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

Published 31 January 2000

Virus: the co-discoverer of HIV tracks its rampage and charts the future Luc Montagnier W W Norton, 256pp, £18.95 ISBN 0393039234

Aids is the first postmodern plague, its brief history marked by horror stories and conspiracy theories. Among my favourite is the ridiculous suggestion that the disease was created by the CIA for biological warfare. A more tenable suggestion - Edward Hooper's - is that the epidemic may have been started accidentally by scientists while developing vaccines against polio.

At the start of the 1980s, we in the west complacently believed that infectious disease had sunk into history. Until, that is, the American Centres of Disease Control began noticing that clusters of homosexual men were contracting a bizarre menagerie of infectious agents. Investigations showed that the immune system, which usually deters microbial intruders with impunity, had virtually disappeared from these men. What had caused this disappearance? The wise money was on another microbe, possibly a virus, and a frantic contest to find its identity ensued. Luc Montagnier, at the Pasteur Institute in Paris, first isolated the human immunodeficiency virus (HIV) which is responsible for the disease. (The lobby, disgracefully championed by Andrew Neil at the Sunday Times, which claimed that Aids is not caused by a virus, is now discredited.)

Montagnier's victory was, however, tainted by rivals competing in the hunt for scientific glory. Robert Gallo led American efforts, and has since been cited as a co-discoverer in a Franco-American agreement ratified by Jacques Chirac and Ronald Reagan, which continues to vex Montagnier. In his autobiographical account of the race to discover the virus, the circumspect Montagnier can barely contain his bitterness at the outcome. He takes sideswipes, not just at what he sees as Gallo's opportunism and inadequate science, but also generally at the scientific establishment.

HIV invades the command centre of the immune system, comprised of "helper T cells", and eventually kills them. The continuous production of these cells means that it can take as long as a decade before the virus depletes the immune system sufficiently to expose the body to the plethora of opportunistic infections which end up killing the afflicted.

The origin of HIV has remained a mystery - which goes some way to explain why CIA-style conspiracies arise. It's true that some monkeys possess viruses similar to HIV, and many investigators agree that such a virus was transferred to humans somewhere in Africa in the late 1950s. Montagnier glosses over the details of this calamitous leap. Perhaps indigenous tribesmen caught the disease through eating chimpanzee meat. Perhaps a playful scratch from a pet monkey was enough to cause the transfer. Other hypotheses, such as that expounded by Charles Gilks at Oxford University, that suggest that the virus was transmitted directly from chimpanzee blood in early experiments on possible malaria vaccines, have as much biological plausibility as the polio link.

Whatever the cause, good science should be published in specialist journals after detailed scrutiny by several experts in the field. This process of peer review evolved specifically to weed out sensationalist speculation from any old Tom, Dick or Edward Hooper.

The system does contain flaws. New ideas are often neglected through misunderstandings or even for less scrupulous reasons. Montagnier himself suffered at the hands of competitors refereeing his work, and every small-time scientist has a conspiracy theory to peddle about a rejected manuscript. In spite of the flaws, however, a better system to ensure that the scientific juggernaut rumbles onward has yet to be devised.

Regardless of the bridging event which brought HIV into humans, another important question remains. How did a major Aids epidemic develop among gays in the USA in the 1980s? The modern shift in sexual behaviour, particularly among homosexuals, is often cited as a key contributory factor. Promiscuity and anal sex may not be a particularly modern invention, but Oscar Wilde and even Joe Orton would surely have blushed at some of the scenes enacted in the New York bathhouses.

Montagnier doubts that such behaviour in such places could alone have been responsible for the epidemic. He believes that other microbes emerged as co-factors promoting the survival of HIV, which succeeds better in individuals already carrying other infections, because they have more activated immune cells to harbour the virus when it enters. This multi-infection link may also explain the enormous prevalence of HIV in Africa.

Recent advances in treating the disease mean that triple combination therapy can keep the virus in check for many years, if not yet eliminate it. Further advances are expected. Vaccines have proven slow in coming, although there is some optimism that a breakthrough may not be far away. Even with these advances, however, it must be remembered that effective treatment for other infections such as malaria and tuberculosis has been available for more than half a century. And yet more people around the world die of these diseases than ever before. Five per cent of the world's HIV-infected population receive therapy. The others are unable to afford treatment. Hard economics, not science, will dominate the final outcome of the global Aids epidemic.

Mike Barrett is a lecturer at the Institute of Biomedical and Life Sciences at Glasgow University

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2 comments from readers

Andrew Maniotis
31 October 2008 at 13:28

Global health strategies on AIDS require evidence not emotions

In July 2000 one of us visited Mseleni General Hospital in the Maputaland area of South Africa (within KwaZulu-Natal province), one of the poorest regions of the country. When the nurses' supervisor was asked to identify the hospital's wards she identified them as follows: 1) ob-gyn, 2) childhood maladies, 3) accidents and personal injury trauma, 4) mental illnesses, and 5) tuberculosis.

Not one word about AIDS or HIV. Perhaps all five wards implicitly incorporated HIV or AIDS? She never said. An explanation for the nomenclature of the wards at Mseleni Hospital may be gleaned from the data available in the May 2006 publication by Statistics South Africa, entitled Mortality and Causes of Death in South Africa, 2003 and 2004: Findings From Death Notification which includes vital statistics back to 1997. [Statistics South Africa, Mortality and Causes of Death in South Africa, 2003 and 2004: Findings from Death Notification, Pretoria, May 2006, Statistical release P0309.3].

This publication arranges data in a statistical category called "Leading Underlying Natural Causes of Death" for South Africa from 1997-2004, an important period in the political history of the country. In 1999, the year that Thabo Mbeki succeeded Nelson Mandela as President of South Africa, there was a total of 9,782 deaths (in a country with a population then of 42

million) whose cause was officially listed as "HIV Diseases." It is well known that these statistics were derived from only one flawed "HIV" test result, a practice which has been completely debunked as having anything to do with generating accurate statistics, but not headed by the AIDS Establishment. Nevertheless, that number represented 2.6% of all deaths in South Africa for 1999. In the province of KwaZulu-Natal (whose northernmost district is Maputaland), in 1999 the total number of deaths attributed to “HIV Diseases” was 1,899, or 2.3% of all

provincial deaths that year. Perhaps officials at Mseleni General Hospital had good reasons not to devote a special ward to “HIV diseases?” For the next five years there ensued bruising scientific debates (which the AIDS orthodoxy scorned as “denialism”) in which a constant questioning of the efficacy of

HAART and ARVs was juxtaposed against the scare-monger predictions of a looming "HIV/AIDS" holocaust about to engulf South Africa.

So what really happened?

In 2004, the total number of South African deaths (in a country then of 47 million) whose cause was officially listed as "HIV Diseases" was 13,220. That number represented only 2.3% of ALL deaths in South Africa that year, a decrease from 2.6% five years earlier.

For both 2003 and 2004, "HIV diseases" were officially ranked #21 in the list of leading causes of death for South Africa. We have no way of ascertaining from this data exactly how any attending physician, health care worker, or coroner knew for certain that so-called "HIV disease" was the underlying cause of death. Meanwhile, in KwaZulu-Natal for 2004, the total number of deaths attributed to “HIV disease” that year was 3044 which corresponded exactly to the same 2.3% of all provincial deaths that were reported five years earlier.

It is our contention that statistics amassed on “HIV disease” and/or “AIDS” are littered with inconsistencies and absurd projections that invite criticism. For an example of how inflationary figures routinely characterize orthodox HIV and AIDS statistics, one need only consult the latest annual volume by S. Buhlungu, et. al. (eds.), State of the Nation: South Africa 2007 especially the chapter by H. Schneider, et. al., entitled, "The Promise and the Practice of Transformation in South Africa's Health System" [Sakhela Buhlungu, et. al. (eds.), State of the Nation: South Africa 2007, Cape Town:

Human Sciences Research Council, 2007].

That chapter utilizes a table that alleges that for 2000, HIV/AIDS was the #1 cause of death in South Africa, accounting for 30% of all the 410,000 deaths reported in the country, or 123,000 HIV/AIDS deaths.

Compare that alarmist data with the sober statistics given in mid-2006 by Statistics South Africa, which state that for 2000, HIV diseases numbered 10,321 or 2.5% of all deaths. In other words, even in 2007 Schneider and her associates retrospectively increased the number of HIV/AIDS deaths for 2000 in South Africa by 12 times! The data on death rates from “HIV diseases” from 1997 to 2004 in South Africa reveals other interesting anomalies from select provinces:

1) In 1997 in KwaZulu-Natal Province, “HIV diseases” accounted for 2.2% of all its

deaths; in 2004, it was 2.3%.

2) In 1997 in Mpumalanga Province, “HIV diseases” accounted for 2.3% of all its deaths;

in 2004 it was >2.2%.

3) In 1997 in Limpopo Province, “HIV diseases” accounted for 2.3% of all its deaths; in

2004, it was >2.0%.

4) In 1997 in Free State Province, “HIV diseases” accounted for 3.9% of all its deaths; in

2004, it was >2.1%.

5) And even for South Africa as a whole, in 1997 “HIV disease” was said to account for

2.0% of all deaths; in 2004 it had risen to 2.3%, but that was down from 2.6% in 1999.

It appears that President Mbeki’s skepticism had some merit and was empirically based. This stands in sharp contrast to his critics, whose resort to personal vilification and vicious slurs, revealed the reflexively irrational and vindictive manner whereby HIV/AIDS mainstreamers respond to anyone who dares to challenge their assumptions.

Several years ago, a Kenyan AIDS trial was interrupted because a 53 percent reduction in acquisition of "HIV" among circumcised men was observed. Out of 2,784 men studied in the trial, 69 men were “HIV” positive: 22 of these were circumcised, and 47 uncircumcised. Many, if not all 69 of them had received prior (or concurrent) treatment for penile infections, and 28 of the 69 had serologic syphilis at the outset. A year before, it was claimed that a trial of 4,996 HIV-negative men in Rakai, Uganda, showed that HIV acquisition was reduced by 48 percent in circumcised men. These results have now been thoroughly debunked with a new study that showed no difference between circumsized versus uncircumsized men.

In the past, AIDS science by press release, has led to horrible consequences for hundreds of thousands during the AIDS era who were experimented on with toxic "life saving" or "life extending" drugs. Uncertainties exist because: data has been acquired at STD clinics or from trial participants with genital ulcer disease (GUD) or other infections, and the relative roles (if any) of biological versus cultural practices that influence "HIV" acquisition have been challenged by the WHO. Uncertainties regarding the damage done by microbicides also exist, which apparently increase the frequency of reported genital lesions and the feared spread of "HIV." The ability or inability to neutralize "HIV" by washing with mild or concentrated detergents is in question, and the transmission of "HIV" from human to human by providing evidence of seroconversion has yet to be provided in a form that constitutes as careful a study as the 10 year study that followed 175 serodiscordant couples for 10 years that found no conversions (the Padian Study). Uncertainties also exist because of the vastly different rates and efficiency of transmission said to be associated with heterosexual, homosexual, and IV drug use in different regions, and, because of the ability of gamma globulin in neutralizing "HIV" among well-nourished and healthy individuals. Uncertainties also exist especially because of the validity (and invalidity) of different test kits to identify "HIV" positive participants, and the role (or non-role) of T-cells in progression to AIDS is also still in question. The role of circumcision in preventing transmission of "HIV" and acquisition of AIDS in Africa is further complicated by compelling evidence from a series of recent studies that identified nosocomial (hospital and doctor-medicated) "HIV" transmission as the single most critically important factor for the spread of AIDS in Africa, which accounts for many anomalies and conundrums that cannot be explained by a sexual transmission hypothesis (see Gisselquist). From the 1950s into the 1980s, unsafe injections may have contributed to the silent spread of HIV-positive test results in Africa in much the same way that other types of vaccination campaigns, including injections for schistosomiasis and other treatments in Egypt, established "hepatitis C-positive" test results as a major blood-borne pathogen. While evidence for nosocomial transmission of "HIV" continues to accumulate since the long established fact that hepatitis B and flu vaccines cause "HIV" positive tests in some individuals, six Bulgarian health care workers (The Tripoli Six) were almost executed by firing squad in Libya for their alleged role in supposedly transmitting "HIV" to 426 Libyan children, which, according to Luc Montagnier were the result of an influx of "Sub-Saharan" health-care workers to Libya (read black people). The sanctity of breast-feeding also has been violated by the champions of the “HIV=AIDS” hypothesis. It is the image in The Vatican of Michaelangelo’s Pieta-Mother Mary holding her dead child. In fact, the practice of brow beating African women to dissuade them from-breast feeding and passing onto their infants “HIV-infection” increased the death-rate in formula-fed infants some 20 times, compared to mother-infant pairs that weren’t dissuaded from breast feeding. For instance, on Monday, July 23, 2007, in Nkange, Botswana, it was reported by Craig Timberg, Washington Post Foreign Service, that in Botswana, steps to cut AIDS proves a formula for disaster:

"Doctors noticed two troubling things about the limp, sunken-eyed children who flooded pediatric wards across Botswana during the rainy season in early 2006: They were dying from diarrhea, a malady that is rarely fatal here. And few of their mothers were breast-feeding, a practice once all but universal."

"After the outbreak was over and at least 532 children had died — 20 times the usual toll for diarrhea — a team of U.S. investigators solved the terrible riddle."

The word, “disaster” appears with alarming frequency in the AIDS literature. For instance the term "Challenger disaster" was used by Robert Gallo to describe the latest of the multi-million dollar "HIV" vaccine failures (that not only have failed to protect anyone from acquiring "HIV's" non-specific molecular markers in 60 vaccine trials to date, but have increased the rate of testing positive so they were halted just last year). Are there other disasters?

Yes. The failure to block transmission of “HIV” or AIDS in mother to child transmission studies (MTCT) is part of George Bush’s PEPFAR pogrom, and also qualifies as an unmitigated disaster. For instance, a recent 2007 study accomplished increased rates of “virological failure” (nevirapine resistance) in 20% to 69% of women and 33% to 87% of infants after exposure to a single, peripartum dose of the black box label drug nevirapine given in Africa to 875,000 mother infant pairs. This 20-69% of women and 33-87% of infants will be now treated as hopeless, drug-resistant “AIDS” patients whose therapy failed to suppress virus (virological failure). Grade IV events aren’t available for previous trials of this kind that failed because the records were washed away in “The Great Flood,” according to Edmont Tremont (one of the heads of the NIH's AIDS program), which is why he felt it was necessary to change the nevirapine trial safety data.

Football strategies and religious ideology also have been used after repeatedly failed human “HIV/AIDS” microbicide trials. Microbicides are noxious chemicals that supposedly kill "germs" like "HIV.” White Western AIDS doctors go to the African continent to encourage the smearing of these toxic microbicide creams on the genitals of Africans. Although a top AIDS researcher, John Moore of Weil Medical College, claimed his multiple monkey "SIV" insemination experiments proved that his “SIV-fighting” (not “HIV-fighting”) microbicide worked because it absolved his monkeys from contracting “SIV” after he inseminated them multiple times, human microbicide trails were halted because these vile mucosal irritants, like the STEP trial vaccines, caused “more” “HIV infections” in microbicide recipients, than it did in placebos. (February 1, 2007, Tests of Drug to Block H.I.V. Infection Are Halted Over Safety: The Conrad Trial. By Lawrence K. Altman):

"Efforts to develop a topical microbicide to prevent H.I.V. infection during sex suffered a surprising setback yesterday when researchers announced that they had stopped two full-scale trials for safety reasons."

"The trials, in Africa and India, involved a chemical, cellulose sulfate or Ushercell, and were the second failure of a potential microbicide in a full-scale trial in recent years. In one of the latest trials, a standard check by an independent scientific committee found an increased risk of H.I.V. infection among women who used cellulose sulfate compared with those who used a placebo gel."

"In 2000, a large full-scale trial showed that the only other microbicide candidate, nonoxynol-9, was unsafe when it had been expected to be effective. Subjects in that trial developed a higher incidence of H.I.V. infection, presumably through ulcers caused by chemical irritation."

To examine the potential value of circumcision versus the possibility of nosocomial transmission, misdiagnosis, and other possibilities regarding the acquisition of AIDS in Africa, we reasoned that examination of both established and new AIDS policies that will affect millions of people should include the vital statistics generated by Africans

themselves if they are available, as well as recommendations by physicians who have

direct, empirical knowledge of African AIDS from their hospital or clinical setting. A wealth of data obtained directly from Statistics South Africa and other sources, which reported for both 2003 and 2004, that "HIV diseases" were officially ranked #21 in the

list of leading causes of death for South Africa, and constituted between 2-3% of all deaths throughout most regions. These statistics, reported by Africans themselves, are supported by historical, sociological, and cultural considerations, by the accounts of

prison officials, as well as by both African and foreign doctors who have written about how serving medical care to Africans has changed or not changed over the period of several decades. These observations further suggest that the state of affairs regarding "HIV/AIDS" in Africa has nothing to do with sexual activities, but reflects the changing nature of African political economies since the late 1970s, its devastation on African lives, in some regions, because of the traumas of civil war violence, and the damage to African culture and society due to a proliferation of "HIV" testing, and flood of "HIV/AIDS" health care opportunism.

Drug studies to date have not been properly evaluated in order to compare with circumcision statistics from Kenya, regardless of what the complete data from the

Kenyan study will show, if they ever are published. It has been admitted unabashedly that more than 875,000 African mother-infant pairs have been experimented on in this fashion.

It is concluded that global health strategies for AIDS, like any other public health activities, should be based on evidence instead of racist notions regarding sexual behavior. Many of the basic assumptions regarding the probability that "HIV" leads to "AIDS" are clearly wrong, contradictory, and defy common sense, to the extent that the "HIV/AIDS" hypothesis should be retracted, and a full examination of where we went wrong, conducted, so we can learn from "mistakes." It is perhaps the individuals in leadership roles in our own government who press release these kinds of distortions and propaganda, or who direct these trials

and distort data, who must be held legally, and criminally responsible?

Andrew Maniotis, Ph.D.,

Visiting Associate Professor of Bioengineering

212 SEO, MC 063

University of Illinois at Chicago

Chicago, IL 60607

Email: amanioti@uic.edu

Phone: 773-960-9084

Charles L. Geshekter, Ph.D.

Professor of African History

California State University

Chico, California 95929

Email: chollygee@earthlink.net

Office phone: (530) 898-6718

Andrew Maniotis
31 October 2008 at 19:34

What I forgot to add is:

"HIV" ORIGINATED FROM THE HUMAN GENOME:

NOT FROM BIZARRE AFRICAN SEXUAL PRACTICES, AFRICAN TOYS, DEAD MONKEYS, CONTAMINATED HEPATITIS B OR OTHER VACCINES, OR THE MILITARY'S SPECIAL VIRUS PROGRAM.

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 suggests 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 "HERV's" (Human Endogenous Retro-Viruses) such as the "Phoenix viruses" (presumptively named because nobody has shown that endogenous infectious "retroviruses" exist). "HERV's" (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 virus's" reverse transcriptase sequence and other parts of it's 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 Thy2. In "HIV/AIDS" patients, the balance was shifted toward Th2 and away from Th1, i.e. a lack of Thy1 and an 3excess 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 awhile. 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 also 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 (=