What is Human Immunodeficiency Virus?
The most basic question: what is HIV, is not an easy one to answer. Depending on what country you are in and who you are talking to the answer varies. The best I can do is summarise some of these and then conclude with my own opinion.
The International Committee on Taxonomy of Viruses lists only Human Immunodeficiency Virus-1 as a species of the family Retroviridae, genus Lentivirus.(1) Elsewhere, scientists talk about 3 HIV species, and 17 different “clades”(2) and then there are enumerable “isolates”, including 106 genetically distinct variants in an asymptomatic AIDS patient(3) and more than 108 in a symptomatic one.(4)
Mainstream science holds that HIV is transmitted in the exchange of blood and sexual secretions, and kills T4 cells. The relative absence of these cells then leads to a breakdown of the immune system or Acquired Immunodeficiency Syndrome (AIDS) which occurs anytime from an average five years after infection to 10 years or longer leaving the hapless host open to disease, even diseases which have nothing to do with the immune system, such as malaria and dementia.
The description leaves several bizarre anomalies, most of them pinpointed by arch sceptic of the HIV cause of AIDS Professor Peter Duesberg who has called HIV the original sin of virology. Paramount among these anomalies, is that HIV was reported to replicate without cytocidal effects, by the very person who proposed it was cytocidal:
“In 1984, in Science, [Robert] Gallo said HIV kills T-cells and that is the cause of AIDS. Also in 1984, in May, he signed under oath to the U.S. Patent Office that this same virus can be produced in permanently growing human T-cells. And these T-cells are still growing in his laboratory, in dozens of companies on this planet, enough to conduct at least 25 million tests per year in this country alone, over 20 million in Russia, millions all over the world. These T-cells have yet to die.”(5)
In the mid-1980s, Duesberg was professor of molecular biology at the University of California-Berkeley, a rising scientific star and leading world expert on retroviruses, a field in which he was a pioneer. He was the National Institutes of Health (NIH) Outstanding Investigator with a $350,000 grant. Then in 1987 he published a paper “Retroviruses as Pathogens: Expectations and Reality“(6) in which he argued that there was no evidence to suggest that retroviruses were anything other than harmless, benign “passengers” of the human genome, where they constituted about 1% or so of the genetic material from our evolutionary history. The Abstract of his follow-up paper in 1989 “Human Immunodeficiency virus and acquired immunodeficiency syndrome: Correlation but not causation”(7) remains the most succinct statement on the paradoxical nature of the HIV-causes-AIDS hypothesis, including the conclusion that Koch’s postulates for the isolation of infectious microbes had not been fulfilled.
The National Institute of Allergy and Infectious Disease/NIH Fact Sheet “The Evidence that HIV causes AIDS” disagrees.(8) While it contains no references for the isolation of HIV, it does claim that Koch’s Postulates have been fulfilled. Unfortunately none of the references supplied demonstrate this. The fact is Koch’s postulates have been variously interpreted by scientists, and modifications have been suggested to accommodate new technologies, particularly with regard to viruses. In the process what exactly constitutes “isolation” becomes a semantic debate over the meaning of “isolation”. When it comes to HIV, the word has different meanings for different people. But in terms of Koch’s postulates, HIV has not been isolated. The four postulates were developed by 19th century bacteriologist Robert Koch to prove a microbe causes a disease:
1. The organism must be present in all cases of the disease; 2. It must be grown and then isolated in pure culture from the cells of individuals with the disease; 3. It must reproduce the disease when introduced into a susceptible host or experimental animals; 4. It must be recovered from said host or experimental animal.
The problem with Koch’s postulates is which virus has been isolated according to these four criteria? As far as I have been able to find out the answer could be none!
The NIAID/NIH fact sheet cites studies that used unpurified cultures or biologic fluids that contained “HIV sequences” as well as other undefined material. No study cited used “a pure isolate of HIV” and therefore cannot be considered as presenting scientific evidence. Some references refer to “cloned HIV in the laboratory”, but a close reading reveals that a pure isolate was not used, so what ever was cloned was propagated along with other undefined agents. There is reference to SIV/SHIVs isolated from chimpanzees with AIDS which caused AIDS when transmitted to uninfected animals. Again a close reading of the study reveals that the virus was not “isolated” from chimpanzees with AIDS. Unpurified supernatants were tested for RT activity. This is detection not isolation. Similarly unpurified and undefined biologic fluids tested for p24 reactivity is not isolation.
Notably absent from the NIAID/NIH Fact Sheet is any reference to the 1983 paper by Professor Luc Montagnier and colleagues at the Pasteur Institute of Paris published in Science, “Isolation of a T-Lymphotrophic Retrovirus from a patient at Risk for Acquired Immune Deficiency Syndrome (AIDS)”(9). Also absent is reference to the four papers by Dr Robert Gallo’s laboratory at the NIH published in Science in May 1984 in which they also claimed isolation of what they called Human T-Lymphotrophic Retrovirus (HTLV-111) in AIDS patients.(10-13) On the 23rd of April 1984, at a Washington press conference held two weeks before the papers were published, Margaret Heckler, then Secretary for Health and Human Services, accompanied by Gallo, announced that his NIH team had discovered the “probable” cause of AIDS and had developed a sensitive blood test to detect the virus in the body, so a vaccine was expected within “two years”. Twenty-two years later it has not yet happened which proves just how sensitive the blood test was!
But this was the start of the single virus cause of AIDS, so the omission of references to these papers in the NIAID/NIH Fact Sheet is significant. It is also worth noting that the International Committee of Taxonomy of Viruses no where lists Gallo’s HTLV1, 11 or 111 in its index of viruses!(1)
It would be really nice if some mainstreamer posted a reference to isolation of HIV so that the debate could be put to rest, but the fact is it has not happened, not in the South African Presidential Aids Advisory Panel, nor in the Durban Declaration signed by virtually everyone than is anyone in mainstream HIV/AIDs worldwide which merely stated that the “evidence was exhaustive and incontrovertible”, nor in the numerous websites, web-boards and blogs on the Internet.
Another way of fudging isolation is to argue that it is not necessary in an age of molecular cloning. Duesberg in 1996 played Devil’s Advocate to present the arguments that full-length HIV DNA (that is virus-specific DNA of 9150 nucleotides that cannot be detected in DNA of uninfected cells) recovered from infected cells and then cloned in bacterial plasmids was a far more rigorous standard than isolation. His argument was rebutted by Eleni Papadopulos-Eleopulos et al from the Royal Perth Hospital, University of Western Australia, in a series of four articles published in Continuum.(14), Running to 50-odd pages, there is no finer demonstration of the complexities and shortcomings in HIV science – and why molecular cloning of full length HIV DNA has not been achievable.
The heart of this exchange, as set out by the Perth Group, is that for “HIV DNA” to be the genome of a unique retroviral particle the most basic requirement is proof for the existence of a unique molecular entity “HIV DNA”, that is, unique fragments of DNA identical in both composition and length in all infected individuals. The claim that a stretch of RNA (cDNA) is a unique molecular entity which constitutes the genome of a unique retrovirus can be accepted if and only if it is shown that the RNA belongs to a particle with the morphological, physical and replicative characteristics of a retroviral particle. Proof of these properties can only by obtained by isolating the putative viral particles, that is, by obtaining them separate from everything else, extracting the nucleic acids and demonstrating that such particles are identical (their constituents including their nucleic acids are identical) and infectious.
To quote the Perth Group, the correct procedures for retroviruses require demonstration that:
- 1. In “infected” cell cultures (cocultures) there are particles with a diameter of 100-120nM containing “condensed inner bodies (cores)” and surfaces studded with projections (spikes, knobs); (82)
- 2. In sucrose density gradients the particles band at a density of 1.16 gm/ml
- 3. At the density of 1.16 gm/ml these is nothing else but particles with the morphological characteristics of retroviral particles;
- 4. The particles contain only RNA and not DNA and that the RNA consistently has the same length (number of bases) and composition no matter how many times the experiment is repeated;
- 5. When the particles are introduced into secondary cultures, but mindful of the critical caveat discussed below:
(a) the particles are taken up by the cells;
(b) the entire RNA is reverse transcribed into cDNA;
(c) the entire cDNA is inserted into the cellular DNA
(d) the DNA is transcribed into RNA which is translated into proteins;
- 6. As a result of 5 the cells in the secondary cultures release particles into the culture medium;
- 7. The particles released in the secondary cultures have exactly the same characteristics as the original particles, that is, they must have identical morphology, band at 1.16 gm/ml and contain the same RNA and proteins.
The caveat is that while the introduction of the majority of infectious particles into cell cultures and subsequent release of similar particles is proof that such particles are indeed infectious, this is not the sufficient case for retroviruses. The basis of this exception is the fact that one of the most striking features that distinguishes retroviruses from all other animal viruses is the presence in the chromosomes of normal uninfected cells, of genomes of infectious viruses.
In fact, a cell may contain the genome of many retroviruses. As far back as 1976 retrovirologists recognised that the failure to isolate endogenous viruses from certain species may reflect the limitations of in vitro cocultivation techniques. In other words, the finding of a retrovirus in both the primary and secondary “infected” cultures/cocultures is not proof that the cells have been infected with an exogenous retrovirus.
As things stand, scientists have not been able to agree on the genome of HIV. While there is broad agreement on it being comprised of three protein coding genes – gag, pol and env – these genes are common to all retroviruses, so cannot be considered as HIV specific, even if the nucleotide sequences of these genes were indentical, which they are not. There is also broad agreement that the full-length HIV genome would contain eight genes that encode regulatory proteins. In practice, researchers have shown that the nucleotide sequences of these genes vary. But in mainstream HIV science their expression, role and functioning is dismissed and ill-understood. Instead, when it comes to HIV scientists talk about “homologies” where a 40% variation in nucleotide sequences is still considered “HIV”.
The fact is genome sequencing cannot replace the need to isolate HIV as an entity with defined dimensions, shape and characteristics – together with evidence that is acquired from outside the body through sexual intercourse or parentally – and is not cellular in origin. Alternately, the real test of a virus, is that it can be crystalised and the unique crystal structure defined. Then it would need to be thawed in saline, introduced into a laboratory animal where it must cause the same disease which infected the donor host. This has not been achieved not even with polio, as I understand the science.
As it stands with no satisfactory purification of HIV, markers are used in “HIV” antibody screening assays. Without purification the possibility that the so-called protein “markers” dubbed “HIV” could be of cellular instead of viral origin cannot be ruled out. Claims of successful HIV “isolation” based on the detection of one of the so-called “markers” (like p24, gp160 or Reverse Transcriptase) are, consequently, scientifically unacceptable.
Attempted “purification” of retroviruses by sucrose gradient centrifugation at the density of 1.16 gm/ml is acceptable only if the resulting “band” is analyzed by electron microscopy (thin section method) and shown to contain practically nothing else but similarly looking retroviral particles. This was easily achieved with murine and avian retroviruses in the 1960s. It has never been achieved with so-called HIV.
It has been well known for more than 30 years that material sedimenting in sucrose gradients at the density of 1.16 gm/ml is frequently contaminated by abundant cell debris. Omitting the electron microscope control of such material makes any rigorous interpretation concerning the origin of the proteins, enzymes, and nucleic acids practically impossible.
At the start of the HIV-cause era reverse transcriptase (RT) activity was regarded as unique to HIV. It has now been established that RT is an enzyme found in most cells, so its detection could originate from contaminating cell debris.
Today, AIDS research still suffers from the scientific fallacy of viral “markers” in the absence of viral particles even though it has been clear for over a decade that HIV particles could never be convincingly seen by electron microscopy in tissue biopsies directly obtained from AIDS patients. Instead, particles with the morphological features of retroviruses have been repeatedly observed by electron microscopy, in complex, hyperstimulated mixed-cell cultures, and computer graphic renderings of these images inundate the medical literature and the media.
Polymerase chain reaction (PCR) is now routinely used to quantify “viral load” in HIV+ individuals and/or in AIDS patients. This is being done worldwide, in spite of repeated warnings by the inventor of the PCR methodology, Dr Kary Mullis, that “measuring” viremia is not an acceptable application of the PCR methodology. Roche, the manufacturer of a widely used test to quantify “viral load” warns that it’s test “is not intended as a screening test for HIV or as a diagnostic test to confirm the presence of HIV infection” (15). How then does it justify identifying 142 nucleotide bases of about 1500 that make up the gag gene as specific to HIV? Gag means group-specific antigen – specific to (retro)viruses – and beyond just retroviruses there is ample evidence that antibodies which react with p24 are ubiquitous in both human and animal sera. This can only be interpreted that either the viral protein p24, the antibodies, or both, are non-specific for HIV. Alternatively most humans as well as most animals species are infected with HIV!
As a final word on “viral load” – patients or seropositive individuals with high “viral load” counts should, if the theory is right, have plenty of HIV particles in their peripheral blood, i.e. viremia. Yet, according to the Roche package insert “the usefulness of p24 antigen as a marker for viral load is limited since antigen detection is detectable in only 20% of asymptomatic patients and 40-50% of symptomatic patients”. Most surprisingly, there is not one report in the medical literature establishing a correlation between high “viral load” quantified by PCR of AIDS patients and the observation of HIV particles by electron microscopy.
I have concluded from my investigations that no research team anywhere in the world has been able to identify HIV-specific proteins. Once a virus was proposed as the cause of AIDS, it became urgent to prevent the spread of the virus by the blood supply. In the absence of isolation of HIV and identification of HIV specific proteins, blood-based antibody tests were created. While I entirely support safety, and even an application of the precautionary principle in the absence of scientific certainty, the fact remains that so-called “HIV” tests are based on detecting non-specific antibodies.
The finer detail of this has been eloquently expressed by Vladimir Koliadin.(16) He makes the point that B-lymphocytes of the immune system normally respond to foreign substances (“antigens”) by increased production of special proteins, known as- immunoglobulins and commonly referred to as antibodies. Some immunoglobulins are non-specific – they are capable of binding to a wide range of antigens. Others bind strongly to a defined antigen and not to others. The ability of specific antibodies to bind only to the antigen which induced their production plays a very important role in biomedical science and serological testing. But in the case of so-called “HIV antibodies” they are indeed non-specific – and this is different to cross reactivity.
As Koliadin explains: “Non-specific reactivity should not be confounded with cross-reactivity. Cross-reactivity is a specific phenomenon, well understood in immunology. Even though cross-reacting antigens differ, they share common determinants, and reaction is specific in respect to these determinants. Normally only a small proportion of antigens cross-react to antiserum against a given antigen. In contrast to the cross-reactions, neither mechanisms of production nor properties of non-specific immunoglobulins are understood in modern immunology. Textbooks of immunology either keep silence or say only a few words about their existence. It is also rarely mentioned in the textbooks, that only a part, maximum 20-30%, of the immunoglobulins produced by B-cells in response to an antigen are capable to bind specifically to the antigen; other 70-80% of the immunoglobulins are non-specific.”
As an additional comment, it has been established that the expression of non-specific immunoglobulins increases radically if B-lymphocytes are over-stimulated, and it is proposed that this effect alone which is common in “HIV” in vitro testing processes leads to positive tests. In vivo, it has been proposed that over stimulation of the immune system due to multiple stressors (infectious, environmental, toxic or lifestyle-related) degrades the system leading to chronic disease. Since, at present, there is no way of distinguishing antibodies presently dubbed “HIV” proteins as distinct from antibodies encoded by endogenous retroviruses, the presence of such antibodies could – and does – indicate that the immune system has been activated, without the need for putative “HIV” virus.
I agree with the conclusion there is no scientific basis for the assertion that there are any “true” HIV antibodies. The only gold standard to establish this would be isolation of “HIV” which has not been achieved. The ultimate answer then, to what is HIV – it is a laboratory marker which should have stayed in the laboratory.
As a concluding note, let me add two things: Firstly, there is abundant evidence that so-called “HIV” proteins are cellular, that is endogenous. This is a Pandora’s Box, that HIV believers are not prepared to open due to pressure to conform to the reigning paradigm of single germ cause of disease, but HIV sceptics have opened this box. Just like the mythological counterpart one of the gifts is hope of huge advances in understanding, treating and preventing chronic diseases be it cancer, AIDS, Chronic Fatigue Syndrome, Gulf War Syndrome or multiple sclerosis etc.
Secondly, I need to counter any interpretation that I support the argument that HIV does not exist and is imaginary. In fact, I am inclined to the proposal that HIV-specific genetic fragments may exist on the genome of many people throughout the world as a result of the development of xenogenic therapies for human disease. That is an evolutionary origin in early preparations of vaccines (maybe even ones currently in use) which have been propagated in monkey renal cells. In people who receive(d) these vaccines there may have been a recombinational integration between non-human retroelements and endogenous retroelements, hence fragments dubbed “HIV” such as have been found, are indistinguishable from simian precursors.
In the US, this may have been contaminated hepatitis B vaccine trialled among volunteers in the homosexual community in the late 1970s-early 1980s, and in the Africa and elsewhere polio vaccines contaminated with simian viruses.
- Burke, DS. Recombination in HIV: An Important Viral Evolutionary Strategy. Emerging Infectious Diseases. Vol 3 No 3. July-September 1997. http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm
- Vartian JP, Meyerhans A, Henry M, et al. High-resolution structure of an HIV-1 quasispecies: Identification of novel coding sequences. AIDS 1992;6:1095-1098.
- Wain-Hobson S. Virological mayhem. Nature 1995;373:102.
- Guccione, B. jnr, Interview with Peter Duesberg. Spin September 1993.
- Duesberg PH. (1987). Retroviruses as carcinogens and pathogens: Expectations and reality. Cancer Res. 47:1199-1220.
- Proc. Natl. Acad. Sci. USA, Vol. 86, pp. 755-764, February 1989. http://www.duesberg.com/papers/ch3.html
- Barre-Sinoussie, F et al.”Isolation of a T-Lymphotrophic Retrovirus from a patient at Risk for Acquired Immune Deficiency Syndrome (AIDS)”. 1983. Science 220:869-871.
10. Gallo RC, Sarin PS, Gelmann EP. (1983). Isolation of Human T-Cell Leukemia Virus in Acquired Immune Deficiency Syndrome (AIDS). Science 220:865-867.
11. Popovic M, Sarngadharan MG, Read E, Gallo RC. (1984). Detection, Isolation,and Continuous Production of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and Pre-AIDS. Science 224:497-500.
12. Sarngadharan M, G., Popovic M, Bruch L. (1984). Antibodies Reactive to Human T-Lymphotrophic Retroviruses (HTLV-III) in the Serum of Patients with AIDS. Science 224:506-508.
13. Schupbach J, Popovic M, Gilden RV, Gonda MA, Sarngadharan MG, Gallo RC. (1984). Serological analysis of a Subgroup of Human T-Lymphotrophic Retroviruses (HTLV-III) Associated with AIDS. Science 224:503-505.
14. Continuum. Vol.4 No.3 Sept./Oct. 1996. http://perso.wanadoo.fr/esprit-libre/continuum/continuum.htm
15. Amplicor HIV-1 Monitor Test. Roche Diagnostics Corporation. 1999. US:83088.
16. Koliadin, V. What Causes a Positive Test for HIV-antibodies? April 1998. www.virusmyth.com