Stealth Virus I have the nosodes for it.

[Alva Irish, PhD, DHM,...]

I have the Nosodes for the Stealth virus.
It contains:
Stealth Virus all forms and mutations, LM6 potency
This also contains:
Simian Cytomegalovirus CMV
Borelia Burgdorferi
Mycoplasma Incognitos
Ehilchiosis
Human Herpesvirus - 6 and 8 all LM6 potency.

$50 for 10 pellets shipping included
Pay thru Paypal:
https://www.paypal.com/affil/pal=Dr.Iri ... eopath.net

Please contact me OFF LIST dr_irish@bellsouth.net
Alva Irish
Stealth Viruses

Explore 10:17-19,2001
John Martin, M.D. Ph.D.
Center for Complex Infectioius Diseases
What are Stealth Viruses?
Viruses are submicroscopic infectious agents that replicate inside cells.
Viral illnesses are normally controlled by the body’s immune system acting
primarily through white blood cells called lymphocytes. These cells
recognize certain viral proteins that provide the antigens targeted by
specific lymphocytes, leading to an anti-viral inflammatory response. Not
all viral proteins, however, can function as antigens for effective
anti-viral immunity. Indeed, for many viruses, only a very few proteins are
involved in lymphocyte recognition of virally infected cells. Loss of these
critical antigenic proteins can allow a virus to essentially go unrecognized
by the cellular immune system. When such viruses have managed to retain the
capacity to damage cells, they can potentially cause a persistent infection
resulting in a prolonged illness. The viral nature of such an illness is
usually overlooked because of the absence of overt inflammation.
Atypically-structured cell-damaging (cytopathic) viruses were initially
identified in patients with the chronic fatigue syndrome and in patients
with more severe neurological and neuropsychiatric illnesses. The term
“stealth” was introduced to highlight their basic property of evading
effective immune recognition, and also because they had gone unrecognized by
the medical community.
Detection of Stealth Viruses
Stealth-adapted viruses can be most readily detected using specialized,
semi-quantitative, viral culture methods developed and refined over the last
decade. Using these procedures, stealth viruses will typically induce a
characteristic vacuolating cytopathic effect (CPE) in cultures of human and
animal-derived cells. Stealth virus infected cultures can be distinguished
from cultures of conventional herpesviruses, adenoviruses, enteroviruses and
retroviruses, by the appearance and host range of the CPE, and also by using
selective immunological and molecular probe based assays, including
polymerase chain reaction (PCR) testing methods.
Cytopathic Effects
A common feature of the CPE-induced, stealth adapted viruses is marked
metabolic disruption. This is expressed as lipid accumulation, cytoplasmic
vacuolization, formation of aberrant protein and lipoprotein inclusions, and
abnormally shaped nuclei. Comparable foamy vacuolating cellular changes with
atypical inclusion-like structures can be seen in detailed examination of
brain and other tissues obtained from stealth virus infected patients and
from animals inoculated with these viruses. Unlike infections caused by
conventional cytopathic viruses, the actual production of readily
identifiable viral particles is uncommon. Seemingly, the infected cells are
metabolically impaired because various energy and other resources are
diverted towards an inefficient and unbalanced synthesis of various virus
coded components at the expense of normal cellular functions. Severe defects
in energy-generating metabolic pathways are also apparent from the marked
mitochondrial changes that are prominent in electron micrographs of
virus-infected cells.
Center for Complex Infections Diseases
Both clinical- and research-based studies on stealth-adapted viruses have
been undertaken at the Center for Complex Infectious Diseases in Rosemead,
California. CCID is a non-profit organization under the National Heritage
Foundation dedicated to understanding the nature, origin, disease
associations, modes of transmission, methods of diagnosis and responses to
therapy of stealth virus infections, and to the dissemination such
information to the medical and lay communities. Information regarding CCID
is available from the internet at www.ccid.org. Additional information is
available from www.EmergingWorlds.com. The following sections provide a
brief overview of some of the ongoing research activities being conducted at
CCID.
DNA Sequencing Studies
A stealth virus isolated from a patient with a chronic fatigue syndrome like
illness was originally noted to have limited DNA sequence homology to human
cytomegalovirus (CMV). As additional sequence data became available, it
became obvious that this virus was a derivative, not of human CMV, but
rather of an African green monkey simian CMV (SCMV). Until the beginning of
last year, these monkeys were routinely used to produce live poliovirus
vaccine. Moreover, although not widely revealed, a joint Food and Drug
Administration/Industry study in 1972 indicated that control kidney cell
cultures from all 12 African green monkeys tested grew out SCMV, and that
most of these isolates were not detectable using standard procedures.
Continued sequencing on the SCMV-derived stealth-adapted virus has shown
interesting changes compared to a typical CMV. Of special note is the uneven
representation of genes that encode various viral components. As expected,
the genes that code the proteins known to provide major target antigens for
anti-CMV cytotoxic T lymphocytes are either absent or mutated. Other genes
are overly represented, including genes that code for various chemokines and
for chemokine receptors. Interestingly, one of the markedly amplified
chemokine receptor coding genes found in the stealth virus genome can also
function as a receptor for HIV, suggesting a possible potentiating role of
stealth viruses in HIV infected patients.
One set of amplified chemokine-coding genes detected in the stealth-adapted
virus is of cellular, rather than viral, origin. Cellular genes can
apparently be incorporated into stealth virus genomes, presumably during
viral replication. The particular chemokine-coding cellular gene identified
within the prototype SCMV-derived stealth virus was probably assimilated as
a partially processed RNA molecule since it lacks the normal introns present
in cellular DNA. This implies that stealth virus DNA replication is
proceeding through RNA intermediates, and that it may, therefore, be
dependent upon reverse transcriptase, as could be provided by an assimilated
endogenous retroviruses. RNA to DNA replication is much more prone to error
than is DNA to DNA replication. This might explain sequence variability
between the three copies of the chemokine-coding cell-derived gene that have
so far been identified within the stealth virus.
Chemokine receptor genes of both viral and cellular origins have been
implicated in the development of several types of malignancies. It is
somewhat worrisome, therefore, that the stealth adapted virus is apparently
employing this type of gene for its survival. On the other hand, many
therapeutic agents that appear to be of some benefit to stealth virus
infected patients are known to inhibit cheomkine production and receptor
activity.
Viteria
It has also been determined that stealth viruses have the ability to acquire
genetic sequences of bacterial and even fungal origin. Normally, viruses
that are infectious for human or animal cells (eukaryotic cells) will not
infect bacteria (prokaryotic cells). Stealth viruses appear to have overcome
this phylogenetic barrier. The term "viteria" has been coined to define
eukaryotic viruses that have acquired bacteria-derived genetic sequences.
The sources of the bacterial sequences include microorganisms that are not
known to grow intracellularly within eukaryotic cells. This strongly
suggests that stealth viruses become viteria by infecting bacteria. Judging
from the bacterial sequences so far identified, genes have been captured
from a wide variety of both gram positive and gram negative bacteria. The
linear arrangements of many of the bacterial-derived sequences are quite
different from any of the known major bacteria, suggesting that an active
ongoing selection process may be occurring to assist in stealth virus
propagation within bacteria. Genetically empowered bacteria, carrying
potentially oncogenic stealth-adapted viruses, could become a far more
threatening biological weapons program then ever envisioned by military
planners.
Bacterial sequences incorporated within stealth-adapted viruses may help
explain positive findings in stealth virus infected patients in various
tests for known bacteria, including Borrelia burgdoferi (the cause of
authentic Lyme disease), mycoplasma (a suggested cause of CFS and Gulf war
syndrome); chlamydia (implicated in coronary artery disease and Alzheimer’s
disease), etc. None of the commonly used assays for these bacteria actually
detect cultured organisms, but instead rely upon broadly reactive molecular
and/or serological testing that could as easily be explained by the presence
of viteria.
Clinical Conditions Associated with Stealth Virus Infections
Stealth-adapted viruses have been recovered from the blood, cerebrospinal
fluid, urine, throat swabs, breast milk, brain biopsies and tumor samples
from patients with various neurological, psychiatric, auto-immune, allergic
and neoplastic diseases. Examples of neurological illnesses are autism,
attention deficit and behavioral disorders in children; depression,
schizophrenia, amyotrophic lateral sclerosis, multiple sclerosis, chronic
fatigue and fibromyalgia in adults; and neurodegenerative illnesses in the
elderly. It is now known that the stealth viruses can infect many organs,
but that the brain is especially prone to manifest the effects of even
limited localized cellular damage. The varying manifestations of a stealth
virus encephalopathy is probably heavily influenced by the timing of
infection, regions of the brain that are mostly involved, genetic
predisposition to particular symptoms and the additive pathology of any
superimposed auto-immune component triggered by the viral induced cellular
damage. CCID's focus is away from strict clinical categorization of stealth
virus infected patients into discrete neurological and neuropsychiatric
illnesses. This viewpoint has been supported by following individual
patients over several years, and also by the not uncommon occurrences of
related, yet diverse, illnesses occurring among other family members and
even among household pets. Community-wide outbreaks of stealth virus
infections have also been observed with individuals showing varying levels
of severity and duration of illness. Neither the reporting of otherwise
unexplainable deaths, nor the apparent “dumbing” of a whole township, as
reflected in the excessive need for special education for its children,
appears to provide adequate Public Health motivation to confirm CCID’s
findings of stealth-adapted viruses.
Cancer can now be added to the list of potential stealth virus-associated
diseases. Positive stealth virus cultures have been seen in virtually all of
the multiple myeloma patients tested, and in several patients presenting
with other types of tumors. A previous history of a fatiguing illness and
clinical indications of impairments in normal brain functions are suggestive
of an underlying stealth adapted virus infection in a cancer patient. It
will be interesting to determine the effect of stealth-virus suppressive
therapy in such patients.
Infection Among Blood Donors
An indication of the probable prevalence of infection among apparently
healthy individuals has come from studies conducted on student blood donors
attending a college campus. Slightly less than 10% of the units tested gave
a positive result. As a requirement of the study, it was not possible to
determine the actual health status of these students. Nor were efforts
allowed to follow recipients of the stealth virus positive blood units. Even
if culture-positive individuals are presently asymptomatic, this would not
preclude their being at risk for subsequent development of a stealth-virus
associated illness. This concern is underscored by the apparent capacity of
stealth-adapted viruses to “capture, amplify and mutate” various additional
genes of viral, cellular and bacterial origins.
Role of Other Infectious Agents in Chronic Illnesses.
Much of the debate over a potential infectious cause for many of the
illnesses that are increasingly being seen within our society has centered
upon conventional microorganisms. Patient support groups and their
affiliating clinicians have championed alternative explanations for these
illnesses. Human herpesvirus-6 (HHV-6), human herpesvirus-8 (HHV-8),
enteroviruses and parvoviruses feature among the viral causes for these
illnesses, while Borrelia burgdoferi, Mycoplasma incognitos and Ehlichiosis
are being promoted as the bacterial causes for a wide spectrum of illnesses.
As is the case for HHV-6 in CFS, HHV-8 in multiple myeloma, enterovirus in
ALS and Borrelia in chronic Lyme disease, when looked at critically, the
actual findings are generally inconsistent with a true etiological
relationship. None of these negative studies exclude the role atypically
structured microorganisms; indeed, if anything they strongly support their
presence. As alluded to above, stealth-adapted viruses can easily be
mistaken in diagnostic tests for conventional viral and bacterial pathogens.
Additional complex associations between stealth adapted viruses and
conventional microorganisms may exist. For example, the lipid-laden cells
infected with a stealth virus appear especially favorable to the growth of
intracellular bacteria, including Borrelia, the causative agent of Lyme
disease. CCID has demonstrated positive stealth virus cultures in blood
samples from over 90% of patients referred with a diagnosis of chronic Lyme
disease. Whether the patients are actually infected with Borrelia remains
unproven, but if so, their growth may be dependent upon an accompanying
stealth virus infection. Synergistic growth patterns between stealth adapted
viruses and the viruses present in several live viral vaccine preparations,
have also been observed. The potential role of stealth virus encoded
chemokine receptors in the evolution and the present day expression of HIV,
is also under consideration.
Clinical Approach to the Diagnosis and Therapy of Stealth Adapted Virus
Infections (SAVI)
Diagnosis: A major challenge in providing medical care for stealth virus
infected patients is the multiple and diverse clinical manifestations of the
patients’ illnesses. Individual patients do not fit comfortably into a
single medical discipline, whether it is psychiatry, neurology,
rheumatology, endocrinology, hematology, or any other. Imprecise diagnostic
labels, such as CFS, fibromyalgia, depression, attention deficit, etc., and
even the better defined diagnostic labels, such as schizophrenia, autism,
ALS, multiple sclerosis, Alzheimer’s disease, etc., tend to obscure the
complex multi-system nature of the patients’ illnesses. Another difficulty
is quantitating the severity of disease processes that can vary widely over
time, and can be influenced by such non-specific factors as stress,
environmental exposures to chemicals, placebo effects, etc.
Disordered brain function can be anticipated in many stealth virus infected
patients. This can be documented using a detailed neurological examination,
with a focus on what are sometimes referred to as “soft” neurological signs.
Ancillary, although expensive, tests such as SPECT scans, quantitative EEG
and formal neurocognitive evaluations, can help substantiate a diagnosis of
stealth adapted virus infection with encephalopathy. Additional syndrome
names can be applied depending on clinical and laboratory findings.
Tabulation of symptoms using a detailed questionnaire can be helpful in
identifying clinical problems and in assessing therapy related improvements.
Therapy: Until the existence of stealth viruses is accepted by Public Health
authorities, there will be no approved standard of care in providing
anti-viral treatments. Several suggestions can be made, however, from what
is currently known about the prototype SCMV-derived stealth virus. Whether
these suggestions are relevant to atypical viruses cultured from other
patients remains to be tested. CCID is now reaching out to clinicians
involved with the care of stealth virus infected patients for assistance
with these clinical trials.
Basically, it seems appropriate to undertake efforts to suppress stealth
virus activation and at the same time to support cellular metabolism,
especially mitochondria function. The remarkable expansion of chemokine and
chemokine-receptor related genes within the prototype SCMV-derived
stealth-adapted virus support the potential use of agents that can down
regulate chemokine pathways. Fortunately, many of the widely used herbal and
generally non-toxic allopathic medicines are known to interfere with
chemokine signaling. It is probably more than a coincidence that many of the
compounds have also been reported to benefit at least a proportion of
patients with CFS and related illnesses. Ideally, patients receiving these
relatively simple therapies would be retested for stealth virus activity. If
there were no apparent reduction in stealth virus activity, and if the
patient remained symptomatic, one could more easily justify the use of
potentially more toxic allopathic medicines, including known anti
herpesviral agents.
For patients with major neurological, psychiatric, autoimmune or malignant
diseases, the stealth virus associated treatments will simply be an aside to
the accepted standard care of the patient’s underlying illness. Once
sufficient supportive data are collected, it may be possible to proceed
directly with anti-stealth virus therapy as the primary treatment for these
severe disorders.
Request for Assistance with Clinical Therapeutic Studies
In support of these studies, CCID has begun to work with medical specialists
treating major medical neurological, psychiatric, rheumatological and
neoplastic illnesses, and also with orthomolecular clinicians experienced in
the uses of alternative medicines. Stealth virus culture activity will be
serially determined and correlated with the use of various therapeutic
modalities and changes in clinical status. CCID can provide copies of
patient questionnaires and an appropriate informed consent form. A database
for integrating laboratory, clinical and pharmaceutical data, will be
established and will be assessable to all participating clinicians. The type
of program is urgently needed to address the major Public Health threat
posed by stealth-adapted viruses and viteria.
Additional information and copies of various research publications on
stealth viruses, requisition forms, etc, can be viewed at www.ccid.org.
Clinicians wishing to participate in stealth virus research should contact
CCID. Stealth virus testing requires an Acid Citrate Dextrose (ACD)
yellow-topped tube of whole blood. While a $250.00 fee is required for an
initial diagnostic assay, a subsequent test on the patient during or
following therapy will be at no charge. Blood samples should be sent via
Federal Express to CCID, accompanied by a physician request for testing.
CCID is located at 3328 Stevens Avenue, Rosemead, CA 91770. Ph. (626)
572-7288, Fax (626) 572-9288, e-mail ccidlab@hotmail.com.