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Monkey business: Or not...
Aids comes from our Human genome   Prt 3
March 01, 2009
Andrew Maniotis, PhD

Expanding on the preceding article, the following is taken from two comments Dr Maniotis posted to an article in the New Statesman where Mike Barrett reviews a book: Virus: the co-discoverer of HIV tracks its rampage and charts the future - by Luc Montagnier

Monkey business:  Aids is still killing millions in Africa
Mike Barrett charts the controversy surrounding its discovery

Comments by
Andrew Maniotis
31 October 2008 at 13:28

... and a further comment by Andrew Maniotis
31 October 2008 at 19:34

What I forgot to add is:



A likely explanation of the origin of “HIV” comes not from notions of monkey or ape-to-human transmission due to Africans smearing monkey blood on their loins for sexual orgies as published in The Lancet and other top journals (1), nor was "HIV" likely transmitted to African children or their parents by playing with or by eating dead monkeys or chimps as "bush-meat" because their parents couldn't find or afford toys or food (2). "HIV" did not emerge from a Special Virus Program conspiracy that the U.S. government planned for population control or for germ warfare. "HIV" did not crawl out from a monkey or chimp kidney culture used during the manufacture the hepatitis B vaccine or other vaccines.

Recent studies in gene research suggest that the so-called specific markers of “HIV” are produced by our own non-specific endogenous DNA sequences called retroelements or "retroids."

A retroid is a special kind of mobile gene sequence that has been associated with diseases such as multiple sclerosis, and with normal biological functions involving the placenta (3). It is known that these retroid sequences make cellular proteins that are expressed by normal uninfected (healthy) yeast, insects, and a variety of mammals (4), 50% of healthy dogs (5), "uninfected" rhesus monkeys, chimps, and humans (6). Retroelements are now known to be important sequences for telomere replication at the tips of normal and cancer cell chromosomes (7). Once claimed by AIDS scientists to be a specific molecular component required for "HIV" replication, retroids and specifically reverse transcriptases (RT) are now seen frequently in market magazines concerning biotechnology stocks (8,9) in the context of normal, non-pathological situations, despite what AIDS proponents continue to claim about the specificity of RT to exogenous retroviruses. p24, another protein once thought to be the unique capsid protein that makes up the proteinaceous shell of “HIV” is now known to be expressed in the thymus glands of "HIV-negative" children (10). An "HIV" positive result can also occur when some infants are exposed to the proteins in cow's or goat's milk (11) as well as after the flu vaccine (12), hepatitis B vaccine (13), in normal pregnant women (14), under conditions of stress caused by disease, drugs, oxidation, or malnutrition, or dozens of other factors or reasons (15), but paradoxically, not after specific "HIV" sequences or proteins are directly injected into "HIV-negative" "HIV-vaccine recipients.

That these endogenous human genetic elements exist but yet are ill-defined has been shown again and again to be likely from studies on presumptively named "HERVs" (Human Endogenous Retro-Viruses) such as the "Phoenix viruses" (presumptively so named because nobody has shown that endogenous infectious "retroviruses" exist). "HERVs" (viral-like particles that look like "HIV" virus particles are supposed to look) can be produced by infecting (transfecting in Petri dishes) cells with certain sequences of DNA or RNA (16), which then are replicated and packaged by the cells into virus-like "enveloped" particles that look identical to "HIV." Modern analyses of the human genome database (which presumably wasn't derived from anyone infected with "HIV") have revealed more than 120,000 full-length retroids containing (once thought to be) specific viral reverse transcriptase transcripts (17).

Although the "HIV=AIDS" Establishment is always saying the "HIV viruses" reverse transcriptase sequence and other parts of its genome are mutating every time a patient dies while on “life saving” anti-retroviral drugs that supposedly target this and other "HIV-specific" gene sequence products, genomic analyses show that these retroid reverse transcriptase elements are among the most stable transcripts that make up these retroids. In other words, amongst gene sequence analysts, it is the sequence stability rather than the instability or mutability of the reverse transcriptase sequence itself that make these 120,000 retroelement sequences possible to classify as distinct sequences (17), while at the same time, the AIDS Establishment points to the mutability of these same sequences as the reason why they have failed to find a stable target in "the AIDS virus."

Clinical evidence that this non-specific retroid hypothesis is correct and is the cause of "HIV's" molecular signature(s) is supported by therapeutic studies conducted in connection with German drug rehabilitation clinics by Heinrich Kremer M.D., who was Medical Director of the Federal Clinics for Juvenile and Young Adult Drug Offenders for five German counties, including Berlin, Bremen, and Hamburg, Dr. Juliane Sacher, and their colleagues, who two decades ago noticed a paradox:

"AIDS patients had high, sometimes extreme amounts of gammaglobulins (immunoglobulins, antibodies), 35-40, even 45% instead of the normal 18%. But Dr. Sacher had learned in her training that T4-cells are called "helper" cells because they enable B-cells to become plasma cells which produce gammaglobulins. How could it be that patients supposed to be low in T4-cells were producing excess gammaglobulins? The answer, shown by research in later years, is that the T4-cells are not destroyed (until anergy results later), they merely absent themselves from the blood and move elsewhere (the lymph nodes)."

"In the late 1980s and early 1990s it was realized that there are two kinds of T4-cells, namely Th1 and Th2. In "HIV/AIDS" patients, the balance was shifted toward Th2 and away from Th1, i.e. a lack of Th1 and an excess of Th2. Those Th2 cells move into the lymph system to assist B-cells to produce gammaglobulins. Hence the oft-noted swelling of the lymph nodes in "HIV/AIDS" patients, reflecting chronic and rather intractable inflammation."

"This [phenomenon] also explains why "cocktail" "HIV/AIDS" therapy works. It is cytostatic---it kills cells---and thereby attacks the processes that caused the inflammation. When the lymph-node inflammation subsides, the count of the T4-cells in the blood increases again as they move back into the blood. Recent work has indeed shown that these cells are not newly generated; they never were destroyed in the first place. To this day no one has shown how "HIV" is supposed to kill T4-cells."

Thus the German "HIV/AIDS" team first proposed that the immune cell Th2/Th1 ratio is imbalanced in "AIDS" patients, and a consequent hypergammaglobulinemia characteristic of "HIV's" molecular signatures result, which can be modulated in profoundly immune suppressed patients through the toxic effects of the ARVs, at least for a while. Although the information about these observations have been suppressed and funding for the studies was withdrawn by the German government without explanation after early enthusiasm for the progress of Drs. Kremer Dr. Sacher and others (18), currently Dr. Kremer and Dr. Sacher and their colleagues claim to have been curing AIDS patients with glutathione, alpha-lipoic acid, patient-specific amino acid profile restoration as well as vitamin, mineral, and trace element restoration in a patient-specific manner for 20 years. Also, cysteine, Ginkgo, proteolytic enzymes, mild aerobic exercise, and other non-toxic means have been employed successfully in these German drug clinics for 20 or more years to reverse immune suppression, "AIDS," and "HIV-disease."

Furthermore, according to these "HIV/AIDS" physicians, in these therapeutic trials, HAART has only occasionally been given for short periods of time successfully in some of the profound immune suppressed cases, because this toxic cocktail antagonizes the imbalanced proliferation (disturbed TH1/TH2 ratio) of these cells, because they are rank cytotoxic poisons. Both in non-symptomatic "HIV" patients and in some profoundly suppressed "AIDS patients," HAART has the ability to dampen the molecular markers that these imbalanced sets of cells generate (and which are read as high viral load although no virus particles have been photographed or isolated). At higher doses HAART may antagonize raging bacterial infections, protozoa, and fungal infections. However, if given chronically, it is now well established that HAART will eventually wipe the immune system out and render the patient anergic and bone-marrow depressed, not to mention the toxic effects of the HAART regimens given chronically exert on the intestines, platelets, and other tissues that lead to mal-absorption disorders, neuropathies, and lypodystrophies, heart failure, and liver destruction.

Dr. Sacher and her colleagues essentially have shown that relatively gentle treatments described above can in most cases reverse "AIDS-indicator illnesses," far more reliably, and completely than HAART.

Although the funding of Dr. Sacher, and her colleagues was abruptly ended without explanation years ago, even the AIDS Establishment now sees the merits of their approach. For example, one of the staunchest supporters of the "HIV=AIDS" hypothesis recently wrote:

Immune Activation in HIV Infection More than Just Markers

By Richard Jefferys

"At the recent International AIDS Society conference in Sydney, Mike Lederman reminded attendees that abnormally high levels of immune activation were described in the first case reports of gay men with AIDS in 1981. The authors of those reports, led by Michael Gottlieb, specifically noted the "increased percentage of cells bearing the thymocyte-associated antigen T10." This antigen is now known as CD38, and an extensive literature—particularly the work of the late Janis Giorgi, an immunologist at UCLA—demonstrates that CD38 expression on CD8 T cells correlates strongly with the rate of disease progression in people with HIV infection" (in many instances, more strongly than viral load and peripheral blood CD4 T cell counts).

Translation: In the absence of any clear mechanism to explain how "HIV" damages immune cells, the AIDS research enterprise is beginning to focus their attention on issues regarding the immune system raised by their early critics such as Dr. Sacher, Heinrich Kramer, The Perth Group, Peter Duesberg, Kary Mullis, and others, that they had fought so hard to silence and many of whose funding was abruptly stopped.

"It has also become clear that immune activation is a broader phenomenon than just CD38 expression on CD8 T cells. CD4 T cells are also over-activated and additional T cell activation markers—such as HLA-DR—are elevated along with levels of pro-inflammatory cytokines including TNF-alpha, IL-6 and IL-1beta."

Translation: In other words, "AIDS patients" are immunologically abnormal in ways that a simple virus infection cannot explain.

"The role of immune activation in HIV infection has generally received less attention than HIV-associated immune deficiency."

Translation: A disproportionate amount of money (all of it) has been directed at how "HIV" works and virtually no money has been directed at hypotheses in which "HIV" doesn't play a major role (like immune activation), or which plays no role at all in immune deregulation syndromes.

"But recently, immune activation has received renewed attention for a number of important reasons:"

Translation: The head of the Swiss Blood Bank, Alfred Hassig, Dr. Kramer, the Perth Group and others have been discussing oxidative stress and immune activation (a more generalized issue than simply immune activation) for years and being censored and defunded: Jefferys and the AIDS Establishment say it's time to look at these hypotheses more closely because the simple virus-centric "HIV=AIDS" paradigm has repeatedly, and without exception failed.

"-Immune activation—but not viral load—has emerged as the critical factor distinguishing pathogenic immunodeficiency virus infections—such as HIV infection in humans and SIV infection in rhesus macaques—from non-pathogenic infections, such as SIV infection in sooty mangabeys and African green monkeys."

"-Results from the large SMART trial, which evaluated the strategy of interrupting ART in a large population of more than 5,000 HIV-infected individuals, clearly showed that the relative risk of clinical events not normally considered to be AIDS-related was higher in people who interrupted therapy."

Translation: Clinical events that are "non-AIDS related" tend to be due to side effects of drugs that cause non-AIDS-indicator syndromes such as heart disease, liver failure, neuropathies, lipodystrophies, coagulopathies, etc. Unfortunately, the trial was prematurely ended, and it didn't have a control group of "HIV-positives" that were given no pharmaceutical intervention.

"Many of the events—such as cardiovascular, liver and kidney disease—are associated with inflammation and immune activation, and recent analyses of the SMART results are suggesting that levels of biological markers known to predict an increased risk of these events were raised by treatment interruption."

Translation: Like hepatitis B infection and liver disease, no clear association between a virus and tissue destruction has been discovered in the context of "HIV/AIDS," so now they are looking for the mysterious "autoimmune" after-effects on major organs never associated with the targets of the "HIV/AIDS" hypothesis before (outside the context of drug toxicity and drug damage often mistaken for the AIDS-indicator diseases). But Jefferys and his AIDS Establishment are 10-20 years late with this view because Robert Root-Bernstein, The Perth Group, Kary Mullis, and others had already proposed autoimmune mechanisms years ago as the basis of AIDS.

"-The effectiveness of ART in restoring immune responses to opportunistic pathogens has greatly reduced the incidence of opportunistic infections, but even individuals on long-term ART with well-suppressed viral load typically show elevated levels of T cell activation compared to uninfected controls as well as markers of incomplete immune restoration (e.g. persistently skewed CD4/CD8 ratios)."

Translation: An activated immune system is characteristic of AIDS and is independent on the level of "virus", and AZT and HAART. And although these drugs do permanent damage to the immune system depending on dosage and duration of treatment, they may be partially effective in some individuals for a while by acting as anti-bacterials and perhaps anti-fungals. Although the drugs may unreliably suppress the responses of the immune system so that "viral load" appears to go down, Jefferys is saying here that these drugs don't appear to affect in most cases the long-term autoimmune oxidation that will destroy tissues of the body in persons who are hyperimmune activated for any one of dozens of reasons. In other words, "HIV," if it existed, isn't suppressing the immune system leading to AIDS. In fact, now the AIDS enterprise is saying that something is stimulating the immune system so that it becomes destructive to tissues that have nothing to do with AIDS-indicator diseases, or which may have nothing to do with "HIV," as is the case with many chronic autoimmune diseases.

"This suggests that these individuals may remain at increased risk for conditions associated with inflammation and/or perturbed T cell homeostasis (e.g. the cardiovascular events mentioned above and autoimmune-like phenomena)."

"Taken together, these findings argue strongly for a renewed focus on unraveling the causes and consequences of immune activation and inflammation in HIV infection."

Translation: There is no correlation between "viral load" and morbidity as much as there is a correlation between the onset or consequences of hyperimmune activation, and the typical autoimmune responses and tissue damage that accompany hightened immune activation (not AIDS which is a depression of the immune response) that has nothing to do with a virus.

"But exactly how this is occurring—particularly the extent to which HIV antigens are involved versus other potential sources of activation such as bacteria leaking across the gut mucosa—remains unresolved."

Translation: There still is no experiment that can account for how "HIV" can cause AIDS.

"These questions are no longer solely of interest to academic immunologists, they are now increasingly recognized to have a vital relation to the transmission and pathogenesis of HIV infection and AIDS."

Perhaps this is why, in 2007, it was announced that viral load is only able to predict progression to disease in 4% to 6% of any HIV-positives studied, challenging much of the basis for current AIDS science and treatment policy for any individual who tests "HIV" positive [24. Rodriquez B, Sethi AK, Cheruvu VK, et al. Predictive value of plasma HIV RNA level on rate of CD4 T-cell decline in untreated HIV infection. JAMA 296(12):1498-506, 2006;Cohen J. Study says HIV blood levels don't predict immune decline. Science 313(5795):1868, 2006].

Everybody has "HIV": p24, the capsid protein of "HIV" is detectable in everybody's cells.

One of the co-founders of the "HIV=AIDS" hypothesis, Dr. Robert Gallo, has claimed that in a stadium full of "HIV-negative" people, not one molecule of "HIV" will be present (personal communication). By contrast, the DAIDS (Division of AIDS) culturing manual claims that if "HIV-infected" cells from human blood express more than 30 units of “HIV-specific” p24 protein on 2 or 3 separate tests ...

Read Part 1 | Part 2 | Part 3
read blog    or this blog

Andrew Maniotis, Ph.D.,
Visiting Associate Professor of Bioengineering
212 SEO, MC 063
University of Illinois at Chicago
Chicago, IL 60607

Charles L. Geshekter, Ph.D.
Professor of African History
California State University
Chico, California 95929

Source: http://www.newmediaexplorer.org/sepp

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