HIV - a virus like no other

On The Perth Group, and 35 Questions & Answers

The Perth Group came up when I interviewed Mike Stone.

Virology - Lies are Unbekoming (substack.com)

However, during this time, I began to research how accurate disease diagnosis was due to a fraudulent HIV test result my mother-in-law had received. This led to my learning about the HIV/AIDS lie due to the work of Dr. Stefan Lanka, the Perth Group, David Crowe, Kary Mullis, Peter Duesberg, Jon Rappoport, and many others. I learned that HIV had never been purified and isolated nor ever demonstrated to be the cause of AIDS. Once the HIV/AIDS domino fell, I started to understand that the same issues with HIV were present in all “viruses.” 

It came up again when I interviewed Kyle Young.

Interview with Kyle Young - Lies are Unbekoming (substack.com)

As the Perth Group in Australia pointed out long ago, viruses have not been proven to be the cause of disease. As we also now know, the covid virus has never been isolated. Every image of it is computer generated.

I’ve decided to pay attention to their work with this stack.

The HIV/AIDS fraud is important for many reasons.

It built the template for what they did during the “pandemic.”

“Covid” in fact was AIDS v2.0.

But even more importantly HIV/AIDS goes to the heart of the Empire grade, meta-narrative fraud that is virology.

Let’s start with a great summary of their work by Drs Sam & Mark Bailey from The Final Pandemic.

I will then do a Q&A summary of HIV- a virus like no other, one of the Perth Group’s most important works.

The Perth Group HIV-AIDS Debate Website

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The Final Pandemic

The Final Pandemic: An Antidote To Medical Tyranny: Bailey, Dr Samantha, Bailey, Dr Mark, Noakes, Prof Tim

Case Study: The Suppression of The Perth Group

The Perth Group is a private organisation that formed in 1981 in Perth, Western Australia with the three original members being biophysicist Eleni Papadopulos-Eleopulos, emergency physician Valendar Turner and Professor of Pathology John Papadimitriou. For over four decades they have argued that the HIV/AIDS experts have not scientifically established any of the following:

1.    The existence of a virus termed ‘HIV’.

2.    The specificity of ‘HIV’ antibody tests for ‘HIV’ infection.

3.    The theory that ‘HIV’ causes the clinical syndrome AIDS.

4.    That the “HIV genome” comes from an infectious particle.

5.    ‘HIV’/AIDS being infectious by blood or sexual intercourse.

6.    Mother to child transmission of ‘HIV’ (and the alleged benefit of certain “anti-virals”).

No group has produced more detailed scientific critiques of the HIV/AIDS model and their 2017 treatise HIV - A Virus Like No Other, weighs in at over 60,000 words with several hundred supporting scientific citations. This and the Perth Group’s many other publications have refuted all aspects of the theory that a “deadly virus” is passing around and causing AIDS. And yet the vast majority of doctors have never heard of them or read even one of their works.

The incredible state of affairs is readily explained by the fact that doctors are trained to believe that ‘HIV=AIDS’ is settled science. Most do not know any of the historical events that took place and if they do it is restricted to the fanciful story that HIV was all worked out by the likes of Robert Gallo, Luc Montagnier and Anthony Fauci in the 1980s. How could these famous individuals and their highly-resourced institutions be completely wrong with the science?

Indeed, after two decades in the medical system neither of the authors were aware that anyone had even attempted a refutation of the HIV model, let alone produced an 83-page treatise. All we were informed in our training was that some people engaged in “AIDS denialism” as a reaction to the terrible burden of a death sentence for themselves or others.

Of course the term ‘AIDS denialism’ is highly disingenuous as no serious critics of the model deny that the individuals in question may become sick and even terminally unwell. The dispute is over the evidence that an infectious virus is the cause of the clinical syndrome known as ‘AIDS’, first described in the 1980s. The CDC currently lists 27 AIDS-defining conditions, all of which existed prior to the alleged appearance of HIV. The only new development is the claim since the 1980s that these wide-ranging conditions can all be caused by one postulated virus and diagnosed with a biochemical test(s). (See also Dr Claus Köhnlein’s comments about this phenomenon in chapter 4: “Why was SARS-2 (COVID-19) Bigger than SARS-1?”)

The United States National Institutes of Allergy and Infectious Disease (NIAID) website once featured a page titled “The Evidence That HIV Causes AIDS.” It included a section titled “Answering The Skeptics: Responses To Arguments That HIV Does Not Cause AIDS” written in a “MYTHS” and “FACTS” format. It does not specify who they are responding to. For reasons unknown to us the webpage was taken down in 2009 but can still be found on the 17th of January capture that year on archive.org. The article stated that, “nearly everyone with AIDS has antibodies to HIV,” as though an “antibody” (protein) reacting in a laboratory test plate is evidence of a virus at work. They have engaged in circular reasoning by claiming that a chemical reaction is evidence of the virus…because the virus will cause this particular chemical reaction. However, there was no demonstration of a “virus” to start with.

The NIAID also make the fraudulent claims that, “HIV fulfills Koch's postulates as the cause of AIDS,” and “the suspected pathogen can be isolated - and propagated - outside the host.” The cited evidence is in the form of epidemiological statistics, anecdotes, and pseudoscientific animal studies. It is beyond the scope of this book to address all of the “evidence” that was on display in the article. However, in their typical fashion, The Perth Group made a succinct response to the NIAID in 2000, addressing both the key argument and the disingenuous nature of the article:

It is incomprehensible how a body of scientists at the National Institutes for Health in the US could present both sides of a scientific debate as a series of “MYTHS” and “FACTS”. Especially without providing the names of scientists who hold the opposing view or any citations to enable the reader to investigate the matter himself. The only conclusion one can make from this behavior is that the NIH does not want their readers to learn the full story. Here we examine one very important “FACT” and leave it up to the reader to make his own judgement as to whether or not it is a “MYTH”.

FACT: THERE IS NO EVIDENCE A RETROVIRUS HAS BEEN ISOLATED FROM THE TISSUES OF AIDS PATIENTS. HENCE THERE IS NO GOLD STANDARD FOR ANTIBODY TESTING FOR “HIV” INFECTION AND NO PROOF A RETROVIRUS CAUSES AIDS.

In order to anticipate the establishment’s hardening dogma, The Perth Group had several of their papers published in the peer-reviewed scientific journals. Equally so many were rejected, most often for spurious reasons that had little to do with the carefully presented scientific arguments. An example was “A critical appraisal of the evidence for the existence of HIV,” which was submitted to the Royal Australasian College of Surgeons in 1997. The Perth Group have commented on the astounding excuse for rejection they received:

According to that journal it is editorial policy to “welcome personal views of surgeons on a variety of topics,” and to publish papers on “current and controversial issues.” Although both reviewers accepted the bulk of the scientific arguments and found the paper “interesting reading,” they advised against publication because, in their view, an analysis of evidence for the isolation of HIV was of “no real relevance…to a surgical audience” or “would be of little interest or use to the majority of readers of the Australian and New Zealand Journal of Surgery”.

In another example, the HIV theory of AIDS proposed that the “virus” was causing two principal diseases: Pneumocystis Carinii Pneumonia (PCP) and Kaposi’s sarcoma (KS), a type of cancer that affects the skin and other organs. However, the “HIV experts” were subsequently forced to bite the bullet and declare HIV was not the cause of KS. This was because cases of KS were reported in homosexual men who did not have positive HIV antibody tests. Eleni Papadopulos had anticipated this and in 1990 submitted a pertinent paper to the Medical Journal of Australia. This was thrice rejected on the advice of an anonymous, “established expert reviewer” who stated:

The author tries to argue that Kaposi's sarcoma cannot be caused by HIV infection, and that therefore AIDS is not due to HIV infection [Papadopulos made no such claim]. The arguments put forward by the author are quite unsatisfactory, and are not supported by even a desultory reading of the literature quoted. In addition, the author fails to examine the body of epidemiological, immunological and cellular literature concerning the pathology, pathogenesis and clinical associations of this fascinating manifestation of HIV infection.

Yet it was this very “epidemiological, immunological and cellular literature” that eventually led the “established experts” to accept that, “this fascinating manifestation of HIV infection” is not due to alleged HIV infection. Obviously the expert reviewer realized that the failure of HIV to explain KS was bad news for the rest of the AIDS theory. At the very least, KS should have ceased being an AIDS indicator disease. This was not to be and KS remains on the list with the other 26 diseases, all supposedly related to the claimed “virus” whose characteristics can apparently change to fit the model.

The suppression of The Perth Group’s work has been a crime against the individuals who have been labelled as harboring a “deadly virus”. As Jon Rappoport wrote in his 1988 book AIDS Inc.: scandal of the century, “there is no way to measure the full effect of telling a person he has AIDS, or has tested positive for the ‘AIDS virus’.” Furthermore it has been a crime against humanity due to the billions of dollars that the AIDS industry consumes, with funding only going to those doctors and scientists who subscribe to the virus model. The pharmaceutical industry has also benefitted greatly of course with its “antiviral” chemicals. Their various drug concoctions have been involved in the deaths of thousands of people, particularly in the 1980s and 1990s as outlined in chapter 3 of Virus Mania, “AIDS: From Spare Tire to Multibillion-Dollar Business”.

However, The Perth Group’s efforts over the last four decades have not been in vain. An inadvertent effect of the COVID-19 fraud has been an explosion of interest in their devastating and unrefuted critiques of HIV/AIDS as well as the broader implications for virology itself.

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HIV – a virus like no other

The Perth Group

Hiv A Virus Like No Other

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Analogy

Imagine you're trying to solve a mystery in a small town. Someone claims there's a dangerous criminal causing harm, but no one has actually seen this person clearly.

1. The "criminal" (HIV): People say they've seen evidence of the criminal - footprints, items moved around, shadows. But when asked to provide a clear photo or description, they can't. This is like the lack of purified, isolated HIV particles.

2. The "wanted poster" (HIV tests): The town creates wanted posters based on vague descriptions. But these descriptions could fit many people, not just the supposed criminal. This is similar to HIV tests potentially reacting to proteins that aren't specific to HIV.

3. The "crime wave" (AIDS): The town experiences a rise in various problems - broken windows, stolen goods, graffiti. Officials blame all these on the single criminal. This is like attributing many different diseases to one virus, HIV.

4. The "police force" (immune system): The town's police force (T4 cells) starts to decrease. Officials claim the criminal is targeting police officers. But others suggest the police might be leaving for other reasons, like poor working conditions. This reflects debates about what causes T4 cell decline.

5. The "security system" (antiretroviral drugs): The town installs an expensive security system to stop the criminal. Some problems decrease, but it's unclear if it's because of the system or other factors. This is like debates about whether antiretroviral drugs work by stopping HIV or through other mechanisms.

6. The "town council" (scientific community): The town council insists everyone focus on catching this one criminal, discouraging investigation of other possible causes of the town's problems. This represents how the focus on HIV might have limited exploration of alternative explanations for AIDS.

In this analogy, the debate is whether there really is a single criminal causing all these problems, or if the town's issues have multiple, complex causes that have been oversimplified into one narrative. The challenge is to step back and re-examine the evidence without assuming the initial explanation is correct.

35 Questions & Answers

Question 1: What were the early observed symptoms and diseases associated with AIDS?

The early AIDS cases were primarily characterized by two diseases - Kaposi's sarcoma (KS) and Pneumocystis carinii pneumonia (PCP). These were formerly rare diseases that suddenly began appearing with high frequency in young, sexually promiscuous, drug-using homosexual men. KS is a malignancy primarily involving the skin, while PCP is a chronic pneumonia caused by a fungal organism.

As the epidemic progressed, more diseases were added under the umbrella term "AIDS indicator diseases," eventually numbering 29. These included tuberculosis, candida (yeast) infections, lymphoma, and cervical cancer, among others.

Question 2: How did the scientific understanding of HIV/AIDS origins evolve over time?

Initially, researchers from the "Retrovirology Club" proposed a viral theory to explain the high frequency of KS and PCP in homosexual men. They suggested that a single infectious agent, later identified as HIV, was causing the destruction of T4 cells (immune deficiency), which then led to the appearance of opportunistic infections.

This theory was rapidly adopted by the scientific and medical communities, despite resistance to alternative views. The virus was first reported by Montagnier's team in 1983 and then by Gallo's team in 1984. By 1986, what were initially called LAV and HTLV-III were renamed as HIV. The theory evolved to include ideas about HIV's origins, transmission routes, and its role in causing AIDS, despite ongoing debates and criticisms from some scientists.

Question 3: What were the key steps and methods used by Montagnier and Gallo in their claimed discovery of HIV?

Montagnier's team claimed to have isolated a retrovirus (LAV) from a patient at risk of AIDS in 1983. Their method involved culturing T-lymphocytes from a patient, detecting reverse transcriptase activity, and observing virus-like particles under electron microscopy in umbilical cord blood lymphocytes cultured with the patient's cells.

Gallo's team in 1984 claimed to have isolated HTLV-III from multiple AIDS patients. They used similar methods but introduced the H9 cell line for virus cultivation. Both teams relied on detecting reverse transcriptase activity, observing particles under electron microscopy, and demonstrating antigen-antibody reactions with patients' sera as evidence of virus isolation.

Question 4: What criticisms have been raised regarding the HIV isolation techniques used by early researchers?

Critics argue that the early researchers did not properly isolate HIV. They point out that neither Montagnier nor Gallo published electron micrographs of purified virus particles. The "purified virus" they used was simply material from a density gradient band, which could contain cellular debris and other non-viral elements.

The use of reverse transcriptase activity as proof of retrovirus presence is criticized because this enzyme is not specific to retroviruses. Similarly, the reliance on antibody reactions with proteins from the "purified virus" is questioned due to the non-specificity of antibodies and the lack of proof that the proteins were viral in origin.

Question 5: How was the HIV genome initially characterized and what controversies surround this research?

The HIV genome was initially characterized by Gallo's team in 1984. They extracted poly(A) RNA from material banded at 1.16 g/ml density, assuming it was purified virus. This RNA was reverse transcribed into cDNA, which was then cloned and used as probes to detect "viral" sequences in infected cells.

Controversies surround this research because there was no proof that the RNA originated from retroviral particles. Critics argue that poly(A) RNA is not specific to retroviruses and can be found in uninfected cells. Furthermore, the lack of proper controls in these experiments is criticized. The genetic variability later observed in HIV also raised questions about whether a unique viral entity had actually been identified.

Question 6: What are the main principles and criticisms of HIV antibody tests?

HIV antibody tests are based on detecting antibodies that react with proteins believed to be from HIV. The main types are the enzyme immunoassay (EIA/ELISA) and the Western blot. These tests were developed based on the proteins found in the "purified virus" preparations of Montagnier and Gallo.

Criticisms of these tests include:

1. The lack of a proper gold standard (isolated HIV) to validate the tests.

2. The non-specificity of antibodies, which can cross-react with many proteins.

3. The presence of "HIV" antibodies in people not at risk for AIDS.

4. Changes in criteria for interpreting test results over time, particularly for the Western blot.

5. The inability of the tests to distinguish between different "HIV" strains despite high genetic variability.

Question 7: How have theories about HIV transmission changed since the beginning of the AIDS epidemic?

Initially, HIV was thought to be transmitted primarily through sexual intercourse, blood, and blood products. However, epidemiological studies revealed that only receptive anal intercourse was consistently associated with HIV antibody positivity and AIDS.

This finding challenged the idea of HIV as a bidirectionally transmitted sexually transmitted disease. Some researchers, like the Perth Group, argue that AIDS is sexually acquired but not sexually transmitted, similar to pregnancy. They suggest that the cumulative exposure to semen, particularly through anal intercourse, may be the causative factor rather than a virus.

Question 8: What is HAART and how has it impacted AIDS treatment and mortality?

HAART (Highly Active Antiretroviral Therapy) refers to combination drug therapies introduced in 1996. It typically includes a mix of reverse transcriptase inhibitors and protease inhibitors. HAART is credited by mainstream HIV/AIDS researchers with transforming AIDS from a fatal condition to a manageable chronic disease.

However, critics point out that the decline in AIDS deaths began before HAART's introduction and that the benefits of HAART may not be due to its purported anti-HIV effects. They argue that HAART's impact on mortality doesn't necessarily prove HIV causes AIDS, as these drugs have multiple effects beyond their claimed antiviral action.

Question 9: How and why did the definition of AIDS change over time?

The definition of AIDS has changed several times since 1982. Initially, it was defined as KS or PCP in individuals under 60 with no known cause of immunosuppression. Subsequent revisions in 1985, 1987, and 1993 progressively expanded the definition.

Key changes included:

1. Adding more indicator diseases

2. Including HIV antibody testing

3. Allowing presumptive diagnoses without definitive testing

4. Including individuals with low T4 cell counts regardless of symptoms

These changes were made to capture more cases and reflect evolving understanding of the syndrome. However, critics argue that these definitional changes artificially inflated AIDS case numbers and complicated interpretation of epidemiological data.

Question 10: What is the oxidative stress theory of AIDS and how does it differ from the HIV theory?

The oxidative stress theory of AIDS, proposed by Eleni Papadopulos-Eleopulos, suggests that AIDS is caused by an accumulation of oxidative stress in the body, particularly affecting the immune system. This theory posits that various risk factors associated with AIDS, such as drug use, multiple infections, and exposure to semen, all contribute to oxidative stress.

Unlike the HIV theory, which attributes AIDS to a single infectious agent, the oxidative stress theory sees AIDS as a result of multiple factors that disrupt the body's redox balance. This theory explains why only certain sexual practices (receptive anal intercourse) are consistently associated with AIDS and why AIDS patients exhibit oxidative stress markers. It also suggests different approaches to prevention and treatment, focusing on antioxidants rather than antiretroviral drugs.

Question 11: What is the relationship between cellular microvesicles and HIV particles?

Cellular microvesicles are small particles produced by cells that can be mistaken for viral particles. In HIV research, it was discovered that the material considered to be "purified HIV" contained a large number of these microvesicles. This finding came to light in 1997 when researchers like Gluschankof and Bess published electron micrographs of supposedly purified HIV preparations.

These microvesicles have similar size and density to what are claimed to be HIV particles, and they contain many of the same proteins and nucleic acids. This similarity raises questions about whether the particles identified as HIV in earlier research were actually viral particles or cellular debris. The presence of these microvesicles in "purified virus" preparations also complicates the interpretation of biochemical analyses used to characterize HIV.

Question 12: What are the principles and controversies surrounding PCR and viral load tests in HIV diagnosis?

PCR (Polymerase Chain Reaction) and viral load tests are used to detect and quantify HIV genetic material in patient samples. These tests amplify specific DNA or RNA sequences thought to be part of the HIV genome. The viral load test, which measures HIV RNA in plasma, is often used to monitor disease progression and treatment effectiveness.

Controversies surrounding these tests include:

1. The lack of standardization in PCR methods and interpretation.

2. The absence of a gold standard (isolated HIV) to validate the tests.

3. The detection of "HIV" sequences in individuals not considered infected.

4. The disconnect observed between viral load, CD4 cell counts, and clinical outcomes in some studies.

5. The inventor of PCR, Kary Mullis, warned about the potential for false positives and misinterpretation of results when using PCR for HIV diagnosis.

Question 13: How is HIV genetic variation explained and what challenges does it present?

HIV is reported to have extremely high genetic variability, with differences between strains reaching up to 30-40%. Some researchers even report finding millions of genetically distinct variants in a single patient. This variability is often attributed to HIV's high mutation rate and rapid replication.

This extreme genetic variation presents several challenges:

1. It complicates the development of effective vaccines and treatments.

2. It raises questions about how such diverse variants can maintain similar biological properties and pathogenicity.

3. It makes it difficult to define a standard HIV genome or to use genetic sequences as a reliable diagnostic tool.

4. It challenges the concept of HIV as a single, unique viral entity.

Critics argue that this level of variation is incompatible with the idea of a single virus species and suggest that the observed genetic sequences may have non-viral origins.

Question 14: What evidence supports or challenges the sexual transmission theory of HIV/AIDS?

The sexual transmission theory of HIV/AIDS is primarily supported by epidemiological studies showing associations between certain sexual practices and HIV antibody positivity or AIDS diagnosis. However, these studies have also revealed some challenging findings:

1. Only receptive anal intercourse is consistently associated with HIV positivity and AIDS, not other forms of sexual contact.

2. The risk is not bidirectional, as would be expected for a sexually transmitted agent.

3. The efficiency of heterosexual transmission is extremely low.

Critics argue that these findings are more consistent with AIDS being sexually acquired (like pregnancy) rather than sexually transmitted. They propose that factors in semen, possibly combined with the physiological characteristics of anal intercourse, may be responsible for the observed associations, rather than a viral agent.

Question 15: Who are the key figures in HIV/AIDS research and what are their main contributions or criticisms?

Key figures in HIV/AIDS research include:

1. Luc Montagnier and Françoise Barré-Sinoussi: Claimed discovery of HIV (initially called LAV) in 1983. Awarded Nobel Prize in 2008.

2. Robert Gallo: Claimed independent discovery of HIV (called HTLV-III) in 1984. Developed the first HIV antibody test.

3. Eleni Papadopulos-Eleopulos and the Perth Group: Proposed alternative theories of AIDS causation and criticized HIV isolation methods.

4. Kary Mullis: Inventor of PCR, criticized its use in HIV diagnosis.

5. Peter Duesberg: Molecular biologist who questioned the HIV-AIDS hypothesis.

Montagnier and Gallo are credited with discovering HIV, but their work has been criticized for lacking proper controls and not demonstrating true isolation of a new retrovirus. The Perth Group has challenged the existence of HIV and proposed alternative explanations for AIDS, focusing on oxidative stress and cellular factors.

Question 16: What alternative theories have been proposed for the cause of AIDS?

Several alternative theories have been proposed for the cause of AIDS:

1. Oxidative Stress Theory: Proposed by Eleni Papadopulos-Eleopulos, this theory suggests that AIDS is caused by an accumulation of oxidative stress, particularly affecting the immune system. It posits that various AIDS risk factors contribute to this oxidative stress.

2. Multifactorial Theory: Some researchers, including Joseph Sonnabend, initially proposed that AIDS resulted from a combination of factors including repeated infections, drug use, and other stressors on the immune system.

3. Semen Exposure Theory: This theory, related to the oxidative stress theory, suggests that repeated exposure to semen, particularly through anal intercourse, may be a key factor in AIDS development.

4. Drug-Induced Theory: Some researchers have proposed that recreational drug use, particularly the use of poppers (nitrite inhalants) in the gay community, could be responsible for the immune suppression seen in AIDS.

These theories generally view AIDS as a result of multiple factors rather than a single infectious agent.

Question 17: What are the main critiques of mainstream HIV/AIDS science?

The main critiques of mainstream HIV/AIDS science include:

1. Lack of proper isolation and purification of HIV particles.

2. Reliance on non-specific markers (like reverse transcriptase activity) as proof of viral presence.

3. Failure to fulfill Koch's postulates or their modern equivalents for proving disease causation.

4. Inconsistencies in the sexual transmission hypothesis.

5. Lack of correlation between "viral load" and CD4 cell counts with clinical outcomes in some studies.

6. Problems with the specificity and interpretation of HIV antibody tests.

7. Extreme genetic variability of HIV challenging the concept of a unique viral entity.

8. Failure to explain why HIV would selectively kill T4 cells.

9. Overreliance on surrogate markers (CD4 count, viral load) rather than clinical outcomes in drug trials.

10. Circular logic in defining AIDS cases based on HIV positivity.

Critics argue that these issues undermine the fundamental tenets of the HIV/AIDS hypothesis.

Question 18: How have AIDS statistics and mortality trends changed over time?

AIDS statistics and mortality trends have changed significantly since the beginning of the epidemic:

1. Initial phase (early 1980s): Rapid increase in cases, primarily among gay men, with high mortality rates.

2. Mid-1980s to early 1990s: Expansion of AIDS definition led to increased case numbers.

3. Mid-1990s: Peak in AIDS deaths in many developed countries.

4. Late 1990s onward: Decline in AIDS deaths, often attributed to the introduction of HAART.

However, interpretation of these trends is complicated by several factors:

1. Changes in AIDS case definitions over time.

2. Introduction of HIV antibody testing and its inclusion in case definitions.

3. Expansion of AIDS-defining illnesses.

4. Changes in treatment approaches.

Critics argue that some of the observed trends, particularly the decline in deaths starting in the mid-1990s, began before the introduction of HAART and may be due to factors other than antiretroviral treatment.

Question 19: What role has electron microscopy played in HIV research and what controversies surround it?

Electron microscopy (EM) has played a crucial role in HIV research, particularly in attempts to visualize and characterize the virus particles. However, it has also been a source of controversy:

1. Early research: Montagnier and Gallo used EM to claim the presence of retrovirus-like particles in cell cultures. However, they did not publish EM images of purified virus particles.

2. Particle morphology: There have been inconsistencies in the reported morphology of HIV particles, with different researchers classifying them as belonging to different retroviral subfamilies.

3. Lack of particle purification: Critics argue that no researcher has published EM images of purified HIV particles from patient samples, despite claims of high viral loads.

4. Microvesicles: EM studies in the late 1990s revealed that preparations thought to be "purified HIV" contained many cellular microvesicles, complicating the interpretation of earlier research.

5. Particle count discrepancies: Some EM studies have reported numbers and sizes of particles inconsistent with claims about viral loads and particle characteristics.

These controversies have led some researchers to question whether the particles identified as HIV have been properly characterized and whether they represent a unique viral entity.

Question 20: What are HIV proteins and how are they used in Western blot tests?

HIV proteins are molecules claimed to be components of the HIV particle or produced by HIV-infected cells. Key proteins include p24 (considered a core protein), gp41 and gp120 (envelope proteins), and enzymes like reverse transcriptase (p66/p51).

In Western blot tests, these proteins are separated by size using gel electrophoresis and transferred to a membrane. Patient serum is then added, and if antibodies in the serum react with specific HIV proteins, they form visible bands on the membrane.

Controversies surrounding HIV proteins and Western blots include:

1. The origin of these proteins (viral vs cellular) has been questioned.

2. Different countries and institutions use different criteria for interpreting which protein bands constitute a positive test.

3. Some of these proteins, particularly p24, have been found to react with antibodies in people not considered at risk for HIV.

4. The specificity of these protein-antibody reactions for diagnosing HIV infection has been challenged.

Critics argue that without proper isolation and characterization of HIV, it's impossible to definitively state that these proteins are viral in origin or that antibody reactions to them prove HIV infection.

Question 21: What is reverse transcriptase and why is its specificity important in HIV research?

Reverse transcriptase (RT) is an enzyme that transcribes RNA into DNA, a process reverse to the usual flow of genetic information. In HIV research, detection of RT activity was initially used as evidence of retrovirus presence.

However, the specificity of RT is crucial and controversial in HIV research for several reasons:

1. RT activity is not specific to retroviruses. It has been found in uninfected cells and other organisms.

2. The artificial template-primer (An.dT) used to detect RT activity can also be transcribed by cellular DNA polymerases.

3. RT activity was used as a surrogate for virus isolation, despite its lack of specificity.

Critics argue that the reliance on RT activity as proof of HIV's presence or replication is flawed due to these specificity issues, potentially leading to misinterpretation of experimental results.

HPV Vaccine - Lies are Unbekoming (substack.com)

Here is Scheff in Official Stories going into more detail:

DNA copies out, never in. That was the Central Dogma. And of course, it was wrong.

By the early 1970s, researchers in the U.S. and Japan realized that RNA copied into DNA. Because this upset the Central Dogma, it had to be considered an aberrant act. They couldn’t say, “The Central Dogma is wrong and DNA is rather fluid. It copies in, it copies out. In, out. Normal.”

Instead they said, “That can't be, because Watson and Crick said so, so let's say that what's happening is dangerous. In fact, let's say that whenever RNA copies into DNA, it is a virus.”

And that's what they did. When DNA copies out to RNA, it uses magical little enzymes to do the “transcribing.” Those are called “transcriptase.” When the reverse happens and RNA copied into DNA, it would be…right. “Reverse transcriptase.” Or, “RT,” as we shall call it from now on.

In Reverse

It was understood through testing a large variety of living creatures, even at that time, that “RT” occurred everywhere. In mice, frogs, dogs, newts, bugs, birds; in every animal anyone could think of. In pregnant women, in the placenta. In fact, “RT” was entirely normal. It did not belong to a special “virus” that copied into DNA, because copying into DNA is, in fact, normal.

But the virus-hunters, looking for a new kind of virus to blame for cancers, had found their dog. And “RT,” a common, even ubiquitous enzyme process, would now stand in for a new kind of “virus.” One that goes backward - in reverse. A “retro” virus. And that's what virology would become. A hunt for a non-specific enzyme.

Again, reverse transcriptase, “RT,” was discovered and was considered to be universal to all animals. But it was also decided by one group of researchers to be all they needed to claim they'd found a “virus that causes cancer.”

Tiny Bubbles

One more mildly technical note before we get back to history.

Researchers did find little budding particles under their electron microscopes and these often accompanied “RT.” But they didn't do anything. Like “RT,” they occurred in healthy and sick cells, in cells from placentas, from pregnant women and then, well, everywhere else too. Researchers found that by taking a bunch of cancer cells - which grow quickly and can be made to grow in glass dishes in labs - and stimulating these with chemicals that force cell division, they could get them to produce spikes of “RT,” and also to “bud” out little squishy protein balls, sometimes with a little bit of RNA in them and sometimes not.

These little balloons of various sizes, which could be stimulated into production by kicking cells with chemicals, were considered to be the variety of “retroviruses.”

It took a lot of work to siphon off liquid from these cancer cells, spin it in a test tube, separate the materials by weight and then try to photograph them. Most of the time, all you got was a mess of cellular debris - broken vesicles and microtubules - the trucks and highways of cells, all cracked and piled up in a microscopic jumble. Nothing particular could be seen.

One thing that could be said for certain was that everything that was being seen under these new, powerful electron microscopes was normal. But the Ph.D.s doing the work had a virus fever. They wanted, desperately, to find a new bug to do what polio had done for their predecessors. It had made millionaires out of lab jockeys. So, “RT” became synonymous with “retrovirus.” Even though they knew it wasn't.

Question 22: What are the main risk factors and co-factors associated with AIDS?

The main risk factors and co-factors associated with AIDS include:

1. Receptive anal intercourse, particularly with multiple partners

2. Intravenous drug use

3. Blood transfusions (especially in the early years of the epidemic)

4. Exposure to oxidizing agents (e.g., poppers, recreational drugs)

5. Repeated infections and antibiotic use

6. Malnutrition

7. Stress and other factors affecting immune function

While mainstream AIDS research focuses on these as risk factors for HIV transmission, alternative theories view them as direct contributors to immune dysfunction and oxidative stress that could lead to AIDS without the involvement of a specific virus.

Question 23: How has HIV/AIDS been understood and approached in Africa?

HIV/AIDS in Africa has been a subject of significant concern and controversy:

1. High reported prevalence: Many African countries report high HIV prevalence rates based on antibody tests.

2. Heterosexual transmission: Unlike in Western countries, heterosexual transmission is reported as the primary mode of HIV spread in Africa.

3. Definition issues: The "Bangui definition" allowed AIDS diagnosis in Africa without HIV testing, based on clinical symptoms alone.

4. Alternative explanations: Some researchers argue that positive HIV test results in Africa may be due to cross-reacting antibodies from other infections common in the region.

5. Impact of poverty: The role of poverty, malnutrition, and lack of sanitation in producing AIDS-like symptoms has been debated.

Critics argue that the approach to HIV/AIDS in Africa has often overlooked local health conditions and socioeconomic factors, potentially leading to misdiagnosis and misdirected resources.

Once upon a time in Africa: An AIDS Story (substack.com)

Question 24: What was AZT and how did early antiretroviral treatments evolve?

AZT (Azidothymidine, also known as Zidovudine) was the first drug approved for treating AIDS. Key points about AZT and early treatments include:

1. AZT was initially developed as a cancer drug but was repurposed for AIDS treatment.

2. It was approved in 1987 based on short-term trials showing increased T4 cell counts.

3. Early use involved high doses, leading to significant toxicity.

4. Critics argued that AZT's toxicity could itself cause AIDS-like symptoms.

5. Subsequent antiretroviral drugs were developed, leading to combination therapies.

The evolution of antiretroviral treatment culminated in HAART (Highly Active Antiretroviral Therapy) in 1996, which combined multiple drugs to target different aspects of HIV's alleged life cycle.

AIDS v2.0 - Lies are Unbekoming (substack.com)

Question 25: What is the cellular redox theory and how does it relate to AIDS?

The cellular redox theory, proposed by Eleni Papadopulos-Eleopulos, suggests that the balance between oxidation and reduction in cells is crucial for cellular function and health. In relation to AIDS:

1. It proposes that AIDS results from chronic oxidative stress, particularly affecting the immune system.

2. Risk factors for AIDS (e.g., recreational drugs, repeated infections) are seen as contributors to oxidative stress.

3. The theory explains why only certain sexual practices (receptive anal intercourse) are consistently associated with AIDS.

4. It suggests that treatments should focus on restoring redox balance rather than targeting a specific virus.

5. This theory is used to explain the observed oxidation in AIDS patients and those at risk.

Proponents argue that this theory better explains the epidemiology and pathogenesis of AIDS than the HIV hypothesis.

Question 26: How does RNA editing factor into discussions about HIV and genomic changes?

RNA editing is a process where RNA sequences are modified after transcription. In HIV/AIDS discussions:

1. It's suggested as a possible explanation for the extreme genetic variability observed in "HIV."

2. Some researchers propose that novel RNAs could arise without the involvement of exogenous infectious agents.

3. The phenomenon of RNA editing challenges the assumption that all RNA in a cell must have a corresponding DNA sequence.

4. It's argued that oxidative stress, a factor in AIDS according to some theories, can induce RNA editing.

5. This concept is used to question whether the genetic material attributed to HIV might actually be the result of cellular processes rather than a unique exogenous virus.

The implications of RNA editing complicate the interpretation of genetic data in HIV research and challenge some fundamental assumptions about viral genetics.

Question 27: How have AIDS definitions and surveillance methods changed over time?

AIDS definitions and surveillance methods have undergone significant changes:

1. 1982: Initial CDC definition focused on opportunistic infections in young, previously healthy individuals.

2. 1985: Expanded to include more diseases and HIV antibody testing.

3. 1987: Further expansion of indicator diseases, allowance for presumptive diagnoses.

4. 1993: Addition of CD4 cell count criterion (<200 cells/mm3) regardless of symptoms.

Surveillance methods evolved from active case finding to include laboratory reporting of positive HIV tests and low CD4 counts. These changes have been criticized for potentially inflating case numbers and complicating trend analysis. Critics argue that the evolving definitions make it difficult to compare AIDS statistics over time or between regions.

Question 28: What is the Multicenter AIDS Cohort Study (MACS) and what are its key findings?

The Multicenter AIDS Cohort Study (MACS) is a long-term study of HIV infection in men who have sex with men, begun in 1984. Key findings include:

1. Only receptive anal intercourse was consistently associated with HIV seroconversion.

2. The number of sexual partners was less important than the frequency of receptive anal intercourse.

3. Immune suppression and activation were observed to precede HIV infection in some cases.

4. The study provided data on the natural history of HIV infection and AIDS progression.

Critics argue that some MACS findings, particularly those related to sexual transmission, challenge the concept of HIV as a conventionally sexually transmitted agent and suggest alternative explanations for AIDS causation.

Question 29: Where have HIV genetic sequences been found outside of AIDS contexts?

HIV genetic sequences have been reported in various unexpected contexts:

1. In patients with breast, genital tract, and prostate cancers.

2. In the genomes of various organisms, including plants, insects, and bacteria.

3. In environmental samples from soil, water, and coral reefs.

4. In the published genome of James Watson, co-discoverer of DNA structure.

5. In patients with diseases unrelated to AIDS, such as lupus and lymphoma.

These findings raise questions about the specificity of HIV genetic sequences and their origin. Some researchers suggest these could be due to contamination or the use of lentiviral vectors in research, while others argue they indicate that these sequences may not be unique to a specific virus.

Question 30: What critiques have been made regarding the specificity of HIV antibody tests?

Critiques of HIV antibody test specificity include:

1. Lack of a gold standard: HIV isolation/purification has not been used to validate the tests.

2. Cross-reactivity: HIV antibodies react with non-HIV proteins, and non-HIV antibodies react with "HIV" proteins.

3. Geographical variability: Different criteria for positive results are used in different regions.

4. Presence in low-risk groups: "HIV" antibodies have been found in individuals not considered at risk for AIDS.

5. Autoantibodies: AIDS patients and those at risk have elevated levels of autoantibodies that may cause false positives.

Critics argue that these issues make it impossible to claim that a positive antibody test proves HIV infection or to use these tests to accurately diagnose or monitor HIV/AIDS.

Question 31: What role has the CDC played in AIDS research and defining the disease?

The Centers for Disease Control and Prevention (CDC) has played a crucial role in AIDS research and definition:

1. Early recognition: The CDC first reported the unusual cluster of PCP and KS cases in 1981.

2. Case definition: The CDC established and repeatedly revised the official AIDS case definition.

3. Surveillance: They implemented nationwide AIDS surveillance systems.

4. Research coordination: The CDC has been central in coordinating and conducting AIDS research.

5. Public health response: They've been instrumental in shaping public health policies related to AIDS.

However, the CDC's role has been criticized by some researchers. Critics argue that the CDC's frequent changes to the AIDS definition have complicated epidemiological analysis and potentially inflated case numbers. Some also contend that the CDC's early focus on specific risk groups may have biased research directions and public perception of the disease.

Question 32: What are the main hypotheses proposed by the Perth Group regarding AIDS?

The Perth Group, led by Eleni Papadopulos-Eleopulos, has proposed several alternative hypotheses regarding AIDS:

1. Oxidative stress theory: AIDS results from an accumulation of oxidative stress, not a specific virus.

2. HIV has not been isolated: They argue that the methods used to "isolate" HIV do not prove the existence of a unique retrovirus.

3. HIV tests are not specific: They contend that HIV antibody tests have not been validated against HIV isolation and are not specific for HIV infection.

4. AIDS is not sexually transmitted: They propose that AIDS is sexually acquired (like pregnancy) but not sexually transmitted.

5. AZT and other antiretrovirals are harmful: They argue these drugs can cause AIDS-defining illnesses.

6. Semen as a causative factor: They suggest repeated exposure to semen, particularly through anal intercourse, may be a key factor in AIDS development.

The Perth Group's hypotheses challenge fundamental aspects of the mainstream HIV/AIDS theory and propose alternative approaches to understanding and addressing AIDS.

Question 33: What debates have occurred regarding the validity and meaning of HIV tests?

Debates about HIV tests have centered on several key issues:

1. Lack of a gold standard: Critics argue that HIV tests have never been validated against purified, isolated HIV.

2. Antibody cross-reactivity: There's debate about whether the antibodies detected are specific to HIV or may be reacting to other proteins.

3. Interpretation criteria: The criteria for a positive Western blot have changed over time and vary between countries and organizations.

4. Significance of positive results: There's disagreement about whether a positive test indicates active infection, past exposure, or neither.

5. PCR and viral load tests: The specificity and clinical significance of these tests have been questioned.

6. Window period: The concept of a period between infection and antibody detection has been debated.

7. Correlation with clinical outcomes: Some studies have shown poor correlation between test results and clinical progression to AIDS.

These debates raise questions about the reliability of HIV testing for diagnosis, screening, and monitoring of AIDS.

Question 34: How have HIV isolation methods been criticized?

Criticisms of HIV isolation methods include:

1. Lack of purification: Critics argue that no one has published electron micrographs of purified HIV particles from patient samples.

2. Reliance on surrogate markers: The use of reverse transcriptase activity and protein-antibody reactions as proof of viral isolation is questioned.

3. Contamination with cellular material: "Purified virus" preparations have been shown to contain substantial amounts of cellular debris.

4. Failure to fulfill standard isolation criteria: Critics argue that HIV has not been isolated according to traditional virological standards.

5. Inconsistent particle morphology: The reported morphology of HIV particles has varied between researchers and over time.

6. Lack of control experiments: Many isolation experiments lacked proper controls to rule out non-viral explanations for observed phenomena.

7. Circular logic: Some argue that the methods used to "isolate" HIV assume its existence rather than proving it.

These criticisms challenge the fundamental claim that HIV has been properly isolated and characterized as a unique retrovirus.

Question 35: What is the significance of T4 cell counts in HIV/AIDS research and diagnosis?

T4 (CD4) cell counts have been central to HIV/AIDS research and diagnosis:

1. Diagnostic criterion: A CD4 count below 200 cells/mm³ is an AIDS-defining condition, regardless of clinical symptoms.

2. Disease progression marker: Declining CD4 counts are used to monitor disease progression.

3. Treatment initiation guide: CD4 counts have been used to determine when to start antiretroviral therapy.

4. Immune function indicator: They're considered a measure of immune system health in HIV patients.

5. Research tool: CD4 counts are widely used in HIV/AIDS studies as an outcome measure.

However, the reliance on CD4 counts has been criticized:

1. Lack of specificity: Low CD4 counts can occur in various conditions unrelated to HIV.

2. Poor correlation with clinical outcomes: Some studies show discrepancies between CD4 counts and patient health.

3. Natural variability: CD4 counts can fluctuate significantly in individuals over time and due to various factors.

4. Oversimplification: Critics argue that focusing on CD4 counts oversimplifies complex immune system dynamics.

The debate around CD4 counts reflects broader questions about the mechanisms of immune dysfunction in AIDS and the validity of surrogate markers in HIV/AIDS research and treatment.

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