government
authorities.
For evidence of cannibalism, Gajdusek also cited Australian arrests
of tribesmen for the alleged crime - which, as it turned out, were
based on hearsay accusations. So perhaps New Guinea natives stand
falsely accused of ritual cannibalism.
In addition, few people outside of Gajdusek's original research team
have ever personally witnessed kuru victims. This means we also
depend on his own descriptions and statistics for our knowledge of
the disease itself, particularly since he claims cannibalism and kuru
both ceased to exist within a few years after his 1957 trip. Phantom
viruses, transmitted through phantom cannibalism, cause phantom disease.
Yet Gajdusek has reshaped the thinking of an entire generation of
biologists, his seductive message of slow viruses having landed on
eager ears. He and the virus hunters inspired by him have built
careers chasing viruses and attributing them to latent periods in
order to connect them to noninfectious diseases.
SMON, the nerve-destroying disease that struck Japan during the
1960s, became one unfortunate example. Japanese virologists, greatly
impressed with Gajdusek's accomplishments, spent years searching for
slow viruses they presumed would cause the disease and thereby
delayed finding the true cause - a prescribed medication.
Another example of a pointless virus hunt involved diabetes.
Beginning in the early 1960s, some scientists tried to blame this
noncontagious syndrome on the virus that also causes mumps. The
evidence has been pathetically sparse, forcing virologists to point
to occasional children who become diabetic after they have also
suffered mumps or, if they really stretch their case, to argue that
both mumps and diabetes become most common during the same annual
season in one county of New York.
Having become soldiers without a war, veteran polio virologists
invaded the diabetes field as well, proposing since the early 1970s
that Coxsackie viruses may cause the disease. Antibodies against
several strains of these harmless viruses, first discovered as
by-products of polio research, have been found in a few diabetic children.
But between 20 percent and 70 percent of young diabetics have never
been infected, and the remainder have already neutralized the virus
with their immune systems long before the onset of diabetes.
Apparently, an equal percentage of non-diabetic children have also
been infected with these Coxsackie viruses. Needless to say, none of
the above viruses meets Koch's postulates for causing diabetes.
Hilary Koprowski, like Gajdusek, typifies the modern virus hunter.
Although Koprowski's virology career began earlier, Gajdusek's work
helped rescue Koprowski from the obsolescence that threatened polio
researchers after the war on polio. Like so many of his colleagues,
he found his newest calling in the war on AIDS.
Koprowski's work on viruses started at the Rockefeller Institute in
New York. By the late 1940s he moved across town to the Lederle
pharmaceutical company, where he worked feverishly to develop a polio
vaccine. By 1954 he had invented one, but Jonas Salk was announcing
the field trials for another vaccine, and Koprowski's already-tested
product was shunted aside by Salk's public acclaim.
Koprowski left Lederle in I957 to take a position as director of the
privately endowed Wistar Institute of Pennsylvania, where he began
tests on humans and stepped up the campaign to get approval for his
vaccine. By now Albert Sabin had tested his own polio immunization on
millions of people in foreign countries, completely overshadowing
Koprowski's equally successful but less-promoted vaccine.
Nevertheless, Koprowski's day did arrive. His vaccine became the
standard used by the World Health Organization in America during the
late 1950s and 1960s.
In the meantime he spent several years studying the rabies virus and
creating a vaccine against that virus, which attacks the brain and
nervous system. But because rabies is relatively rare, Koprowski's
vaccine never achieved the stardom of other immunizations. More
important, however, his rabies research placed him squarely in the
field of neurological diseases just in time to meet up with
Gajdusek's kuru work.
The news of slow viruses enticed Koprowski with visions of
groundbreaking science. He quickly realized that the notion of slow
viruses could become a useful tool, allowing him to source slow,
noninfectious diseases to viruses, so long believed to be fast-acting
agents. He participated as a "program advisor" in Gajdusek's first
major conference on slow and unconventional viruses held in 1964 at
the NIH head-quarters in Bethesda, Maryland. From that point forward,
Hilary Koprowski joined the new virus-hunting trend from which he
would never turn back.
His first big opportunity to take a crack at slow viruses came at the
end of the 1960s. Subacute sclerosing panencephalitis (SSPE), a
mouthful of a name for such a rare condition, attacks a small number
of schoolchildren and teenagers each year, causing dementia, learning
disabilities, and finally death.
Doctors first recognized SSPE in the 1930s, and by the 1960s the
virus hunters were searching for an SSPE germ. At that time, the most
fashionable viruses for research belonged to the myxovirus family,
which included the viruses that caused influenza, measles, and mumps.
Animal virologists therefore started by probing for signs of myxoviruses.
Excitement mounted after trace quantities of measles virus were
detected in the brains of SSPE patients, and in 1967 most of the
victims were found to have antibodies against measles. The facts that
SSPE affected only one of every million measles -- infected people
and that this rare condition appeared from one to ten years after
infection by measles were no longer a problem: Researchers simply
hypothesized a one- to ten-year latency period. Little wonder they
could also easily rationalize that one virus could cause two totally
different diseases.
Koprowski's foray into SSPE research began in the early 1970s. He
began isolating the measles virus from dying SSPE victims, a nearly
impossible task because their immune systems had long before
completely neutralized the virus (some SSPE cases, more-over had
never had measles, merely the measles vaccine). His characteristic
patience nonetheless paid off, yielding a tiny handful of virus
particles from some patients that could be coaxed to begin growing
again, if only in laboratory cell culture.
In other patients only defective viruses that were unable to grow had
remained so many years after the original measles infection.
Rather than concluding the measles virus had nothing to do with SSPE,
he employed the new logic of virus hunting to argue that a defective
measles virus caused SSPE!
Koprowski continued this line of SSPE research for several more
years. But in 1985 Gajdusek himself entered the SSPE fray, publishing
a paper with leading AIDS researcher Robert Gallo in which they
proposed that HIV, the supposed AIDS virus, caused SSPE while
remaining latent. With hardly a blink, several leading virologists
jettisoned the old measles-SSPE hypothesis in favor of a newly
popular, but equally innocent, virus.
Multiple sclerosis (MS), the notorious disease that also attacks the
nervous system and ultimately kills, has provided yet another
opportunity for the virus hunters.
First, they blamed the measles virus starting in the 1960s, since
many MS patients had antibodies against the virus. Ten years later
others suggested the mumps virus, which is similar to measles. The
early I980s brought the coronavirus hypothesis of MS, the category of
virus better known for causing some colds. In 1985, with Gajdusek
stealing his thunder for SSPE, Koprowski also published a scientific
paper that year in Nature with Robert Gallo, in this case arguing
that some virus similar to HIV now caused MS. Unfortunately for
Koprowski, even this hypothesis was abandoned within just a few years.
Phantom Viruses and Big Bucks
Most virus hunters prefer chasing real, if arguably harmless, viruses
as their deadly enemies. But Gajdusek's "unconventional" viruses -
the ones neither he nor anyone else have ever found - have been
making a comeback in recent years. Given the abundance of research
dollars being poured into biomedical science by the NIH and other
agencies, opportunistic virus hunters have been finding creative ways
to cash in. One increasingly successful method utilizes modern
biotechnology to isolate viruses that may not even exist.
Hepatitis, or liver disease, has yielded profitable virus-hunting
opportunities in recent years. Hepatitis can be a truly painful
affliction, starting like a flu but progressing to more severe
symptoms, including high fevers and yellow skin. At least three
varieties seem to exist.
Hepatitis A is infectious, spread through unsanitary conditions, and
is caused by a conventional virus.
Hepatitis B also results from a virus (discovered in the 1960s) and
is transmitted mostly between heroin addicts sharing needles, among
sexually active and promiscuous people, or in the Third World from
mothers to their children around the time of birth.
A third type of hepatitis was found in the 1970s, again restricted to
heroin addicts, alcoholics, and patients who have received blood transfusions.
Most scientists assumed these cases were either hepatitis A or B,
until widespread testing revealed neither virus in the victims.
Roughly thirty-five thousand Americans die each year of any type of
the disease, a fraction of those from this "non-A, non-B hepatitis,"
as it was known for years.
Today it is called hepatitis C. This form of hepatitis does not
behave as an infectious disease, for it rigidly confines itself to
people in well- defined risk groups rather than spreading to larger
populations or even to the doctors treating hepatitis patients. Yet
virologists have been eyeing the disease from the beginning, hoping
one day to find a virus causing it.
That day arrived in 1987. The laboratory for the job was no less than
the research facility of the Chiron Corporation, a biotechnology
company located directly across the bay from San Francisco. Equipped
with the most advanced techniques, a research team started its search
in 1982 by injecting blood from patients into chimpanzees. None of
monkeys contracted hepatitis, although subtle signs vaguely
resembling infection or reddening did appear.
For the next step, the scientists probed liver tissue for a virus.
None could be found. Growing desperate, the team fished even for the
smallest print of a virus, finally coming across and greatly
amplifying a small piece of genetic information, encoded in a
molecule known as ribonucleic acid (RNA), that did not seem to belong
in the host's genetic code.
This fragment of presumably foreign RNA, the researchers assumed,
must be the genetic information of some undetected virus. Whatever it
was, liver tissue contains it only in barely detectable amounts. Only
about half of all hepatitis C patients contain the rare foreign RNA.
And in those who contain it, there is only one RNA molecule for every
ten liver cells - hardly a plausible cause for disease.
The Chiron team used newly available technology to reconstruct pieces
of the mystery virus. Now they could test patients for antibodies
against this hypothetical virus and soon discovered that only a
slight majority of hepatitis C patients had any evidence ofthese
antibodies in their blood.
1. Koch's first postulate, of course, demands that a truly harmful
virus be found in huge quantities in every single patient.
2. His second postulate requires that the virus particles be
isolated and grown, although this supposed hepatitis virus has never
been found intact.
3. And the third postulate insists that newly infected animals, such
as chimpanzees, should get the disease when injected with the virus.
This hypothetical microbe fails all three tests. But Koch's standards
were the furthest thing from the minds of the Chiron scientists when
they announced in 1987 that they had finally found the "hepatitis C" virus.
Now more paradoxes are confronting the viral hypothesis. Huge numbers
of people testing positive for the hypothetical hepatitis C virus
never develop any symptoms of the disease, even though the "virus" is
no less active in their bodies than in hepatitis patients.
And according to a recent large-scale study of people watched for
eighteen years, those with signs of "infection" live just as long as
those without. Despite these facts, scientists defend their
still-elusive virus by giving it an undefined latent period extending
into decades.
Paradoxes like these no longer faze the virus-hunting research
establishment. Indeed, rewards are generally showered upon any new
virus hypothesis, no matter how bizarre. Chiron did not spend five
years creating its own virus for nothing. Having patented the test
for the virus, the company put it into production and began a
publicity campaign to win powerful allies.
The first step was a paper published in Science, the world's most
prestigious science magazine, edited by Dan Koshland, Jr., professor
of molecular and cell biology at the University of California at Berkeley.
Edward Penhoet, chief executive officer for Chiron, also holds a
position as professor of molecular and cell biology at the University
of California at Berkeley. The NIH-supported virology establishment
soon lent the full weight of its credibility to the hepatitis C virus
camp. As Chiron's CEO boasted, "We have a blockbuster product."
A regulatory order from the Food and Drug Administration (FDA) to
test the blood supply would reap enormous sales for Chiron.
Their big chance presented itself in late 1988 as a special request
from Japanese Emperor Hirohito's doctors. The monarch was dying and
constantly needed blood transfusions; could Chiron provide a test to
make sure he received no blood tainted with hepatitis C? The biotech
company jumped at the opportunity, making for itself such a name in
Japan that the Tokyo government gave the product its approval within one year.
The emperor died in the meantime, but excitement over Chiron's test
was fueled when the Japanese government placed hepatitis C high on
its medical priority list. Chiron's test kit now earns some $60
million annually in that country alone.
By the middle of 1990, the United States followed suit.
The FDA not only approved the test, but even recommended the
universal testing of donated blood.
The American Association of Blood Banks followed suit by mandating
the $5 test for all 12 million blood donations made each year in this
country - raking in another $60 million annually for Chiron while
raising the nation's medical costs that much more.
And all this testing is being done for a virus that has never been isolated.
Profits from the test kit have generated another all-too-common part
of virus hunting. With Chiron's new income from the hepatitis C test,
Penhoet's company bought out Cetus, another biotech company, founded
by Donald Glaser, who, like Penhoet, also holds a position as
professor of molecular and cell biology at the University of
California at Berkeley. And Chiron made an unrestricted donation of
about 12 million to the Department of Molecular and Cell Biology at
the University of California at Berkeley that generates $100,000 in
interest each year.
Unfortunately for Peter Duesberg, who belongs to the same department,
his supervisor is yet another professor who consults for Chiron
Corporation - and displays little sympathy for Duesberg for
challenging modern virus hunting by restricting his academic duties
to undergraduate student teaching and by not appointing him to
decision-making committees.
Such conflicts of interest have become standard fixtures in
university biology departments.
The modern biomedical research establishment differs radically from
any previous scientific program in history. Driven by vast infusions
of federal and commercial money, it has grown into an enormous and
powerful bureaucracy that greatly amplifies its successes, all the
while stifling dissent.
Such a process can no longer be called science, which by definition
depends on self-correction by internal challenge and debate.
Despite their popularity among scientists and their companies,
"latent," "slow," and "defective" viruses have achieved only little
prominence as hypothetical causes of degenerative diseases before the
AIDS era. Their hypothetical role in degenerative diseases, which
result from the loss of large numbers of cells, remained confined to
rare, exclusive illnesses like kuru and hepatitis C.
However, because latent, slow, and defective viruses cannot kill
cells, such "viruses" eventually achieved prominence as hypothetical
causes of cancer and thus entered the courts of health care and
medical research. The next chapter describes the terms under which
these viruses were promoted as causes of cancer and how some of these
terms were eventually used to promote latent, slow, and defective
viruses as causes of degenerative diseases including, above all, AIDS.
Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto
*****
http://www.duesberg.com/
Peter H. Duesberg, Ph.D. is a professor of Molecular and Cell Biology
at the University of California, Berkeley. Biographical Sketch
http://www.duesberg.com/about/pdbio.html
He isolated the first cancer gene through his work on
retroviruses in 1970, and mapped the genetic structure of these
viruses. This, and his subsequent work in the same field, resulted in
his election to the National Academy of Sciences in 1986. He is also
the recipient of a seven-year Outstanding Investigator Grant from the
National Institutes of Health.
On the basis of his experience with retroviruses, Duesberg has
challenged the virus-AIDS hypothesis in the pages of such journals as
Cancer Research, Lancet, Proceedings of the National Academy of
Sciences, Science, Nature, Journal of AIDS, AIDS Forschung,
Biomedicine and Pharmacotherapeutics, New England Journal of Medicine
and Research in Immunology. He has instead proposed the hypothesis
that the various American/European AIDS diseases are brought on by
the long-term consumption of recreational drugs and/or AZT itself,
which is prescribed to prevent or treat AIDS. See The AIDS Dilemma:
Drug diseases blamed on a passenger virus.
For a detailed discussion of American/European AIDS as opposed
to African AIDS, see The African AIDS Epidemic: New and Contagious or
Old Under a New Name.
This is Duesberg's official site, containing his written works
on the subject, as well as other scientists that support his views
such as Kary B. Mullis. Kary Mullis won the 1993 Nobel Prize in
Chemistry for his invention of the polymerase chain reaction
technique for detecting DNA. This is the technique used to search for
fragments of HIV in AIDS patients.
Prof. Duesberg's findings have been a thorn in the side of the
medical establishment and drug companies since 1987. Instead of
engaging in scientific debate, however, the only response has been to
cut-off funding to further test Professor's Duesberg's hypothesis.
You can show your support by contributing a tax deductible
donation to help support Prof. Duesberg's lab at the University of
California Berkeley.
More here http://www.duesberg.com/papers/the%20enigma.pdf The Enigma
of Slow Viruses
http://www.virusmyth.com/aids/hiv/pdslowvir.htm
http://www.vaclib.org/basic/gk/pdf/DUESBERG.pdf
This is a great article showing how real the whole issue of viruses
is (not) and how baseless the issue of vaccines for so-called viral
illnesses are.
And what a scam and lie 'slow' viruses are.
Don't be quick to buy into this lie.
Long article but excellent
http://www.healtoronto.com/slowvirus.html
Slow Viruses: The Original Sin Against the Laws of Virology
By Peter H. Duesberg and Bryan J. Ellison
from "INVENTING THE AIDS VIRUS", Regnery publishing, 1996
Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto
From the discovery of tobacco mosaic virus through the polio
epidemic, scientists have found and legitimately blamed many viruses
for a variety of diseases, each having passed the acid test of Koch's
postulates. But for every truly dangerous virus, many more perfectly
harmless passenger viruses can be found in humans and animals.
NIH-sponsored polio research during the late 1950s proved the point.
Researchers trying to isolate new strains of poliovirus accidentally
found numerous closely related passenger viruses -- such as Coxsackie
and echoviruses - that, like polio, infected the digestive system.
Scientists classified some of these viruses as "orphans" - viruses
without corresponding diseases.
The virus hunters could not bring themselves to believe microbes
could exist without being harmful and expected even these "orphan"
viruses would someday find appropriate sicknesses.
When trying to blame a passenger virus for a disease, how-ever, one
nagging problem haunts the virus hunter: The laws of virology dictate
that the illness will strike the victim soon after infection. When
microbes infect a new host, they cause sickness within days or weeks
at most. In order to cause disease, viruses need to grow into
sufficient numbers to take over the body; otherwise, the host's
immune defenses will neutralize the invader and prevent disease altogether.
The rate-determining step of such fast, exponential growth is the
generation time of the virus. Since the generation time of all human
viruses is between eight and forty-eight hours, and since the
infected cell produces one hundred to one thousand viruses per day,
viruses multiply exponentially, increasing in numbers hundred- to
thousand-fold per day. Within a week or two, one hundred trillion
(1014) cells can be produced-one for each of the one hundred trillion
cells in the human body.
Therefore, if scientists wish to convict an innocent virus, they must
invent a new property for it that allows the virus to violate the
laws of virology.
For example, they can hypothesize a "latent period" of months or
years between the time the virus invades the body and the appearance
of symptoms - hence, a "slow" virus.
However, the slow virus concept has never been reconciled with the
short generation time of viruses and the immune system. Once the
virus lies totally dormant, an intact immune system will never allow
any virus to be reactivated to multiply into numbers that would
threaten the host.
For a virus to be reactivated, the immune system first must be
destroyed by something else - the real cause of a disease. A
reactivated virus would just contribute an opportunistic infection.
Thus, there are no slow viruses, only slow virologists.
A conventional virus could, however, be slow acting in a defective
immune system.
Indeed, some exceptional victims suffer pre-existing health problems
that prevent their immune systems from reacting decisively against
the virus, allowing it to continue growing and damaging the host for
a long period of time. This can happen with virtually any type of
virus, but it is extremely rare. When such a chronic infection does
occur, as with a small percentage of hepatitis cases whose immune
system is damaged by alcoholism or intravenous drug addiction, the
virus keeps growing abundantly in the body and can easily be found by
experimental tests.
Other germs, like herpes viruses, can hide out in some recess of the
body, breaking out periodically to strike again when the immune
system passes a seasonal low.In both examples, only the weakened
immune system of the host allows the infection to smolder or
occasionally reappear from hibernation.
By contrast, a slow virus is an invention credited with the natural
ability to cause disease only years after infection - termed the
"latent period" - in previously healthy persons, regardless of the
state of their immunity. Such a concept allows scientists to blame a
long-neutralized virus for any disease that appears decades after
infection. The slow virus is the original sin against the laws of virology.
The slow-virus or latent-period concept, now used to connect HIV with
AIDS, can be traced back to the days of the war on polio. The
researcher who popularized this modern myth is today an authority for
AIDS researchers and one whose career epitomizes the evolution of the
virus hunters over the past three decades.
Dr. Carleton Gajdusek is a pediatrician who has worked as a
virologist at the NIH for decades. Having spent a great deal of time
studying contagious childhood diseases around the world, Gajdusek was
sponsored by the NFIP and sent to New Guinea in 1957.
There, a doctor with the local health department introduced him to a
disease called kuru, a mysterious ailment that attacked the brain,
rendering the victim increasingly spasmodic or paralyzed until death
within months. The syndrome existed only among the thirty-five
thousand tribal villagers in one set of valleys, mostly the Fore tribe.
Before Gajdusek's arrival, no outsider had ever described kuru,
although the Fore tribesmen told him the condition had begun
appearing a few decades earlier.
Gajdusek's initial study assumed the disease to be infectious. He
reported that the natives routinely cannibalized the brains of
relatives for ritual purposes, a practice that they told him had
begun around the same time as the arrival of kuru.
Gajdusek later explained to one interviewer that cannibalism
"expressed love for their dead relatives," and that it also "provided
a good source of protein for a meat-starved community."
Gajdusek decided that kuru was transmitted by the eating of deceased
victims' brains. Yet when he searched for a virus, he ran into a
baffling absence of evidence. None of the typical signs of infection
could be found in the patients. Their bodies showed no inflammation
and no fever, no changes were registered in their supposedly infected
spinal fluid, their immune systems failed to react as if any microbe
had invaded the body, and those people with suppressed immune
defenses had no greater risk of catching the disease.
Another scientific group soon arrived from Australia and concluded
that kuru might be genetically inherited.
Upon arriving back in the United States, Gajdusek was hired by the
NIH to work at its institute for studying neurological disease. While
continuing to monitor kuru incidence, he devoted his time to
laboratory study of the condition.
Word of his discovery of kuru meanwhile made its way to England,
where another virus hunter was investigating a sheep disease known as
scrapie, which involved symptoms of brain degeneration. The English
researcher suggested to Gajdusek that kuru might be caused by a slow
virus, one with a long latent period.
Gajdusek was immediately hooked by the revolutionary idea, despite
his own "misgivings" that genes, toxins, or nutritional deficiencies
might be the cause of kuru.
Again determined to find an elusive virus, he tried to transmit kuru
from victims to chimpanzees. But none of the animals became sick when
injected with blood, urine, or other bodily fluids from kuru
patients, nor from the cerebrospinal fluid that surrounds the brain,
which should have been full of the alleged brain-destroying virus.
Indeed, the monkeys contracted no disease even from eating
kuru-affected brains - the authentic animal model of cannibalism.
Only one bizarre experiment did work, in which the brains of kuru
patients were ground into a fine mush and injected directly into the
brains of live monkeys through holes drilled in their skulls.
Ultimately, some of the experimental monkeys suffered coordination
and movement problems.
Surprisingly, though, even this extreme method could not transfer
kuru to dozens of other animal species. And no virus could be seen in
the brain tissue, even using the best electron microscopes.
At this point, one might expect Gajdusek would have suspected
something was seriously wrong with his virus hypothesis. If evidence
for the invisible virus could not be found anywhere but in unpurified
brain tissue, if it did not elicit any defensive reactions by the
body, and if it could not be transmitted in pure form to animals,
then probably no virus existed at all. The homogenized brain tissue
of dead kuru patients - full of every imaginable protein and other
compounds-should in itself be toxic when inoculated into monkeys' brains.
Nevertheless, the sick monkeys convinced Gajdusek and his colleagues
he had found a virus. Since he could not isolate it apart from the
brain tissue, he decided to study the virus and its structure with a
standard experiment.
He would define which chemical and physical treatments would destroy
the microbe, thereby gathering clues about its nature. But to his
astonishment, almost nothing seemed to harm the mystery germ.
Powerful chemicals, acids and bases, boiling temperatures,
ultraviolet and ionizing radiation, ultrasound-no matter how he
treated the brain tissue, it still caused "kuru" in his lab monkeys.
Further tests also proved that no foreign genetic material, which all
viruses require for their existence, could be found anywhere in
kuru-affected brains.
Employing the strongest virus-destroying treatments, Gajdusek had
failed to render the kuru brain tissue harmless in his experiments.
His results lent themselves to one obvious interpretation: No virus
existed in the first place, so it could not possibly be destroyed.
But Gajdusek clung to his virus hypothesis. Despite his disappointing
experiments, he turned the results upside down and argued that the
"kuru virus" was actually a new type of super-microbe or, as he put
it, an "unconventional virus." This new virus also needed to act as a
slow virus, since long periods of time elapsed between an act of
cannibalism and the onset of kuru; he liberally suggested latent
periods extending into years or even decades.
At an earlier time, and in another context, Gajdusek probably would
have been ignored by orthodox scientists. But he offered this
hypothesis to a generation of scientists dominated and impressed by
virus hunters.
The year was 1965, polio had largely disappeared, and the burgeoning
ranks of NIH-funded virologists welcomed any new research direction
on which to use their skills. Thus, they embraced Gajdusek's slow
virus hypothesis enthusiastically.
They listened uncritically when he claimed a similar unconventional
virus caused Creutzfeld-Jakob disease, a rare brain disorder that
seems to strike mostly Westerners having undergone previous brain
surgery (obviously such medical operations might well be suspected as
the real cause).
Gajdusek proposed slow or even unconventional viruses as the causes
of a huge laundry list of nerve and brain disorders, ranging from
scrapie in sheep to multiple sclerosis and Alzheimer's disease in
humans, and he was taken seriously even though he offered no
proof.Entranced, his peers awarded him the 1976 Nobel Prize for
medicine, specifically for the kuru and Creutzfeld-Jakob viruses he
has yet to find. And the NIH promoted him to head its Laboratory of
Central Nervous System Studies.
In the meantime another crucial, if embarrassing, bit of information
has emerged as a challenge to Gajdusek's virus-kuru hypothesis. The
published transcript of his Nobel acceptance speech, in a 1977 issue
of Science magazine, included a photo ostensibly showing New Guinea
natives eating their cannibalistic meal. The photo is not very clear.
When colleagues asked Gajdusek if the photo truly showed cannibalism,
he admitted the meal was merely roast pork. According to Science, "He
never publishes actual pictures of cannibalism, he says, because they
are 'too offensive.'" Unconvinced, anthropologist Lyle Steadman of
Arizona State University has investigated and directly challenged
Gajdusek, claiming "there is no evidence of cannibalism in New Guinea."
Steadman, who spent two years doing fieldwork in New Guinea, noted
that he often heard tales of cannibalism but when he probed, "the
evidence evaporated."
Gajdusek, angered by the hint of malfeasance, has insisted that "he
has actual photographs of cannibalism, but he would never publish
them because they 'so offend the relatives of the people who used to
do it.'" This statement contradicts his earlier claims that the
tribesman proudly ate their dead relatives out of respect, quitting
the practice only in deference to outside pressure from government
authorities.
For evidence of cannibalism, Gajdusek also cited Australian arrests
of tribesmen for the alleged crime - which, as it turned out, were
based on hearsay accusations. So perhaps New Guinea natives stand
falsely accused of ritual cannibalism.
In addition, few people outside of Gajdusek's original research team
have ever personally witnessed kuru victims. This means we also
depend on his own descriptions and statistics for our knowledge of
the disease itself, particularly since he claims cannibalism and kuru
both ceased to exist within a few years after his 1957 trip. Phantom
viruses, transmitted through phantom cannibalism, cause phantom disease.
Yet Gajdusek has reshaped the thinking of an entire generation of
biologists, his seductive message of slow viruses having landed on
eager ears. He and the virus hunters inspired by him have built
careers chasing viruses and attributing them to latent periods in
order to connect them to noninfectious diseases.
SMON, the nerve-destroying disease that struck Japan during the
1960s, became one unfortunate example. Japanese virologists, greatly
impressed with Gajdusek's accomplishments, spent years searching for
slow viruses they presumed would cause the disease and thereby
delayed finding the true cause - a prescribed medication.
Another example of a pointless virus hunt involved diabetes.
Beginning in the early 1960s, some scientists tried to blame this
noncontagious syndrome on the virus that also causes mumps. The
evidence has been pathetically sparse, forcing virologists to point
to occasional children who become diabetic after they have also
suffered mumps or, if they really stretch their case, to argue that
both mumps and diabetes become most common during the same annual
season in one county of New York.
Having become soldiers without a war, veteran polio virologists
invaded the diabetes field as well, proposing since the early 1970s
that Coxsackie viruses may cause the disease. Antibodies against
several strains of these harmless viruses, first discovered as
by-products of polio research, have been found in a few diabetic children.
But between 20 percent and 70 percent of young diabetics have never
been infected, and the remainder have already neutralized the virus
with their immune systems long before the onset of diabetes.
Apparently, an equal percentage of non-diabetic children have also
been infected with these Coxsackie viruses. Needless to say, none of
the above viruses meets Koch's postulates for causing diabetes.
Hilary Koprowski, like Gajdusek, typifies the modern virus hunter.
Although Koprowski's virology career began earlier, Gajdusek's work
helped rescue Koprowski from the obsolescence that threatened polio
researchers after the war on polio. Like so many of his colleagues,
he found his newest calling in the war on AIDS.
Koprowski's work on viruses started at the Rockefeller Institute in
New York. By the late 1940s he moved across town to the Lederle
pharmaceutical company, where he worked feverishly to develop a polio
vaccine. By 1954 he had invented one, but Jonas Salk was announcing
the field trials for another vaccine, and Koprowski's already-tested
product was shunted aside by Salk's public acclaim.
Koprowski left Lederle in I957 to take a position as director of the
privately endowed Wistar Institute of Pennsylvania, where he began
tests on humans and stepped up the campaign to get approval for his
vaccine. By now Albert Sabin had tested his own polio immunization on
millions of people in foreign countries, completely overshadowing
Koprowski's equally successful but less-promoted vaccine.
Nevertheless, Koprowski's day did arrive. His vaccine became the
standard used by the World Health Organization in America during the
late 1950s and 1960s.
In the meantime he spent several years studying the rabies virus and
creating a vaccine against that virus, which attacks the brain and
nervous system. But because rabies is relatively rare, Koprowski's
vaccine never achieved the stardom of other immunizations. More
important, however, his rabies research placed him squarely in the
field of neurological diseases just in time to meet up with
Gajdusek's kuru work.
The news of slow viruses enticed Koprowski with visions of
groundbreaking science. He quickly realized that the notion of slow
viruses could become a useful tool, allowing him to source slow,
noninfectious diseases to viruses, so long believed to be fast-acting
agents. He participated as a "program advisor" in Gajdusek's first
major conference on slow and unconventional viruses held in 1964 at
the NIH head-quarters in Bethesda, Maryland. From that point forward,
Hilary Koprowski joined the new virus-hunting trend from which he
would never turn back.
His first big opportunity to take a crack at slow viruses came at the
end of the 1960s. Subacute sclerosing panencephalitis (SSPE), a
mouthful of a name for such a rare condition, attacks a small number
of schoolchildren and teenagers each year, causing dementia, learning
disabilities, and finally death.
Doctors first recognized SSPE in the 1930s, and by the 1960s the
virus hunters were searching for an SSPE germ. At that time, the most
fashionable viruses for research belonged to the myxovirus family,
which included the viruses that caused influenza, measles, and mumps.
Animal virologists therefore started by probing for signs of myxoviruses.
Excitement mounted after trace quantities of measles virus were
detected in the brains of SSPE patients, and in 1967 most of the
victims were found to have antibodies against measles. The facts that
SSPE affected only one of every million measles -- infected people
and that this rare condition appeared from one to ten years after
infection by measles were no longer a problem: Researchers simply
hypothesized a one- to ten-year latency period. Little wonder they
could also easily rationalize that one virus could cause two totally
different diseases.
Koprowski's foray into SSPE research began in the early 1970s. He
began isolating the measles virus from dying SSPE victims, a nearly
impossible task because their immune systems had long before
completely neutralized the virus (some SSPE cases, more-over had
never had measles, merely the measles vaccine). His characteristic
patience nonetheless paid off, yielding a tiny handful of virus
particles from some patients that could be coaxed to begin growing
again, if only in laboratory cell culture.
In other patients only defective viruses that were unable to grow had
remained so many years after the original measles infection.
Rather than concluding the measles virus had nothing to do with SSPE,
he employed the new logic of virus hunting to argue that a defective
measles virus caused SSPE!
Koprowski continued this line of SSPE research for several more
years. But in 1985 Gajdusek himself entered the SSPE fray, publishing
a paper with leading AIDS researcher Robert Gallo in which they
proposed that HIV, the supposed AIDS virus, caused SSPE while
remaining latent. With hardly a blink, several leading virologists
jettisoned the old measles-SSPE hypothesis in favor of a newly
popular, but equally innocent, virus.
Multiple sclerosis (MS), the notorious disease that also attacks the
nervous system and ultimately kills, has provided yet another
opportunity for the virus hunters.
First, they blamed the measles virus starting in the 1960s, since
many MS patients had antibodies against the virus. Ten years later
others suggested the mumps virus, which is similar to measles. The
early I980s brought the coronavirus hypothesis of MS, the category of
virus better known for causing some colds. In 1985, with Gajdusek
stealing his thunder for SSPE, Koprowski also published a scientific
paper that year in Nature with Robert Gallo, in this case arguing
that some virus similar to HIV now caused MS. Unfortunately for
Koprowski, even this hypothesis was abandoned within just a few years.
Phantom Viruses and Big Bucks
Most virus hunters prefer chasing real, if arguably harmless, viruses
as their deadly enemies. But Gajdusek's "unconventional" viruses -
the ones neither he nor anyone else have ever found - have been
making a comeback in recent years. Given the abundance of research
dollars being poured into biomedical science by the NIH and other
agencies, opportunistic virus hunters have been finding creative ways
to cash in. One increasingly successful method utilizes modern
biotechnology to isolate viruses that may not even exist.
Hepatitis, or liver disease, has yielded profitable virus-hunting
opportunities in recent years. Hepatitis can be a truly painful
affliction, starting like a flu but progressing to more severe
symptoms, including high fevers and yellow skin. At least three
varieties seem to exist.
Hepatitis A is infectious, spread through unsanitary conditions, and
is caused by a conventional virus.
Hepatitis B also results from a virus (discovered in the 1960s) and
is transmitted mostly between heroin addicts sharing needles, among
sexually active and promiscuous people, or in the Third World from
mothers to their children around the time of birth.
A third type of hepatitis was found in the 1970s, again restricted to
heroin addicts, alcoholics, and patients who have received blood transfusions.
Most scientists assumed these cases were either hepatitis A or B,
until widespread testing revealed neither virus in the victims.
Roughly thirty-five thousand Americans die each year of any type of
the disease, a fraction of those from this "non-A, non-B hepatitis,"
as it was known for years.
Today it is called hepatitis C. This form of hepatitis does not
behave as an infectious disease, for it rigidly confines itself to
people in well- defined risk groups rather than spreading to larger
populations or even to the doctors treating hepatitis patients. Yet
virologists have been eyeing the disease from the beginning, hoping
one day to find a virus causing it.
That day arrived in 1987. The laboratory for the job was no less than
the research facility of the Chiron Corporation, a biotechnology
company located directly across the bay from San Francisco. Equipped
with the most advanced techniques, a research team started its search
in 1982 by injecting blood from patients into chimpanzees. None of
monkeys contracted hepatitis, although subtle signs vaguely
resembling infection or reddening did appear.
For the next step, the scientists probed liver tissue for a virus.
None could be found. Growing desperate, the team fished even for the
smallest print of a virus, finally coming across and greatly
amplifying a small piece of genetic information, encoded in a
molecule known as ribonucleic acid (RNA), that did not seem to belong
in the host's genetic code.
This fragment of presumably foreign RNA, the researchers assumed,
must be the genetic information of some undetected virus. Whatever it
was, liver tissue contains it only in barely detectable amounts. Only
about half of all hepatitis C patients contain the rare foreign RNA.
And in those who contain it, there is only one RNA molecule for every
ten liver cells - hardly a plausible cause for disease.
The Chiron team used newly available technology to reconstruct pieces
of the mystery virus. Now they could test patients for antibodies
against this hypothetical virus and soon discovered that only a
slight majority of hepatitis C patients had any evidence ofthese
antibodies in their blood.
1. Koch's first postulate, of course, demands that a truly harmful
virus be found in huge quantities in every single patient.
2. His second postulate requires that the virus particles be
isolated and grown, although this supposed hepatitis virus has never
been found intact.
3. And the third postulate insists that newly infected animals, such
as chimpanzees, should get the disease when injected with the virus.
This hypothetical microbe fails all three tests. But Koch's standards
were the furthest thing from the minds of the Chiron scientists when
they announced in 1987 that they had finally found the "hepatitis C" virus.
Now more paradoxes are confronting the viral hypothesis. Huge numbers
of people testing positive for the hypothetical hepatitis C virus
never develop any symptoms of the disease, even though the "virus" is
no less active in their bodies than in hepatitis patients.
And according to a recent large-scale study of people watched for
eighteen years, those with signs of "infection" live just as long as
those without. Despite these facts, scientists defend their
still-elusive virus by giving it an undefined latent period extending
into decades.
Paradoxes like these no longer faze the virus-hunting research
establishment. Indeed, rewards are generally showered upon any new
virus hypothesis, no matter how bizarre. Chiron did not spend five
years creating its own virus for nothing. Having patented the test
for the virus, the company put it into production and began a
publicity campaign to win powerful allies.
The first step was a paper published in Science, the world's most
prestigious science magazine, edited by Dan Koshland, Jr., professor
of molecular and cell biology at the University of California at Berkeley.
Edward Penhoet, chief executive officer for Chiron, also holds a
position as professor of molecular and cell biology at the University
of California at Berkeley. The NIH-supported virology establishment
soon lent the full weight of its credibility to the hepatitis C virus
camp. As Chiron's CEO boasted, "We have a blockbuster product."
A regulatory order from the Food and Drug Administration (FDA) to
test the blood supply would reap enormous sales for Chiron.
Their big chance presented itself in late 1988 as a special request
from Japanese Emperor Hirohito's doctors. The monarch was dying and
constantly needed blood transfusions; could Chiron provide a test to
make sure he received no blood tainted with hepatitis C? The biotech
company jumped at the opportunity, making for itself such a name in
Japan that the Tokyo government gave the product its approval within one year.
The emperor died in the meantime, but excitement over Chiron's test
was fueled when the Japanese government placed hepatitis C high on
its medical priority list. Chiron's test kit now earns some $60
million annually in that country alone.
By the middle of 1990, the United States followed suit.
The FDA not only approved the test, but even recommended the
universal testing of donated blood.
The American Association of Blood Banks followed suit by mandating
the $5 test for all 12 million blood donations made each year in this
country - raking in another $60 million annually for Chiron while
raising the nation's medical costs that much more.
And all this testing is being done for a virus that has never been isolated.
Profits from the test kit have generated another all-too-common part
of virus hunting. With Chiron's new income from the hepatitis C test,
Penhoet's company bought out Cetus, another biotech company, founded
by Donald Glaser, who, like Penhoet, also holds a position as
professor of molecular and cell biology at the University of
California at Berkeley. And Chiron made an unrestricted donation of
about 12 million to the Department of Molecular and Cell Biology at
the University of California at Berkeley that generates $100,000 in
interest each year.
Unfortunately for Peter Duesberg, who belongs to the same department,
his supervisor is yet another professor who consults for Chiron
Corporation - and displays little sympathy for Duesberg for
challenging modern virus hunting by restricting his academic duties
to undergraduate student teaching and by not appointing him to
decision-making committees.
Such conflicts of interest have become standard fixtures in
university biology departments.
The modern biomedical research establishment differs radically from
any previous scientific program in history. Driven by vast infusions
of federal and commercial money, it has grown into an enormous and
powerful bureaucracy that greatly amplifies its successes, all the
while stifling dissent.
Such a process can no longer be called science, which by definition
depends on self-correction by internal challenge and debate.
Despite their popularity among scientists and their companies,
"latent," "slow," and "defective" viruses have achieved only little
prominence as hypothetical causes of degenerative diseases before the
AIDS era. Their hypothetical role in degenerative diseases, which
result from the loss of large numbers of cells, remained confined to
rare, exclusive illnesses like kuru and hepatitis C.
However, because latent, slow, and defective viruses cannot kill
cells, such "viruses" eventually achieved prominence as hypothetical
causes of cancer and thus entered the courts of health care and
medical research. The next chapter describes the terms under which
these viruses were promoted as causes of cancer and how some of these
terms were eventually used to promote latent, slow, and defective
viruses as causes of degenerative diseases including, above all, AIDS.
Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto
*****
http://www.duesberg.com/
Peter H. Duesberg, Ph.D. is a professor of Molecular and Cell Biology
at the University of California, Berkeley. Biographical Sketch
http://www.duesberg.com/about/pdbio.html
He isolated the first cancer gene through his work on
retroviruses in 1970, and mapped the genetic structure of these
viruses. This, and his subsequent work in the same field, resulted in
his election to the National Academy of Sciences in 1986. He is also
the recipient of a seven-year Outstanding Investigator Grant from the
National Institutes of Health.
On the basis of his experience with retroviruses, Duesberg has
challenged the virus-AIDS hypothesis in the pages of such journals as
Cancer Research, Lancet, Proceedings of the National Academy of
Sciences, Science, Nature, Journal of AIDS, AIDS Forschung,
Biomedicine and Pharmacotherapeutics, New England Journal of Medicine
and Research in Immunology. He has instead proposed the hypothesis
that the various American/European AIDS diseases are brought on by
the long-term consumption of recreational drugs and/or AZT itself,
which is prescribed to prevent or treat AIDS. See The AIDS Dilemma:
Drug diseases blamed on a passenger virus.
For a detailed discussion of American/European AIDS as opposed
to African AIDS, see The African AIDS Epidemic: New and Contagious or
Old Under a New Name.
This is Duesberg's official site, containing his written works
on the subject, as well as other scientists that support his views
such as Kary B. Mullis. Kary Mullis won the 1993 Nobel Prize in
Chemistry for his invention of the polymerase chain reaction
technique for detecting DNA. This is the technique used to search for
fragments of HIV in AIDS patients.
Prof. Duesberg's findings have been a thorn in the side of the
medical establishment and drug companies since 1987. Instead of
engaging in scientific debate, however, the only response has been to
cut-off funding to further test Professor's Duesberg's hypothesis.
You can show your support by contributing a tax deductible
donation to help support Prof. Duesberg's lab at the University of
California Berkeley.
More here http://www.duesberg.com/papers/the%20enigma.pdf The Enigma
of Slow Viruses
http://www.virusmyth.com/aids/hiv/pdslowvir.htm
http://www.vaclib.org/basic/gk/pdf/DUESBERG.pdf