FYI Hiv to AIDS Disease model revised

[Didi Ananda Rucira]

Greetings all,

FYI: from www.keephopealive.org
there's this and more. go and visit the site!
didi
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Journal of Immunity

Vol 4 No 4 Annual Summary Edition 2006/07

Hiv to AIDS Disease model revised
"Monkey business"

C LeBeau / M Konlee

In this issue, the Sooty Mangobey, a long tailed monkey infected with SIV, gives up its secrets and profoundly changes our understanding of the current HIV to AIDS disease model.

This special edition summarizes the 6 past issues of JOI (2005/06) plus the latest updated news on immune-based medicine in the treatment of HIV, cancer and other conditions. The full unedited versions of JOI can be found online at keephopealive.org.
Keep Hope Alive Forum
"speaking truth to power"

This edition also introduces the Keep Hope Alive Forum, where local and international issues that adversely affect the human race will be discussed and proposed solutions offered. Our first topic is Iraq. We offer a detailed plan to bring stability and peace to Iraq and American troops home. We hope that our plan for peace and stability becomes part of the national dialogue about ending the violence in this troubled land. If you agree with our proposals, tear off the last page of this newsletter and mail it to your Congressman or Senator with a note asking them to support these proposals or make copies for distribution.

Other issues that will be addressed in the future will include plans for low cost health care that will require the federal government to test and approve hundreds of new and old low-cost medical treatments from any and all sources including dietary supplements, botanicals, oxidative medicine, folk medicine, alternative meds and drugs whose patents have expired.

Other topics will include environmental issues, clean and renewable energy, wind, solar and geothermal plus monetary and banking reform, interest rate and debt reduction.
Sooty Mangobey - SIV does not cause AIDS in this monkey due to down regulation of immune response by SIV's nef gene

(See related article on page 3)
HIV to AIDS disease model revised
Will the National Institute of Health correct a flawed disease model?

We have constructed a new disease model for AIDS that turns the old disease model of the past 25 years on its head. The widespread belief that HIV-1 (referred to usually as HIV) is a virus that attacks and destroys the immune system is simply wrong. Say what?

Scientific research finds that HIV-1 is not a pathogenic immune deficiency virus and AIDS is not an immune deficiency disease, but rather, is one of dysfunction. HIV-1 is actually a harmless virus in-vitro but causes immune dysfunction in-vivo (in a person) by being there and provoking an antibody response.
If there were no antibody response to HIV, there would be no disease called AIDS. In a few words, what people with HIV-1 need is an immune system tranquilizer - one that specifically slows down the part of the immune system that is overactive and ineffective - the HIV antibodies.

In the Sooty Mangobeys infected with Simian Immunodeficiency Virus (SIV), the virus from which HIV-2 evolved does not cause immune dysfunction due to down-regulation of the immune response by its nef gene. This occurs in spite of viral loads in the hundreds of thousands. HIV-2, like SIV in Sooty Mangobeys, is not pathogenic.

HIV-1 causes AIDS in humans because it over-stimulates the TH2 arm of the immune system. TH2 B-cell activity then suppresses TH1 immunity that is effective.

HIV-1 provokes an antibody immune response by inflammatory cytokines (protein immune modulators) interleukin 6 (IL-6), tumor necrosis factor a (TNF-a) and Nuclear factor kappa B (NF-KappaB).
"HIV" should be renamed "HOV"

This overactive antibody response is also called humoral immunity or TH2 type immunity. HIV should be renamed Humoral Overactivity Virus (HOV) and AIDS should be renamed Acquired Immune Dysfunction (not deficiency) Syndrome.

This revised disease model provides the rational basis for using anti-inflammatory treatments and drugs (glucocorticoids - cortisol, prednisolone et al) that help balance the TH1 and TH2 arms of the immune system by suppressing TH2 type cytokines that drive humoral immunity. Lowering the TH2 arm of the immune system has the teeter-tooter effect of raising the TH1 arm that is cell-mediated immunity that is effective against the disease process in AIDS and cancer.
Medical Advisory Board

David Miyauchi MD, Honolulu, HI 808-949-8711 Richard Simmons MD Westerville, OH 614-895-0102 Susan Groh, MD Merrick , NY Ronald Peters MD Cave Creek, AZ Bruce Levine DC Syosset, NY 516-364-3382 Gayle Eversole CRNP, PhD, AHG Lake Stevens, WA Christina White BA, Richland Ctr, WI Robert Carson MD, Hawthorne, NY

Keep Hope Alive Ltd is an IRS approved 501 (C) 3 non-profit organization. All donations are tax deductible.

Keep Hope Alive publishes the Journal of Immunity quarterly.

Keep Hope Alive, PO Box 270041, West Allis, WI 53227 414-545-6539

To receive the Journal of Immunity, see the last page of this magazine. Interim reports of this journal that are 8 pages in length are published every 3 months with one annual report at year's end that includes reprints of the quarterly reports.

The Journal of Immunity supplements information in the new Immune Restoration Handbook 2nd edition that has now replaced the earlier edition. All current and past newsletters can be accessed on our internet website at www.keephopealive.org that also contains over 1000 pages of information on nutritional and immune-based therapies and an interactive Message Board
Board Of Directors: Conrad LeBeau, Patrick Raess, Tina Otto.
Balancing TH1 and TH2 immunity

The branch of the immune system called TH1 or cell-mediated immunity (CMI) is the effective one against cancer and AIDS. CMI is stimulated in part by the cytokines IL-2, IL-12 and gamma interferon. CD8 cytotoxic lymphocytes and Natural Killer cells are white blood cells that provide immunity against cancer and AIDS. In practice, stimulating TH1 cytokines has failed to restore normal immune function because of over expressed TH2 cytokine activity.

The immunological shift from TH1 to TH2 substantially weakens the immune response against AIDS, cancer and other health related conditions like Autism while strengthening the antibody immune response against the common cold and seasonal flu. Other cytokines are cross-regulatory and affect both branches of the immune system. The key to normalcy and immune restoration is immune balance.
HIV = AIDS disease model is wrong

To stop HIV progression to AIDS, we needed to find a way to suppress and control the inflammatory cytokines that drive the TH2 arm of the immune system. The inflammatory cytokines we know about today are NF-Kappa B, TNF-a and IL-6 but there could be more that will be discovered in due time. It was not only Alfred Plechner, DVM, whose 30 plus years of treating over 35,000 dogs, cats and other pets with prednisolone and thyroid that finally opened our eyes to scrapping the disease model of the past 25 years that HIV is pathogenic and directly causes immune deficiency but also the research in Germany of Albrecht Ulmer et al in a controlled study that demonstrated that even a low dose of just 5 mg daily of prednisolone could single handedly keep the CD4 counts high and AIDS at bay over a 2 year period.

Ulmer, who has published over 166 articles in peer reviewed medical journals, did not hype the results of his study, but we are and for good cause. (See the abstract from his research a few pages in this newsletter).

Just one headline story about the amazing benefits of immunotherapy (low-dose glucocorticoids) in treating AIDS in any one of our major media (CNN, MSNBC, FOX, ABC, CBS, NBC etc) would have a worldwide impact and could open minds globally on new treatment options that could save millions of lives. The 1980s motto of ACT-UP that "Silence = death" is true.

There are the studies of the National Institute of Health in the 1990's that short term use of high dose prednisone could more than double the CD4 counts in as little as 3 weeks. Unfortunately, research with low cost immunotherapy using glucocorticoids stopped and research with low dose glucocorticoids never started.
Correcting the HIV to AIDS disease model

We are trying to present a new disease model because someone has to do it. So many people, including ourselves got it wrong in the past 25 years. We thought HIV was pathogenic, that is it would attack and destroy CD4 cells, the Generals of the immune system. We thought HIV was an immunodeficiency virus and AIDS were an immunodeficiency disease. We were wrong but we learned to evolve our understanding of this illness by having an open mind and searching for definitive cause and effect relationships.

HIV is not an immunodeficiency virus, it is a Humoral Overactivity Virus or abbreviated as HOV. The tragic mistake today is that doctors and the pharmaceutical drugs they use to treat AIDS is not to treat AIDS as a disease of the immune system, but as a viral infection.

After 10 years of HAART with protease inhibitors used in combination with reverse transcriptase inhibitors and NNRTIs, nearly half of all patients now believe that the side effects of the drugs are as bad if not worse than the HIV virus. Today a very noticeable effect of long-term drug combos for AIDS is wasting syndrome - loss of lean muscle mass. Low dose glucocorticoids like cortisol could help reverse this and stimulate weight gain and help in immune restoration, if only the doctors and the patients knew.
The immune system reaction to "HIV-1" is how it "causes" AIDS

HIV causes AIDS by simply being in the body as a foreign presence. HIV is not pathogenic; that is, it does not directly kill any cells. It presence is like a red flag in front of a bull. It drives an antibody response (TH2) by just being there as well as constantly mutating. The T cell type 2 response (TH2) strongly activates inflammatory cytokines including nuclear factor kappa B (NF-Kappa B), tumor necrosis factor a (TNF-a) and interleukin 6 (IL-6). This leads to the continuous overworking of the CD4 helper cells and thus shortens their life span. If the immune system could be taught to ignore HIV, this virus would never cause AIDS and would in and of itself cause no illness.

This is a profound concept and is the basis for using anti-inflammatory immune-based therapies that reduce and even suppress TH2 type immune activity. AIDS is not a disease of immune deficiency, but rather one of immune exhaustion. In a few words, the CD4 helper cells and other white blood cells literally work themselves to death to remove this foreign entity called HIV that is perceived as a threat. The evolving realities of what AIDS really is calls for an immune-based therapy that is a tranquilizer for the immune system to give it a rest and stop the apoptosis (death) of the T cells.

AIDS is not caused directly by HIV, but rather by the immune systems reaction to the presence of HIV, a virus that is actually benign and "harmless in a laboratory."

Today's faulty disease model implies that HIV destroys the immune system single-handedly and causes AIDS. Nothing could be further from the truth. This flawed disease model feeds the sales of patented drugs that continue their relentless attack against this harmless virus while patients continue to die from immune dysfunction or the side effects of the drugs they have been told they must take all their life or until death do they part. For many, these words are all too true.

For pulsed therapy or short-term use, the strictly ant-viral drugs for HIV are beneficial as they reduce the foreign presence or stimulus that drives the inflammatory immune reaction.

Why are patients with CD4 counts above 350 being told to take their antiviral meds when the government guidelines only recommend to start using the anti-HIV meds when the CD4 count drop below 350? This is a contradiction. When a person is first diagnosed with HIV and the CD4 counts is above 350, the person is not required to take the meds. Note: Current NIH guidelines do not recommend anti-viral HIV drugs when the CD4 count is above 350 unless the viral load is over 100,000. The NIH guidelines suggest that the CD4 count is more important than the viral load. On this point we agree whole heartedly with the NIH. Pharmaceutical salesmen have misled medical doctors into believing that keeping an HIV viral load non-detectable is a primary therapeutic goal for patient survival. Clinical research finds that keeping CD4 counts above 200 and especially above 300 is the key to a symptom free life, survivial and normal immune function. Today, many long term survivors with non-detectable viral loads have falling CD4 cell counts and loss of lean muscle mass subjecting them to life threatenting opportunistic infections. With the loss of lean muscle mass associated with elevated levels of il-6 and TNF-a, these patients also have higher than average outbreak of various types of cancer.

Another argument promoted by big Pharma is that stopping the use of the anti-viral meds for several months will promote viral resistance. It is impossible to develop resistance to a drug you are not using. In fact, clinical experience shows that an extended drug vacation restores sensitivity to the anti-viral drugs that you previously used. One recent study claims that pulsing the drugs use - one week on and one week off was not as effective after a year as using them continuously. This study does not prove that the anti-viral meds are the only option available to patients. There is the alternative of immunotherapy that continues to be ignored by the mass media and most of the media that reaches the HIV+ audience. This newsletter single handedly addresses the issue of "immune restoration" that continues to be ignored by the other media (GMHC, POZ magazine and Project Inform etc) organizations that are funded by pharmacuetical companies and/or advertisements for the anti-viral drugs. It may seem ironic here that the following article comes from AIDSmeds.com but the nef gene in SIV found in monkeys supports the hypothesis of using glucocorticoids to down regulate the immune response and stopping HIV (HOV) progression to AIDS in humans.
SIV "nef protein" prevents immune system decline in monkeys (mimicking the effects of glucocorticoids in humans with HIV-1)
An Accident of Evolution

by Tim Horn, Senior Writer & Editor, AIDSmeds.com

HIV's ability to damage the human immune system might amount to an accident of evolution, notably the loss of the protective function of a viral protein called Nef. Like HIV in humans, related strains of simian immunodeficiency virus (SIV) are rampant among many species of monkeys. Unlike HIV in humans, many primates infected with SIV don't experience immune suppression or suffer the symptoms associated with AIDS.

The evidence, published by an international team of researchers in the June 2006 issue of Cell, is the first to offer an explanation for this striking difference.

The group found that a viral protein known to help the virus evade the immune system, thereby allowing the SIVs that infect monkeys to persist and multiply with high efficiency, also has a protective role in the host immune system. The SIV Nef protein ratchets down the activation of T-cells following infection in primates, thereby limiting the harmful effects that can be caused by chronically strong immune activation.

While chronically strong immune activation may seem like a good thing when it comes to fighting HIV infection, it ends up causing the death of many T-cells and ultimately exhausts the immune system - two factors that can lead to AIDS.

The HIV Nef protein, and those of its closest related simian viruses, however, lack this protective function, leaving those infected susceptible to the heightened immune activation associated with progression to AIDS, according to the new research.

"Nef-mediated suppression of T-cell activation is a fundamental property of primate lentiviruses that likely evolved to maintain viral persistence in the context of an intact host immune system," Dr. Frank Kirchhoff of the University of Ulm in Germany said. "The findings suggest that the gene function was lost during viral evolution in a lineage that gave rise to HIV-1 and may have predisposed the simian precursor of HIV-1 for greater pathogenicity in humans."

"Heightened immune activation is the only clear-cut difference between pathogenic and non-pathogenic infections with the immunodeficiency viruses," Dr. Kirchhoff added. "The observed difference in Nef function may provide, for the first time, a mechanism to explain why many monkey species naturally infected with SIV do not develop disease."

Study coauthor Dr. Beatrice Hahn of the University of Alabama has previously shown that the two forms of HIV that infect humans originated from related SIVs found in different species of African.

HIV-1 - most closely related to an SIV strain found in chimpanzees - is the more virulent of the two human strains and the source of the majority of HIV infections throughout the world. The less pathogenic HIV-2 evolved from a virus that infects long-tailed relatives of baboons called sooty mangabeys. While HIV and SIV strains all infect T-cells that are critical for a functional immune response, SIV usually does so without causing serious damage in their natural primate hosts.

Of more than 30 SIVs that have been molecularly characterized, all encode a Nef gene. However, information about the gene's function has come from studies involving the HIV-1 version of Nef. In turn, Dr. Kirchhoff and his group examined Nef genes taken from a variety of SIV types.

According to the research conducted by Dr. Kirchhoff's group, Nef variants from the great majority of primate SIVs, including the less virulent human strain HIV-2, suppress the expression of a receptor normally found on the surface of T-cells, making the immune cells less responsive to activation. In contrast, the Nef gene of HIV-1 and a subset of closely related SIVs failed to limit T-cell activation and death.

"Intriguingly, this loss of Nef-mediated suppression of T cell activation appears to have occurred twice, once in the ancestor of a group of viruses infecting Cercopithecus monkeys, and once in SIVcpz, the ancestor of HIV-1 which infects chimpanzees," noted study coauthor Dr. Paul Sharp, of the University of Nottingham, who is a leading expert in HIV and SIV evolution.

"What these viruses have in common is a Vpu gene, not found in other SIVs, and so it's tempting to speculate that the presence of Vpu is somehow causally related to the change in Nef function," Dr. Sharp added.

The findings expand on previous studies that found that Nef-deficient SIV failed to cause symptoms in a monkey species normally susceptible to disease.

Other researchers have reported in the past that rhesus macaques infected with the Nef-deficient virus had extremely low viral loads and limited evidence of disease progression. Similarly, humans infected with Nef-defective HIV progress to disease symptoms slowly, if at all.

While altering HIV's Nef gene may not be a therapeutic possibility for those infected with the virus, these results - along with research conducted by several other teams - suggest the use of treatments that could carefully limit immune system activation in humans. This, Dr. Kirchhoff says, would mimic the tight immune system-virus balance seen in non-human primates.

"A strong immune response can be good in the short term, but if sustained for a long time as in those with HIV, it can exhaust the immune system," Dr, Kirchhoff said. "If you could somehow dampen the response, it might effectively convert the condition to the more chronic, asymptomatic infection seen in monkeys."

Source:
Schindler M, Münch J, Kutsch, et al. Nef-mediated suppression of T cell activation was lost in a lentiviral lineage that gave rise to HIV-1. Cell 125:1055-67, 2006.

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SIV "nef gene" research supports our hypothesis that stimulation of the immune system is how HIV causes AIDS. Conrad LeBeau

I could not agree more with Dr. Kirchhoff statement that "Heightened immune activation is the only clear-cut difference between pathogenic and non-pathogenic infections with the immunodeficiency viruses,"

The implications of this latest published research are profound. Will doctors now appreciate the benefits of using low dose immuno-suppressive drugs to stop HIV progression to AIDS in humans? Clearly low dose glucocorticoids (prednisolone, hydrocortisone) can mimic the effects of the SIV nef gene in monkeys who remain healthy in spite of their high viral loads.
Sincerely,
Didi Ananda Ruchira
Director, Abha Light
visit: www.abhalight.org
tel: +254 20 445-0181 / cells: 0733-895466 / 0723-869133
skype: anandarucira
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