AIDS and the end of the world

Peter Arguriou,
from the book to be published
"Public Health Wars: Guildening the pill of corporatocracy"



Peter Arguriou is an author and a public health investigator. Born in 1973, Peter studied medicine in the University of Athens and had a brief course in Homeopathic. His latest work, "The Placebo effect, the triumph of Mind over Body" has been translated in 5 languages.
His upcoming book handles the corporate take over and the political manipulations regarding western medicine, a science and practice that sadly appears to have lost it's commitment towards the human entity and wellbeing.   

---

Chapter: AIDS and the end of world

(Scare tactics: “Research studies now project that one in five – listen to me, hard to believe – one in five heterosexuals could be dead from AIDS at the end of the next three years. That's by 1990. One in five. It is no longer just a gay disease. Believe me.” – Oprah Winfrey, The Oprah Winfrey Show, February 18, 1987)

AIDS is by far the greatest terrorist of our times: Its abbreviation contains only four letters yet the syndrome is accountable for millions of deaths. Like the rest of the “novel epidemics”, AIDS presented an idiomorphic distribution: AIDS showed a particular taste for Africa, especially for her subsaharian regions (2/3 of overall HIV carriers are located in those regions).

The AIDS ( Acquired immunodeficiency syndrome) scourge awoke somewhere in the early 80's. At first it exhibited a biblical sense of morality, affecting mainly gays and junkies. That is the reason why one of the early AIDS medical descriptions was Gay Related Immune Deficiency.

The virology of AIDS was verified originally in 1983 when French researcher Luc Montagnier and his colleagues at the Pasteur Institute isolated a new retrovirus in a cell culture originating from the lymph nodes of a homosexual patient suffering from lymphadenopathy1 and suggested a correlation between the new retrovirus (later named LAV-Lymphadenopathy-Associated Virus) and the AIDS entity. LAV was similar but not identical to another retrovirus, HTLV-1, that American researcher Robert Gallo of the National Cancer Institute had isolated a few years earlier. Gallo was back with a vengeance: In 1984 his team isolated “independently” Montagnier's new retroviral entity, renamed it to HTLV-III (Human T lymphotropic virus type III) and proposed not only a correlation between AIDS and the retrovirus but rather a causal exclusive relation2. On the 23rd of April 1984, Gallo and Margaret Heckler, the then Health and Human Services Secretary, rushed to a press conference to announce that Gallo and his co-workers had found the cause of AIDS and had developed a sensitive test capable of determining the "AIDS virus" presence in blood. Gallo's papers were published in Science on May 4, that is Gallo made the announcement before the publication of his findings, an action typical of the informational war and gold rush that took over the AIDS research. Intrique and controversy followed HIV from the first days of its discovery: The priority over HIV discovery was the apple of discord for Montagnier and Gallo. There were claims of Gallo's usurping Montagnier's cell cultures. Gallo's cell cultures were indeed found to be contaminated by the original Montagnier's retrovirus3. The scientific dispute between the two researchers took international proportions and the AIDS cold war era between France and US embarkes: The two countries insist on using different names for AIDS ( SIDA and AIDS respectively) and for it's virus (LAV and HTLV-III). On May 1986, the International Committee on Taxonomy of Viruses rejects the existing nomenclature and adopts the name HIV (Human Immunodeficiency Virus) for the proposed AIDS retrovirus.4 The scientific dispute is finally resolved with an unprecedented in scientific chronicles political settlement: In 1987, US President Ronald Reagan and French Prime Minister Jacques Chirac made a joint announcement crediting Gallo and Montagnier jointly with the AIDS virus discovery and with the patent rights to a blood test that came from that discovery (a key mediator to the negotiations was Mr Polio Vaccine, Jonas Salk)5. This “grandiose” political deal teared apart the notion of scientific integrity and autonomy: science had officially come to terms with politics.


AIDS Facts?


HIV posseses a unique mechanism: It attacks the immune system rendering it helpless against oppurtunistic infections. CD-4 counts drop dramatically as the disease progresses. What makes the virus even more dreadful is that one of its major transmission routes is sexual contact. Once again sex is medicalized, demonized and witch-hunted for humanity's evils.


By 1984 the sinister retrovirus had been isolated but his origins remained a mystery. The hypothesis that eventually gained ground was the African origins of the virus: HIV was (and still is) thought to be a mutation of the SIV (Simian Immunodeficiency Virus) virus, endemic of chimp subspecies (pan troglodytes troglodytes)6 that jumped to humans. As with other viral diseases, the epizootic disease approach is chosen as the leading explanatory model. The message is clear: Nature is man's greatest foe, the fountain of unaccountable threats- viruses are her hired killers. These kind of phobic-irrational projections, this pseudo scientific guise of modern superstitions abound in AIDS' philology: it was the chimps and the primitive, uncivilized Africans that were hunting them for meat that brought about this viral malice and introduced it to humanity7. But the ambassadors of the epizootic-African hypothesis failed (or didnt even bother) to explain why and when exactly did a new virus appear and cross-jumped in a relatively constant cultural environment: These Africans have been consistently hunting and eating and being bitten by chimps for centuries. Furthermore, the chimp virus (SIV) does not cause immune deficiency to its natural hosts. HIV does not afflict chimps and SIV can not be transmitted to humans, that is, there is a well defined biological barrier between these species. So, despite the cursory interpretations, the question still remains: Why HIV, why know?


AIDS is a disease with an intense social context: Homosexuals and drug addicts, marginalized minorities secluded by intolerant societies together with the financially and culturally raped and desolated Africans are sentenced by a mysterious viral entity to a quarantined life and to a slow and humiliating death. This view of a smart, socially conscious, picky and discriminating virus led to a partisan against the official dogma of AIDS, giving birth to sometimes serious and other times utterly ludicrous conspiracy theories that reflect the intuitive perception that the eclectic activity of HIV in specific populations defined by race, sexual behavior, deviant or marginal behavior and class was too focused to stem from a random biological artifact.


Aids and vaccination programs


Though resembling a preposterous idea originating from the Oort cloud of conspiracy theories, the correlation between AIDS and mass vaccination programs, causal or occasional, is well evidenced. In 1987, London Times published an exciting article revealing a possible relation between WHO's (World Health Organization) mass vaccination program against smallpox that took place in Africa during the 70s and the subsequent african AIDS outbreak. The Times article originated from a whistleblower, a former WHO outside consultant who contacted Times veteran science editor, Pearce Wright. The whistleblower was hired by WHO to investigate possible correlations between vaccinations and the African AIDS outbreak. According to the researcher's findings, it turned out that there was a statisticaly significant relation connecting these two parameters. The consultant stated that in “.. obliterating one disease (smallpox), another (AIDS) was transformed”8. Robert Gallo, the backbone of the AIDS establishment, did not refute the possible AIDS-mass vaccinationions program. In his own words: “The link between the WHO program and the epidemic is an interesting and important hypothesis. I cannot say that it actually happened, but I have been saying for some years that the use of live vaccines such as that used for smallpox can activate a dormant infection such as HIV."9

Pierce Wright did not content himself with the confessions of the whistleblower. He compared AIDS distribution to the vaccine programme implementation and found that the was a geografical coincidence between AIDS incidence and WHO vaccinations. Africa's more infected regions were those who were systematicaly vaccinated. Haiti's AIDS cases rised dramatically after 14000 Haitians got the smallpox vaccine shot while visiting Africa. This explosive piece of journalism by Wright, indicated that mass smallpox vaccinations might have triggered the HIV virus and turned it from a harmless endemic viral agent to a global assassin.

Similarly, journalists Curtis and Hooper attributed in 1991 the manifestation of the African AIDS epidemic to vaccination trials in African population during the 50s and 60s. For Curtis and Hooper the fuse for the AIDS explosion was vaccines prepared in chimps' kidneys and blood that bridged the species barrier and allowed SIV to jump into human carriers and mutate into HIV10.

Although explanations differ slightly from researcher to researcher, the AIDS-vaccine relation seem to repeat itself frequently in the relative literature. And there might be a good reason for it. Despite the fact that mass vaccinations have proved benefactory, even life-saving in respect to some diseases, their immunomodulating activity might hold some undetected, unpredected and unaccoounted for dangers. And the risks can get bigger when the vaccines are contaminated with viruses, or virus particles originating from the organisms that were used for vaccine preparation. Even when the vaccines are free of contaminants, the massive insertion of antigens produced in one organism to an alltogether different organism might induse dangerous genetic recompinations and favour the creation of novel diseases. We can brag about our immunological omniscience as much as we want, but the truth of the matter is that we dont know all that much about immune response. If we did, we would have found a cure for allergies and for autoimmune diseases like multiple sclerosis and type II diabetes. To use vaccines for certain medical conditions is prudence, to proclaim them panacea is reckless arrogance. Virologist Veljko Veljkovic has been warning us since the 90s about the dangers surrounding the development of an AIDS vaccine. In particular, HIV's envelope glucoprotein gp120, resembles to the immunoglobulin region responsible for antigen binding. AIDS vaccines containing the gp120, can interact with the immune system with more than one ways and can occasionally render it not more resilient to the virus as anticipated but more susceptible to it, resulting to a more aggressive progression of the disease.11 Veljkovic is also considering the possibility of genetically recombined viruses containing gp120 or its gene leading to the creation of new pathogens, viruses and bacteria with unforeseen consequences. That is, an AIDS vaccine containing gp120 which is a good choice of viral protein in order to induce specific immune response to the virus and ensure effective immunization can:

promote autoimmunity, with immune cells attacking the gp120-like immunoglobulin region,

promote genetic instability in a region characterized as a recombination hot spot, leading to chronic diseases, or to random recombinant strains of viruses, or even randomly creating all together new viruses and pathogens.

And Veljkovic is not alone in this. Geoffrey Hoffmann, a theoretical immunologist at the university of British Columbia in Vancouver shares the notion that a recombinant vaccine might backfire and provoke autoimmunuty.

Researcher Howard Urnovitz meditatively states that “there appears to be a limit on how much foreign material to which the human body can be exposed before some level of genetic damage occurs and a chronic disease initiates” and ponders whether we are “embarking on a course that will vaccinate people against their own genes?” 12

An inquisitor turned heretic


All the formentioned theories are in accordance with the central AIDS dogma: that is that the causal agent of AIDS is the AIDS virus HIV. But there exist within the scientific community certain clusters of experts that are denouncing the central AIDS dogma and are claiming that HIV is not highly pathogenic by itself, that other agents prod HIV to turn pathogenic, and experts that challenge the AIDS dogma to its very core, claiming that HIV is not a causal agent of AIDS at all, that HIV is just a passenger virus.

The champion of the dissidents and perhaps the man who started it all is Peter Duesberg. Duesberg's fall from grace could as well be a theme from ancient tragedy: Duesberg, once a scientific hero, commits Hubris by challenging the Gods (the AIDS establishment) and is punished for his insolence. The nemesis of the AIDS establishment stripped Duesberg of glory, of status and validity and ultimately of funds. Duesbeg is a modern scientific Sisyphus, trying to carry the boulder of his AIDS hypothesis to the top of the hill of mainstream science.

Duesberg, was the first to isolate a cancer gene. He is a lifetime member of the National academy of sciences and in 1986 he received an Outstanding Investigator Grand (OIG) from the National Institutes of Health (NIH). So what has happened to this outstanding investigator? Has he gone out of his mind?

It is worth noting that before his AIDS heresy, Duesberg was thought to be the leading expert in retroviruses. And HIV is a retrovirus.

Duesberg's free fall from excellence to notoriety partly happened because of his meticulousness, because he choose to stick to the text books of biology. For decades, microbiology had a safe guideline: The Koch postulates, a compilation of criteria enabling microbiology to identify infectious agents -pathogens with diseases, to establish accurate causal relations between microbes and diseases. If you are a microbe and you have the ambition of becoming infectious and cause a particular disease, well then you have to follow the Koch postulates and a) be present in all cases of the disease you claim to cause b) you must be isolated from a diseased organism and be grown in pure culture c) when introduced to a healthy organism you must really make him sick, d) you must once again be isolated from the ex-healthy organism you experimentally infected, to be double sure it was you who caused the disease at the first place. If you can't satisfy the for postulates, don't dare to call yourself infectious.

Duesberg claims that HIV does not satisfy a single Koch postulate regarding AIDS.13. And his arguments extent far beyond HIVs inability to satisfy the Koch Postulates.

Duesberg argues that the plenitude, severity and type of AIDS symptoms do not match the viral profile and activity of HIV. HIV allegedly affects the Human immune system and propagates inside T-cells, cells responsible for the recognition and interception of intruders. The HIV activity supposedly, on the long run leads to a dramatic CD4 cell depletion. Duesberg argues that the ratio of HIV-infected CD4 cells (approximately 1 out of 100 CD4 cells are infected at any given time)14 cannot account for the ultimate picture of immunosuppresion exhibited by AIDS patients. To give some credit to the outstanding investigator, the AIDS establishment does not have any definite answers to HIVs cytotoxic effects. We really don't know how exactly HIV causes CD4 depletion and ultimately immunosuppresion. Duesberg claims that it is the other way around. HIV does not cause immunosuppresion, but rather, it appears in already immunosuppressed organisms, much like any other opportunistic infection. HIV, if existent, could as well be a collateral infection, not a causal one.

Duesberg also comments on the AIDS epidemic selectivity: hemophiliacs, homosexuals, drug addicts are the virus' primary targets. And this is quite unusual. Traditional epidemics kill weak, or weakened portions of the general population: infants, elders, asthenics are the traditional high risk groups. But AIDS is an exception to the usual epidemics' distribution. Duesberg along with other researchers deem that high AIDS incidence in AIDS risk groups is due to particular lifestyle choices or circumstances typical of these groups that have put their immune system under continuous stress, ultimately damaging it. HIV is irrelevant. For hemophiliacs it was the foreign proteins inserted to the patient through transfusion that overstimulated the immune system to the point of exhaustion (the foreign protein immunodeficiency hypothesis)15. For homosexuals it was poppers, nitrites inhalants that the gay community abused for recreational purposes during the 70s16 along with the excessive use of antibiotics for the treatment of venereal diseases frequent amongst the gay community17. For intravenous drug users it was the sharing of syringes, the immune effect of drugs and overall poor personal hygiene and nutritional habits.18 Researcher Papadopulos-Eleopulos of the Perth dissident Group investigates the role of oxidative agents in immune-collapse as observed in AIDS and perceives AIDS as a result of accumulative oxidative stresses instead of an infectious viral disease19. The role of oxidative factors has been regognized by Luc Montagnier, the very same person that isolated and purified HIV. 20 Papadopulos-Eleopulos also believes that Gallo did not follow a strict isolation protocol regarding HIV. The researcher also claims that the usual diagnostic tests used for AIDS diagnosis, Elisa and Western Blot are not specific enough to safely determine and detect the presence of HIV. 21 If this is the case, thousands of persons have been and will continue to be misdiagnosed.

Duesberg has been critical of the use of the drug AZT for the treatment of AIDS. In fact, Duesberg claimes that AZT and like treatments amplified the AIDS phenomenon and contributed largely to its pathogeny and epidimiology. Duesberg is describing an AZT induced AIDS, were the administration of AZT in its usual pharmacological dosage can lead an organism to developing clinical features similar to those of AIDS. The truth of the matter is that AZT was a cancer drug that was withrew from the cancer treatment field to be enrolled decades later in the war against AIDS. That is, an obsolute and totally failed toxic cancer drug was deployed for the treatment of AIDS. And this is not the only contribution the war on cancer made to the war on AIDS. Gallo and his teamates were veterans of the war on cancer that volunteeraly transferred to another battlefield when their favorite cancer-virus hypothesis failed to provide impresive results and therefore funds. So if they could no longer strongly associate viruses with cancer in general, what about viruses and this new disease, AIDS? Why not project our work to the new provocative research field? Allegoricaly speaking, both AZT's and AIDS' sign of zodiac was that of the cancer.

AZT causes a wide range of sideffects and pathogenies. It also causes depletion of mitochondrial DNA (mtDNA) and other mitochondrial abnormalities with unknown longterm effects22. Duesberg holds AZT responsible for a plethora of AIDS related symptoms that appear to be indepentant from the HIV pattern of activity, predominantly symptoms from the central nervous system such as dementia. HIV barely infects neurons. There are only theoretical models on how HIV can directly damage neurons. On the other hand, AZT crosses the blood-brain barrier23 and affects neurons. Duesberg is so certain of AZT's disastrous effects that he describes the administration of AZT to Aids patients as genocide, iatrogenic genocide of gay populations.


HIV's expertises in infecting CD4, yet a large number of AIDS patients demonstrate such a plethora of central nervous system (CNS) symptoms that they define a syndrom by themselves, the so called ADC (AIDS Dementia Complex). ADC symptoms can vary from patient to patient and include cognitive impairment, motor dysfunction, speech problems and behavioral change. HIV's behaviour in the CNS is not clear. HIV-1 is thought to infect several brain cells such as macrophages, microglia24 and astrocytes25 that are subsequently indirectly or directly damaging neurons26. This pluropotent virus that can affect not only immune cells but can also attack CNS cells, becomes stranger by the hour: HIV strains that are located in the CNS are different from the strains that are circulating in the blood of the same patient! And it gets ever weirder: HIV clones lodged in the same brain differ from region to region!27

The HIV infecting CNS theory explains that different cellural enviroments encountered by the virus in different brain regions and compartments force the virus to mutations.28 How can it be? A virus that is clever enough to trick the immune system can also affect the brain and under the cellular enviroment's evolutionary pressure it can mutate and produce new quasispecies in less than five years. This doesn't sound like a virus but rather like an extravagant, vigilant biological lab possesing a unique insight on the human organism. Perhaps we have got it all wrong? Are we building a scientific giant on feet of clay?

It is hard to imagine how any pharmaceutical concoction can succesfully face such a slipery virus in all its cunningness. Even the state of the art antiretroviral coctails that we are using today (HAART-highly active antiretroviral therapy ) fail to confront the elusive HIV encephalopathy (the ADC).29 To make things even more complicated, HAART theoriticaly has the potential to damage the brain by impairing endothelium function. The relation between HAART and endothelium function has been demonstrated in the cardivascular system.30 Perhaps it is then HAART, not HIV that increases blood brain barrier permeatability and leads to the dramatic events of magrophage invasion of the brain, neural apoptosis (death of nerve cells) and gradually to ADC.


To test this hypothesis we can compare ADC in the western world with ADC in a country that is largely still in the pre-HAART era. ADC in the western world afflicts roughly 10% of AIDS patients31 while in still the pre-HAART India, the percentage drops down to 1-2%.32 Is this statistical assymetry attributable to differences in HAART usage?


Duesberg although marginalized, scorned and even slandered by colleagues who previously held him at high esteem (Robert Gallo for example eagerly turned his back on Gallo and has repeatedly rediculed him in his public appearances) is not alone in his quest for AIDS-HIV disassociation. Prominent scientists jeopardized their stature in order to stand for what they believed, what they reasoned was right, scientists like Kary Mullis, Walter Gilbert, David Rasnick and Rodney Richards. Scientinsts who still hold science to be an open process, free of censorship and indisputable dogmas, an ongoing investigation, an earnest dialogue with existance and not a theatrical monologue. Nobelist Kary Mullis, the inventor of the PCR (Polymerase Chain Reactin) method which was later applied as a diagnostic test for HIV, rejects the single-factorial interpretetion of AIDS. David Rasnick, one of the original designers of the AIDS class drugs called PIs (Protease Inhibitors), states that the risks that they pose do not outweight their benefits in AIDS treatment33.

Rodney Richards, a researcher involved in the development of diagnostic tests (including diagnostic tests for AIDS) concluded that neither Montagnier, nor Gallo followed a sctrict isolation protocol regarding HIV. He also holds that the available diagnostic test for HIV (including Elisa, Western Blot, viral load, p24 antigen test) are of dubious diagnostic value and defenitily not conclusive for HIV presence or absence. The Perth researcher, Papadopulos-Eleopulos, concurs with the above positions. So, we have leading experts in their fields arguing AIDS' official interpretation, aetiology, diagnosis and treatment. Are they raving lunatics who want to bring the world to an end, or meticulous researchers that demand a more scholarly approach to the greatest health problem of our times? An approach free of financially driven tendentiousness, personal ambitions, political interventions and institutional authoritarianism.

One point that deserves attention is that AIDS is defined as a syndrome. It is not a particular, well defined disease but rather a wide collection of symptoms consisting of old diseases ((Tuberculosis (TB), Pneumocystis carinii, Toxoplasmosis etc) , varying from patient to patient, from risk group to risk group and from continent to continent . The establishment's answer is slick: well, the immune shield is down so typical of populations infections do occur, and every population has its own epidemiological profile, its own characteristic incidence of diseases. And what about the malignancies ( Kaposi's sarcoma, cervical cancer, lymphomas etc) that are one of the leading causes of death amongst AIDS patients today? Well these deaths occur because there is a co-infection with an oncogenic virus. Everything sounds so convenient. The only problem is that AIDS is becoming more complicated by the hour, absorbing insatiably and embodying other pathogenic entities. Pathology must have really redefined itself in order to accommodate AIDS.

Duesberg and others are blaming WHO (World Health Organization) for artificially inflating worldwide AIDS statistics in his agony to keep the pandemic tale alive. It is partly due to WHO's strenuous efforts and the misclassification of irrelevant diseases under the AIDS tag that the syndrome has came to acquire such a colorful, kaleidoscopic clinical image. WHO is systematically stretching AIDS definition further and further and is stuffing more traditional diseases into the AIDS entity. This policy has recently led to the displacement of tuberculosis from the primacy of deadly diseases with AIDS getting the first. Duesberg is cauterizing this AIDSfying tendency, saying that every single disease will be defined as AIDS if accompanied by an HIV positive diagnosis. For Duesberg, the African AIDS especially, is a WHO compilation of old endemic diseases the are rebaptized as AIDS.


On October 1993, The Sunday Times presented a breathtaking article by Neville Hodgkinson that was examining the African-AIDS experience of two humanitarian workers, the Krynens. In 1988 the couple set off for Africa to provide humanitarian assistance to African children. They chose to settle in the Kagera region of Tanzania. Kangera at this point of time, was regarded as the epicenter of a great AIDS outbreak. The situation seemed hopeless, and to contain the epidemic immediate measures had to be taken. But when the Krynens got acquainted with life and death in Kagera, the AIDS epidemic perspective vanished into thin air. The couple were taken aback when they realized that regardless of HIV diagnosis, people were suffering from the same “conventional” maladies and regardless of HIV diagnosis they doing equally well on “conventional” remedies. AIDS seemed irrelevant. Sanitation and classical treatment of classical diseases had everything to do with life and death in Kagera. It was not the HAARTs nor expiremental vaccines that halted the Kageran AIDS epidemics. Simple drugs against malaria and tuberculosis and parasitic diseases, along with elementary hygiene was what did all the work. This hindsight obliged Evelyn Krynen to all of a sudden “put all she had been told about the disease in the garbage can, and try to reconsider'”. Phillipe Krynen has been more vocal about his first hand experiences in Kagera that led to his African AIDS desillusionment: “'There is no AIDS. It is something that has been invented. There are no epidemiological grounds for it; it doesn't exist for us” and suggests that "it is time to come back to science and abandon magic thinking"34. Phillipe is wrong about one thing: it is not magic thinking, it is theological thinking, dogmatized commantments of the AIDS priesthood.


However convincing and touching, the Krynen experience can not structure a scientific observation moreover counter the given statistical fabric that describes the AIDS epidemic. But UN experts can. UN experts allready did.

According to the Washington Post:


...The United Nations top AIDS scientists plan to acknowledge this week that they have long overestimated both the size and the course of the epidemic, which they now believe has been slowing for nearly a decade, according to U.N. documents prepared for the announcement....

The latest estimates, due to be released publicly Tuesday, put the number of annual new HIV infections at 2.5 million, a cut of more than 40 percent from last year's estimate, documents show. The worldwide total of people infected with HIV -- estimated a year ago at nearly 40 million and rising -- now will be reported as 33 million...


..Some researchers, however, contend that persistent overestimates in the widely quoted U.N. reports have long skewed funding decisions and obscured potential lessons about how to slow the spread of HIV. Critics have also said that U.N. officials overstated the extent of the epidemic to help gather political and financial support for combating AIDS. "There was a tendency toward alarmism, and that fit perhaps a certain fundraising agenda," said Helen Epstein, author of "The Invisible Cure:Africa, the West, and the Fight Against AIDS." "I hope these new numbers will help refocus the response in a more pragmatic way." ...


...Among the reasons for the overestimate is methodology...


...The United Nations' AIDS agency, known as UNAIDS and led by Belgian scientist Peter Piot since its founding in 1995, has been a major advocate for increasing spending to combat the epidemic. Over the past decade, global spending on AIDS has grown by a factor of 30, reaching as much as $10 billion a year.

But in its role in tracking the spread of the epidemic and recommending strategies to combat it, UNAIDS has drawn criticism in recent years from Epstein and others who have accused it of being politicized and not scientifically rigorous.

For years, UNAIDS reports have portrayed an epidemic that threatened to burst beyond its epicenter in southern Africa to generate widespread illness and death in other countries. In China alone, one report warned, there would be 10 million infections -- up from 1 million in 2002 -- by the end of the decade.

Piot often wrote personal prefaces to those reports warning of the dangers of inaction, saying in 2006 that "the pandemic and its toll are outstripping the worst predictions."

But by then, several years' worth of newer, more accurate studies already offered substantial evidence that the agency's tools for measuring and predicting the course of the epidemic were flawed...


...The revisions affect not just current numbers but past ones as well. A UNAIDS report from December 2002, for example, put the total number of HIV cases at 42 million. The real number at that time was 30 million, the new report says...


...Beyond Africa, AIDS is more likely to be concentrated among high-risk groups, such as users of injectable drugs, sex workers and gay men...”35


The dissedents validity regarding their criticism towards the ill received and processed statistical data is finally reistituted. They were right. Not only were the numbers reported for years inflated, but the methodology that was used to develop them was flawed and perhaps affected by political and economic tendentiousness. The dissidents were speaking of an all permiting methodology, of a statistical elasticity beyond the strech limits of proper science, when it appears that numbers were tampered and fixed to fit in the canvas of a wanna be pandemic. One could claim that errors are in the human nature. But even in an accidental car crash there is accountability. If one man is injured or dies because of an accident there is accountability. What of millions of miscatigorized people, what of millions of dollars that where diverged from a usefull social flow to dam up an “emerging pandemic” that was full of hot statistical air, what of the public health policies that were indignated by selfserving numerologists? Ooops, sorry, we made a mistake is just an excuse, a cheap one. And after decades of fear mongering and of social and sexual isolation and incarceretion, this ever expanding quite pandemic that it took the alarming and preaching voice of the medical establishment to manifest itself in the public opinion and public awareness, after all this high pitched hysterical voices proclaiming the advent of the sexual devastator and maneater HIV, after all that they have done to us, today they say that AIDS is shrunck and receeding to it's original realm, in specific subpopulations that were traditionally subject to prejudice. And something from an epidiolocal point of view. Epidimiology is all about biological trends and habbits, molecular exchanges and population kinetics. During the lifespan of the AIDS epidemic, there was a period prior to the virus alibi, a silent period when populations and science were unaware of the culprit's molecular identity and certainly knew nothing of what to do to protect themselves and their beloved ones from the mystirious disease. It was an era of sexual liberty for the most parts of the western Hemisphere. Still, when the virus was isolated, an epidemiological snap-shot of the disease distrubution, revealed that the virus had spred predominantly into the so called high risk groups, homosexuals, hemophiliacs, drug addicts and Africans. The dissemination of the virus in the general population was minimal. The many years that the “silent period” lasted, should suffice for an outburst or at least an allready situated and established epidimiological picture. Yet, only after the virus' isolation and name-giving did the epidemy cross jumped populations and entered the heterosexual western world. How could that be? Only when the populations became aware of the cause behind the disease, of HIV's transmissions, only after the informative campaigns and the dissemination of preventive measures, only then did the epidemic materialized in the heterosexual western world and appeared to have upward trends year after year. This is an oxymoron, an additional oximoron that can not be easily expained unless, the dissidents were wright about an artifecial statistical inflation overstated the real numbers. And they were. UN's report proved them so. And one can not help but wonder: If the statistics went so colosally wrong, what about the underlying biology?


The Great picture of HIV


Let's follow for a while the train of thought that equates HIV with the cause of AIDS and admit that HIV is a deadly trickster, a deviant and eclectic retrovirus. Really, what does it look like? So far, the virus structure has been described as spherical36, icosahedral37, and recently as conical.38 But to immortalize this microbial criminal in film has proven extremelly difficult. Perhaps the slow killing virus wants to travel incognito or avoids being photographed, sharing a belief with indiginous people of old times that a photograph has a soul. A soul possening virus? Allegorecaly speaking, the answer is pretty much yes. The clever virus seems to posses a mind of it's own, a particular taste for cell and human populations, a killing art of penetration, why not a soul? But then again, soul, mind, art and taste are as far as one can tell human qualities. Could it be possible that these “human qualities” that the virus posseses are such because there are mere human projections on the microscopic level? That we are facing an artefact of an anthropocentric virology?

When Luc Montagnieng tried to take pictures of the unwilling microscopic invader, he willingly admited the hardships that his efforts encountered and decsribed the photo venture as “a Roman effort”39. In 2006, a UK-German team performed an outstanding feat: they reconstructed the map of the HIV by compiling hundreds of different viruses pictures. It was another Roman effort. But why is the virus soooo illusive that feel like raising a roman triumphal arch each and everytime we captured it in film?? Oxford University's Professor Stephen Fuller, a participant in the 3D depicting team that modelled HIV said to BBC: "You say can you show me the structure of the HIV virus and the question is which one.”

"HIV is very variable. It varied in diameter by a factor of three."40

Which one”? So, there is no such thing as a standard morphology for HIV. Taken. Viruses in general often refuse to pose for the striving scientist and can be polymorphic. But morphology is a crucial arm of taxonomy. So forget the golden standards of taxonomy and if the allegations that HIV does not fullfill the Koch postulates are grounded, forget microbiology too. And most certainly forget what you knew of epidemiology as the AIDS statistical methodology was proven flawed.

No taxonomic, epidemiologic, microbiologic golden standarts. This is the realm of an exceptional virus, the realm of the no exact science, of the somehow science, the realm of the AIDS science. Science as we know is irelavant. But is it really the HIV an exception to viruses or perhaps the HIV science is an exception to science alltogether? Desperate times require desperate measures. Ok. But while the researchers desparation is relieved with the concoction of HIV, the populations desperation persists. All these decades of invested research and funds and still no succesfull cure, no succesfull vaccine. AIDS striken people still suffer and new cases are constantly emerging despite the milliondollar campaigns. The only good the HIV science ever did them is to buy them some time at best. But is it quality time?


First do no harm”. Hippocrates and the HIV/AIDS drugs adverse effect connection.

Usually, in a serious article, there is no place for personal confessions. You speak through your research and material and strive to maintain objectivity and keep equal distances. But I really feel obliged to make a confession. At the beggining of my research in the topic, I felt like these people from different but relavant scientific disciplines, the so called “dissidents”, had a point. But I also felt extremely restrained, not to make judgements and by god, not to take sides. There was this dreadfull chance that the dissidents were wrong, deadly wrong. Even if the error possibility was slim, even if that was really the case, even so, the stakes were unacceptably high. People by the millions could forget their special resposibilites as HIV carriers, abandon their medications, do all the AIDS no nos and transform the epidemic into a full case pandemic. Even one unjust death of a misleaded by the dissedents view of non HIV-AIDS would suffice, let alone million deaths and a remerging pandemic. The chance that the are still wrong remains, but it gets slimer and thiner by the time. After all, all we are talking about is scientific arguments, not real life, not deaths. But scientific arguments affect life and death. Decisions are taken upon scientific arguments. Life and death desicions. The responsibility was enormous. And that burden did obscure my judgement. For example, when I examined the observed and possible AZT originaly and afterwards HAART adverse effects, I miss out on something alltogether obvious, pretty much everyone else missed it: The obvious and not the possible RTI's and AIDS Dementia Complex connection.

One of the advantages of the antiretrovitral drugs category defined as Reverse Transcriptase Inhibitors, was supposed to be their specificity. They are targeting an enzume that is vital for retrovirus activity. Guess what? They are not specific. The enzyme is used by different types of organeles and molecules in the human organism. Mitochondria, the organism's power plants, are perhaps the most characteristic and important site of cell funtion impairement that accumulates over time to manifest systemic or localized pathological conditions under the influence of the “virus specific” Nucleoside analogues Reverse Transcriptase Inhibitors with some times devastating effects. Mitochondria carry their own DNA which are far more susceptible to damages then the nucleus DNA as it lucks the complexe repair mechanisms of the latter. That is an additional reason why NRTI's are creating a molecular havoc inside them that in the progress leads to mtDNA damage, mtDNA depletion, and ultimately to perillous health conditions. The rare but often deadly

acidosis/hepatic steatosis syndrome is a well descrided condition that is attributed to iatrogenic mitochondrial damage. NRTI's can do that to you41. Lypodystrophy is another NRTI gift42. Cumulative skeletal myopathy also occurs in a significant fraction of AZT and later on HARRT treated AIDS patients43.

But what is really spectacular is that all AIDS's disseases regarding the Central Nervous System, from AIDS Dementia, to peripheral neuropathy and vacuolar muelopathy, conditions that cripple patients lifes, all of them, with no exception, have their counterparts in medical conditions whose pathogenesis is mitochondrial damage or malfunction. Moreover, all of AIDS's manifestations on the Central Nervous System are yet unexplained. Direct or indirect involment of HIV have been suggested, theoritical models have been set, but nothing conclusive, not a single evidence that a theory proposing a mechanism of how HIV causes neurological damage has been ever presented or, to by more precise, no argument of a neurotoxic HIV mechanism has ever been proved.

So once again, science is excluded: Pathology is determined in a wide variaty of medical cinditions, without an underlying, proven pathophysiological mechanism. So after the deconstruction of epidiology, of taxonomy, of microbiology, neurolophysiology and pathophysiology in general are taken apart for the sake of this malevolent virus.

An exciting detail of AIDS Dementia Complex is that it is a late AIDS symptom-disease. Yet its incidence and morbidity is higher in children than in adults, another of these peculiar, unaccounted AIDS phenomenons. AIDS Dementia is a manifestation of late AIDS, years or even decades after its progression yet it is more often and dangerous in children: How can it be?

One possible link is that the child's mitochondrial DNA originates directy from the mother. If there is an agent that is doing extensive damage to the mother's mitochondrial DNA then, there is a good chance that the defective mtDNA will be directly transfered to the child, and the child will develope any of the plethora of the conditions that both AIDS and mitochondrial damage originating diseases express. Why is it then that almost all of the AIDS CNS diseases are attributable to HIV and not to the pharmaceutical treatment that often damages mitochondrial DNA and results to AIDS-like types of dissorders and degenerative diseases? There are too many parallels between the two cases to tell the difference: retrovirus or the antiretrovirus drugs? Which is the predominant cause in AIDS related diseases? Because there can be no doubt that NRTI's can cause pretty much the same health conditions that they are suppose to treat, at least regarding encephalopathy, peripheral neuropathy, cardiomuopathy, skeletal muopathy, and perhaps cancers.

Taking into consideration the involment of mitochondrial damage and oxidative stress in oncogenesis, one might look at the AIDS defining cancers in an altogether different light. It could be that even AIDS more intimate cancers are sometimes encouraged by the NRTI's. And possible another clue of NRTI's involment in AIDS cancers, is that telomerase which is a reverse transcriptase is also targeted by NRTI's. The role of telomere regions in the aging and cancer processeses is still under investigation.

So where does the “virus toxicity” stops and where does pharmaceutical toxicity begins? This issue really perplexes any treatment approach. How can we make a differential diagnosis between such parallel health conditions when the same general syndrom is involved? How can anyone draw the line? The obscurities of the AIDS science are disabilitating even therapeutics.

Mitochondrial dysfunction is an hypothesis that satisfies a great portion of AIDS pathophysiologal profile and one could easily jump to the conclusion that AIDS, as defined by the AIDS science is partly an iatrogenic syndrome. But what is undisputable is that anti-AIDS drug can theoreticaly mimic AIDS related or defining diseases. And this consists a really insurmountable problem in therapeutics.

Beyond Duesberg

When Duesberg attributed gay AIDS to poppers he was in accordance with the mitochondrial damage AIDS mimicry hypothesis. Poppers, recreational nitric inhalants are stored in cells as NO2 which in turn is associated with mitochondrial damage.44

Duesberg presented as an example of “non HIV (A)IDS” another type of immune deficiency called idiopathic CD4 lumphocytopenia (ICL). However, there was a mismatch between AIDS and ICL. AIDS presents an elevated CD8 count, ICL doesn't. Despite Duesberg's scientific stature his analogy was governed by a narrow approach of the observed deficiency, an approach typical of Gallo's work. If there is a deficiency of CD4 immune cells, then the problem must be within the cells, what is killing them is in the cells. Thus the virus hypothesis was conceived. But within the enormous complexity of the immune system, a system that is designed to interact with the inner and outer enviroment, autonomous, localized causalities are not self-evident.

An essential component of the intricate immune system is the Major Histocompatibility Complex (MHC), a set of molecules displayed on cell surfaces that are responsible for lymphocyte recognition and "antigen presentation". The MHC molecules control the immune response through recognition of "self" and "non-self". They are in the same time “maestros” and “ushers” of the immune orchestra. Now, there is this rare health condition, called MHC class II deficiency. This condition leads to CD4+ T cells deficiency, an AIDS defining critirion. At the same time, CD8+ T cell counts are proportionally increased. This increase also occurs in AIDS. Patients are susceptible to oppurtunistic infections as in AIDS.45

MHC II molecules expression is dependant not only on MHC II genes but also on four other regulatory genes.46 One if these genes is encoding the CIITA transactivator, a very important regulator of the MHC. It is obvious that the Major Histocompatibility Complex is indeed very complex. HIV posseses its own regalatory genes. TAT and Nef are two of them. Now what is really interesting is that the HIV-1 Nef protein inhibits the function of the class II Major Histocompatability Complex function47, and the HIV's very own TAT transactivator inhibits the Human CIITA transactivator 48 and that in turn, the human CIITA inhibits HIVs TAT and inhibits viral replication.49

HIV is present in very different aspects of the Immune, the cental nervous, the sceletical muscle system. It is an omnipresent and highly sophisticated virus that “reads” the human biology long perhaps better than we can do. But then again, perhaps it is the human mind that projects both knownedge and superstition on a mere strand of RNA. Perhaps the complexities of the virus are virtually the complexities of the human body. Perhaps we are facing an anthropocentric science once again. Perhaps what we have been following and researching all these years are the molecular marks of immune systems in distress, it is something that is inside of us and not an omniscient endleslly mutative invader.

But there is a virus, isn't there? There is RNA and reverse transcriptase and protein membranes, aren't there? They have been reported and recorded and writen down in text books. Yes?

Certainly. When Luc Montagnier, a meticulous researcher, tried to isolate the killing virus, one of his main concers were endoretroviruses, that the RNA he was searching for could belong to endoretroviruses. Endoretrovirous are viruses once infectious that were incorporated in the human genome and became inactive through succesive mutations. Now they are harmelss genetical drifters in the journey of evolution comprising 5 to 8% of the human genome.50 Montagnier guickly dropped the idea of endoretroviruses because they were inactive, let alone toxic or infectious. But that was hysteron proteron. They were looking for something toxic and infectious inside the CD4+ cells to explain AIDS, but as is exhibited by the MHC II deficiency example and the TAT, NEF, CIITA, MHC II interactions, such a focalization was neither necessary nor usefull. The “HIV” should be isolated and defined first and related to toxicity and infectiousness afterwards if the Koch Postulates were to be honoured. But it didn't happened that way. The endoretroviruses were dismissed, because they were inactive, non infectious and non toxic. But are they not? Research suggests that: “Expression of reverse transcriptase sequences in human tissues may have biological consequences. The described sequences are similar to elements which cause carcinoma and are immunoregulatory in mice. It remains to be seen whether human sequences also have such functions.”51

But what about the photos, the EM photos, the HIV photos?

What the photos are showing are vesicles, granted. Virus particles? Are those vesicles virus particles?

A new hypothesis of how HIV exits the host cell gains ground. It proposes that HIV utilizes the exosome release pathway. Exosomes are nanovesicles released by leukocytes and epithelial cells. They are bags of cellular membrane that have been endocytosed, broken to smaller fragments that form vesicles and finally released from the cell. They can express MHC I and MHC II molecules, and are immunogenic, triggering and modulating immune respnse. Exosome is an additional, novel to us way of intracellular communication and antigen presentation. Exosomes are capable of transporting mRNA and microRNA, the so called "exosomal shuttle RNA" which is shipped from one cell to another and can interfere with the protein production of the recepiant cell52. The exosome release pathway, or trojan exosome model of retrovirus virology has been proposed by Hildreth, Gould and Booth as they were constantly facing numerous observations that just couldn't fit the existing model of HIV biology.53 Hildreth described the driving force behind this propasal eloquently: “so many aspects of retroviral biology have not been reconciled, including HIV, that we have to take a broader view...”

...Much of our work and that of others has shown that the biology of HIV is more complex than would be anticipated from the genes present in its genome.  Furthermore, the large number of host proteins associated with the virus suggest that HIV probably utilizes a cellular pathway for biogenesis and release.  Recently, a number of investigators have shown that gag  proteins of retroviruses directly interact with host proteins involved in formation of or trafficking of late endosomes.  In addition, HIV budding in macrophages occurs in large class II MHC loading compartments or multivesicular bodies (MVBs).  These compartments serve as sites for  formation of exosomes, virus-sized vesicles formed within MVBs and released into the extracellular space.  In collaboration with Dr. Stephen Gould of Johns Hopkins University we have proposed that HIV and other retroviruses are cargo of this pathway (the Trojan Exosome Hypothesis).  In a recent paper, we presented evidence that HIV budding in macrophages occurs through the exosome release pathway and similar observations have been made for HTLV-1...”

The virus is fully an exosome in every sense of the word”

Why the dual personality? Because we have patented HIV as the AIDS causal agent and we are unable or unwilling to reconsider?

The Trojan exosome Hypothesis has been furthered even more towards scientific extremity: It has been suggested that retroviruses evolved from retrotransposons. Retrotransposons are mobile elements of the genome, genetical drifters whose only function appears to be selfprocraation that's what earned them the characterization of “selfish DNA parasites”. They have been associated with Hemophilia, cancer and immunodeficiency, all of them being AIDS related conditions. Hildreth argued that a mutation that redirected a retrotransposon's RNA into the exosome-assembly pathway could have offered a way to package that RNA, get it out of a cell, and introduce it to another cell, hence, a retrovirus is born. (Interestingly enough, the VDJ segment of the immune system, a recompination hotspot that accomplishes immune response diversity, is directed by enzymes that are believed to originate for transposases encoded from trasposons).



That is what they isolated back in 1983: an RNA containing exosome whose existance they didn't know, not even in theory.



That is the reason why the HIV envelope contains a structural MHC class II homology consistent with an alloepitope. That why HIV budds. It is virtually an exosome. That is why no two HIV genomes are the same54, that's why it is constantly mutating, because it was never a specific RNA entity, that's why when you ask Fuller to show you the structure of the HIV virus he answers back with the question: which one? That's why HIVs TAT antagonizes human CIITA, because it is an human endogenous or allogenous transactivator, thats why HIV is different from cell to cell, from organ to organ, from population to population. That's why when Hoffmann expsosed HIV uninfected mouse to allo-mouse cells he got antibodies for gp120 and p24, “specific HIV antibodies”55. That is why when James Stott infected macaques with human uninfected T-cells he amazingly got an immune response for SIV56. That is why hemophiliacs developed AIDS, because of MHC molecules and their receptors in allo-lymphocytes and anti-anti-self MHC57. Not because of a specific RNA virus but because of the speficity of the highly personalized immune system.

AIDS appears to be a endogenous immune condition, triggered by endogenous or exogenous stimuli and perplexed even more by AIDS mimicking treatment. That is what AIDS probably is.

End of the story. Lets only hope that the death of millions will contribute to a better understanding of the enigmatic immune system and its interactions.


1Science, 220, 868-871 (1983), Isolation of a T-Lymphotropic Retrovirus from a Patient at Risk for Acquired Immune Deficiency Syndrome ( AIDS), F. Barré-Sinoussi, J.C. Chermann, F. Rey, M.T. Nugeyre, S. Chamaret, J. Gruest, C. Dauguet, C. Axler-Blin, F. Vézinet-Brun, C. Rouzioux, W. Rozenbaum, L. Montagnier

2Science, 1984 May 4:224(4648):500-3,Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS, Gallo RC, Salahuddin SZ, Popovic M, Shearer gm, Kaplan M, Haynes BF, Palker TJ, Redfield R, Oleske J, Safai b et al

3 Chang S-YP, Bowman BH, Weiss JB, García RE, White TJ (1993) The origin of HIV1 isolate HTLV-IIIB. Nature 363:466-469

4Science. 1986 May 9; 232(4751):697, Human immunodeficiency viruses, Coffin J, Haase A, Levy JA, Montagnier L, Oroszlan S, Teich N, Temin H, Toyoshima K, Varmus H, Vogt P, et al

5New York Times, 1 April 1986, US and France end rift on AIDS, by Lawrence K. Altman

6Nature 397, 436-441 (04 February 1999), Origin of HIV-1 in the chimpanzee Pan troglodytes troglodytes, Feng Gao, Elizabeth Bailes, David L. Robertson, Yalu Chen, Cynthia M. Rodenburg, Scott F. Michael, Larry B. Cummins, Larry O Arthur, Martine Peeters, George M. Shaw, Paul M. Sharp, Beatrice H. Hahn

7BBC, 25 May 2006, HIV origin found in wild chimps

8 London Times, 11 May 1987, Smallpox vaccine 'triggered Aids virus', by Pearce Wright

9London Times, 11 May 1987, Smallpox vaccine 'triggered Aids virus', by Pearce Wright

10 The River: A Journey to the Source of HIVand AIDS, by Edward Hooper, Little, Brown, N.Y 1999

11Prljic J, Veljkovic N, Colombatti A, Johnson E, Metlas R. and Veljkovic V. Identificaion of an active Chi recombinational hot spot within the HIV-1 envelope gene: consequences for development of AIDS vaccine. Vaccine 1999: 17: 1462

12Testimony of Dr. Howard B. Urnovitz, August 3, 1999, at the Committee On Government Reform And Oversight

13J. Albert et al., J. Med. Virol. 23, 67 (1987).

L.A. Falk, D. Paul, A. Landay, H. Kessler, N. Engl. J. Med. 316, 1547 (1987).

G.M. Shaw et al., Science 226, 1165 (1984).

D. Richman, J. McCutchan, S. Spector, J. Infect Dis. 156, 823 (1987).

C.-Y. Ou et al., Science 239, 295 (1988).

M.E. Harper, L.M. Marselle, R.C. Gallo, F. Wong-Staal, Proc. Natl. Acad. Sci. U.S.A. 83, 772 (1986).

A. Ranki et al., Lancet ii, 589 (1987).

P.H. Duesberg, Cancer Res. 47, 1199 (1987).

H. von Briesen et al., J. Med. Virol. 23, 51 (1987).

D. Gallo, J. Kimpton, P. Dailey, J. Clin. Microbiol. 25, 1291 (1987).

J.W. Curran et al., Science 239, 610 (1988).

G.H. Friedland and R.S. Klein, N. Engl. J. Med. 317, 1125 (1987).

J. Coffin et al., Science 232, 697 (1986).

14 A. Fauci, ibid. 239, 617 (1988).

D. Richman, J. McCutchan, S. Spector, J. Infect Dis. 156, 823 (1987).

M.E. Harper, L.M. Marselle, R.C. Gallo, F. Wong-Staal, Proc. Natl. Acad. Sci. U.S.A. 83, 772 (1986).

A. Ranki et al., Lancet ii, 589 (1987).

15 Foreign-protein-mediated immunodeficiency in hemophiliacs with and without HIV, Peter H.Duesberg, Genetica 95: 51-70, 1995

16 Haverkos H W, Pinsky P F, Drotman DP, Bregman DJ, 1985 Disease manifestation among homosexual men with acquired immuodeficiency syndrome: a possible role of nitrites in Kapoisi's sarcoma; J. Sex. Trans. Dis. 12 203-208

17Is The AIDS Virus A Science Fiction? (Immunosuppressive Behavior, Not HIV, May Be the Cause of AIDS) by Peter H. Duesberg & Bryan J. Ellison, Policy Review Summer 1990

18Is HIV Cause Of AIDS? By Peter H. Duesberg & Brian J. Ellison , Policy Review Dec. 1990

19Papadopulos-Eleopulos E. Reappraisal of AIDS: Is the oxidation caused by the risk factors the primary cause? Medical Hypotheses 1988; 25:151-162.

20Piedimonte G, Guetard D, Magnani M, et al. Oxidative, protein damage and degradation in lymphocytes from patients infected with human immunodeficiency virus. JInfect Dis 1997;176:655–64

21 Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D. The Isolation of HIV: Has it really been achieved? Continuum 1996; 4:1s-24s.

Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Is a positive Western blot proof of HIV infection? Bio/Technology 1993; 11:696-707.

Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Has Gallo proven the role of HIV in AIDS? Emergency Medicine [Australia] 1993; 5:113-123.

22 Damien Freyssenet, Martino DiCarlo, Patricia Escobar, Janice Grey, Jeremy Schneider, and David A. Hood, Zidovudine (AZT) induced alterations in mitochondrial biogenesis in rat striated muscles, Can. J. Physiol. Pharmacol.77(1):29–35(1999)

De la Asunción JG, del Olmo ML, Sastre J, Pallardó FV, Viña J, Zidovudine (AZT) causes an oxidation of mitochondrial DNA in mouse liver, Hepatology. 1999 Mar;29(3):985-7.

23 Katsuko Takasawa, Tetsuya Terasaki, Hiroshi Suzuki and Yuichi Sugiyama, In Vivo Evidence for Carrier-Mediated Efflux Transport of 3'-Azido-3'-Deoxythymidine and 2',3'- Dideoxyinosine Across the Blood-Brain Barrier via a Probenecid-Sensitive Transport System, Pharmacology and Expirimental Therapeutics Vol. 281, Issue 1, 369-375, 1997

24 Bagasra O, Lavi E, Bobroski L, Khalili K, Pestaner JP, Tawadros R, et al. Cellular reservoirs of HIV-I in the central nervous system of infected individuals: identification by the combination of in situ polymerase chain reaction and immunohistochemistry. AIDS 1996; 10 : 573-85

25 Tornatore C, Chandra R, Berger JR, Major EO. Abstract HIV-I infection of subcortical astrocytes in the pediatric central nervous system. Neurology 1994; 44 : 481-7.

Ranki A, Nyberg M, Ovod V, Haltia M, Elovaara I, Raininko R, et al. Abundant expression of HIV Nef and Rev proteins in brain astrocytes in vivo is associated with dementia. AIDS 1995; 9: 1001- 8.

26McArthur JC, Haughey N, Gartner S, Conant K, Pardo C, Nath A, et al. Human immunodeficiency virus-associated dementia: an evolving disease. J Neurovirol 2003; 9:205-21

27Chang J, Jozwiak R, Wang B, et al. Unique HIV type 1 V3 region sequences derived from six different regions of brain: Region- specific evolution within hostdetermined quasispecies. AIDS Res Hum Retroviruses 1998, 14 : 25-30.

Smit TK, Wang B, Ng T, Osborne R, Brew B, Saksena NK. Varied tropism of HIV-1 isolates derived from different regions of adult brain cortex discriminate between patients with and without ADC: Evidence for neurotropic variants. Virology 2001; 279; 509-26

28 Chang J, Jozwiak R, Wang B, et al. Unique HIV type 1 V3 region sequences derived from six different regions of brain: Region- specific evolution within hostdetermined quasispecies. AIDS Res Hum Retroviruses 1998, 14 : 25-30.

29Langford TD, Letendre SL, Masliah E. Changing patterns in the neuropathogenesis of HIV during HAART era. Brain Pathology 2003; 13 : 195-210.

30Fiala M, Murphy T, MacDougall J, Yang W, Luque A, Iruela-Arispe L, Cashman J, Buga G, Byrns RE, Barbaro G, Arthos J., HAART drugs induce mitochondrial damage and intercellular gaps and gp120 causes apoptosis. Cardiovasc Toxicol. 2004;4(4):327-37.


Debasis Mondal; Leena Pradhan; Mussa Ali; Krishna C. Agrawal, HAART Drugs Induce Oxidative Stress in Human Endothelial Cells and Increase Endothelial Recruitment of Mononuclear Cells: Exacerbation by Inflammatory Cytokines and Amelioration by Antioxidants Cardiovascular Toxicology, Volume 4, Number 3, August 2004 , pp. 287-302(16)

  1. 31H. E. Gendelman, I. Grant, I. Everall, S. A. Lipton, and S. Swindells, The Neurology of AIDS, Oxford University Press, 357-373

  1. 32Satishchandra, P., Nalini, A., Gourie-Devi, M., Khanna, N., Santosh, V., Ravi, V., Desai, A., Chandramuki, A., Jayakumar, P. N., and Shankar, S. K. (2000). "Profile of neurologic disorders associated with HIV/AIDS from Bangalore, south India (1989-96)". Indian J. Med. Res. 11: 14-23

Wadia, R. S., Pujari, S. N., Kothari, S., Udhar, M., Kulkarni, S., Bhagat, S., and Nanivadekar, A. (2001). "Neurological manifestations of HIV disease". J. Assoc. Physicians India 49: 343-348.

33 BJM, rapid responses, 5 Aprill 2004, HAART: One foot on the gas pedal, the other on the break, David Rasnick

34The Sunday Times (London) 3 October 1993, The plague that never was, by Neville Hodgkinson

35 U.N. to Cut Estimate Of AIDS Epidemic

Population With Virus Overstated by Millions

By Graig Timberg

Washington Post Foreign Service
Tuesday, November 20, 2007

36Ehrlich LS, Liu T, Scarlata S, Chu B, Carter CA, HIV-1 capsid protein forms spherical (immature-like) and tubular (mature-like) particles in vitro: structure switching by pH-induced conformational changes.Biophys J 2001 Nov;81(5):2992.

37 Nermut MV, Grief C, Hashmi S, Hockley DJ., Further evidence of icosahedral symmetry in human and simian immunodeficiency virus, AIDS Res Hum Retroviruses. 1993 Oct;9(10):929-38.

38 3D structure of HIV is 'revealed' BBC news Tuesday, 24 January 2006

39 Interview, Luc Montagnier
Did Luc Montagnier Discover HIV?

By Djamel Tahi

Continuum Winter 1997

403D structure of HIV is 'revealed' BBC news Tuesday, 24 January 2006

41 Chattha, G, Arieff AI, Cummings C, and Tierney LM, Jr. Lactic acidosis complicating the acquired immunodeficiency syndrome (see Comments). Ann Intern Med 118: 37-39, 1993

Boubaker, K, Sudre P, Flepp M, Furrer HJ, Haensel A, Hirschel B, Boggian K, Chave JP, Bernasconi E, Opravil M, Rickenbach M, and Telenti A. Hyperlactatemia and Antiretroviral Therapy in the Swiss HIV Cohort Study (SHCS). In: 7th Conference on Retroviruses and Opportunistic Infections, San Francisco, CA, 2000.


42Saint-Marc, T, Partisani M, Poizot-Martin I, Bruno F, Rouviere O, Lang JM, Gastaut JA, and Touraine JL. A syndrome of peripheral fat wasting (lipodystrophy) in patients receiving long-term nucleoside analogue therapy. AIDS 13: 1659-1667, 1999

43Dalakas, MC, Leon-Monzon ME, Bernardini I, Gahl WA, and Jay CA. Zidovudine-induced mitochondrial myopathy is associated with muscle carnitine deficiency and lipid storage (see Comments). Ann Neurol 35: 482-487, 1994

44Nitric oxide-mediated mitochondrial damage: A potential neuroprotective role for glutathione

Juan P. Bolaños, Simon J. R. Heales, Stefan Peuchen, Jane E. Barker, John M. Land and John B. Clark

Free Radical Biology and Medicine, Volume 21, Issue 7, 1996

45Reith W and Mach B. The bare lymphocyte syndrome and the regulation of MHC expression. Annu Rev Immunol 19: 331–373, 2001

46Reith W and Mach B. The bare lymphocyte syndrome and the regulation of MHC expression. Annu Rev Immunol 19: 331–373, 2001

47Stumptner-Cuvelette P, Morchoisne S, Dugast M, Le Gall S, Raposo G, Schwartz O, Benaroch P.

Nef impairs MHC class II antigen presentation and surface expression.

Proc N atl Acad Sci U.S.A 2001 Oct 9;98(21):12144-9HIV-1

48Kanazawa S, Okamoto T, Peterrlin BM

Tat competes with CIITA for the binding to P-TEFb and blocks the expression of MHC class II genes in HIV infection.Immunity. 2000 Jan;12(1):61-70

49The MHC class II transactivator: prey and hunter in infectious diseases

Accolla R. S., De Lerma Barbaro A., Mazza S., Casoli C., De Maria A., Tosi G.

Trends Immunol. 2001;22:560–563

50International Human Genome Sequencing Consortium (2001) Nature 409:, 860–921

51P. Medstrand and J. Blomberg

Characterization of novel reverse transcriptase encoding human endogenous retroviral sequences similar to type A and type B retroviruses: differential transcription in normal human tissues.

J Virol. 1993 November; 67(11): 6778-6787

52 Valadi et al.,

sRNA,

Nat Cell Biol 2007 Jun;9(6):654-9

53Gould, S.J., Booth, A.M. , and Hildreth, J.E.K. The trojan exosome hypothesis,  Proc. Nat. Acad. Sci. USA 100:10592-10597, 2003

54 Wain­Hobson, S., 1989. HIV genome variability in vivo. AIDS 3: supp 1; 13­9

55Hoffmann, Geoffrey W. "Anti-HIV and Anti-Anti-MHC Antibodies in Alloimmune and Autoimmune mice." Science, vol. 253 (September 6, 1991), pp. 1138- 1140

56Stott, E.J. (1191). Anti-cell antibody in macaques. Nature 353(6343), 393

57G W Hoffmann, T A Kion, and M D Grant An idiotypic network model of AIDS immunopathogenesis.Proc Natl Acad Sci U S A. 1991 April 15; 88(8): 3060–3064.


Login Sitemap | | Design by... | Powered by CMSimple