필독 궁금남님과 자유인님의 질문에 대한 HEAL Toronto의 상세한 답변

[바라꽃]

Below is some information addressing the questions you asked.

Best regards,

Robert Johnston

HEAL Toronto

website: http://healtoronto.com

email: endaids@hotmail.com

NIAID say, as the evidence that HIV causes AIDS, "HIV fulfills Koch's postulates as the cause of AIDS."

HIV Fails Koch's Postulates.

David Rasnick has specialized in protease inhibitor research for over twenty years, and was past president of the Group for the Scientific Reappraisal of AIDS. He responded to statements posted by the NIH that HIV fulfilled Koch's postulates (NIAID/NIH, 1995). See Dr. Rasnick뭩 review: http://healtoronto.com/durban/koch.html

>
>We think all these three issues are equally important but in particular, NIAID explains article 2 as follows.
>
>"Modern culture techniques have allowed the isolation of HIV in virtually all AIDS patients, as well as in almost all HIV-seropositive individuals with both early- and late-stage disease. In addition, the polymerase chain (PCR) and other sophisticated molecular techniques have enabled researchers to document the presence of HIV genes in virtually all patients with AIDS, as well as in individuals in earlier stages of HIV disease."
>

PERTH GROUP ON JACKSON et al

http://www.virusmyth.com/aids/data/epreplypd.htm

8.2 "For example, Jackson et al. have tested blood cells of 409 antibody-positives including 144 AIDS patients and 265 healthy people. In addition 131 antibody-negatives were tested. HIV- specific DNA subsets-defined in size and sequence by HIV-specific primers (start signals for the selection amplification)-were found in 403 of the 409 antibody-positive, but in none of the 131 antibody negative people (Jackson et al., 1990)".

8.2.1. Apparently, up until 1987 Jackson et al considered the detection of RT (reverse transcription determined by transcription of A(n).dT15 in cultures synonymous with HIV isolation! However, they had an "isolation rate of 57% in patients with acquired immunodeficiency syndrome". By 1988 the "reverse transcriptase assay was replaced with the Abbot Laboratories HIV-1 antigen detection assay", which "primarily detects the p24 core antigen of HIV-1...A culture was considered positive for HIV-1 antigen if two serial supernatant samplings were positive, with the later sampling showing greater activity"! "HIV-1 was isolated from the PBMC of 141 (99.3%) of 142 HIV-1 antibody positive patients".(235) In their 1990 paper Jackson et al reported that "Between February 1987 and October 1988, peripheral blood mononuclear cells (PBMC) from 409 individuals who were antibody positive for HIV-1 by Western (immuno) blot (56 AIDS patients, 88 patients with ARC, and 265 asymptomatic in! dividuals) were cultured". Using a sensitive technique previously described", the p24 assay noted above, they reported that "HIV-1 can be isolated from 100% (56 of 56) of AIDS patients, 99% (87 of 88) of ARC patients, and 98% (259 of 265) HIV- 1 antibody positive asymptomatic individuals". Not one of "131 HIV- 1 antibody-negative individuals has a positive culture". Using the same p24 assay (Abbot) they tested the serum from 403 out of the 409 individuals. The test was positive in 23/56 (42%) AIDS patients, 31/88 (57%) ARC patients and 44/259 (17%) asymptomatic antibody positive individuals. For unstated reason(s) a positive serum test is considered proof for the detection of "HIV-1 antigen in serum" while the same positive culture test is considered proof for "HIV-1 isolation" from the culture. There are many reasons to question the interpretation of the p24 assay: (a) The p24 assay is an antibody/antigen reaction and is subject to ubiquitous background reactivity. In this ! context, even if "two serial supernatant samplings with the later sampling showing greater reactivity", even if double or triple, for example, 30 and 60 or 30 and 90, both readings may be nothing else but background readings. Jackson and colleagues' criteria are not even in agreement with those used by Ho et al which are equally as arbitrary; "A culture was considered positive if the concentration of p24 antigen in the supernatant exceeded 1000pg per milliliter (typical cutoff value approximately 30pg per milliliter) on a single determination or ?200pg per milliliter on two or more determinations".(51) In this regard it is important to note that no amount of experimental variations and technological improvements in the p24 test can,change the underlying nature of the test. The test solely detects antibody/antigen reactivity and the reason underlying such reactivity cannot be determined on the basis of an arbitrary cut off. A priori, there is no reason why conditions leading! to non-specific reactivity should not be present at a sufficient level to drive the reaction above cut off, nor any reason to prevent the reverse, that is, specific reactivity below cut off. The only way to resolve this issue is to compare reactivity with the presence or absence of HIV as determined by virus isolation. To date, this has not been reported. Even without a gold standard, the non-specificity of the p24 antigen test is so obvious that it is accepted by no less an authority on HIV testing than Philip Mortimer and his colleagues from the UK Public Health Laboratory Service, "Experience has shown that neither HIV culture nor tests for p24 antigen are of much value in diagnostic testing. They may be insensitive and/or non-specific".(236) The fact that in experiments with "serial dilution studies of culture supernatants" the p24 test is more likely to be positive than RT is not proof that the p24 test is "at least 100-fold more sensitive that reverse transcriptase as! says". Sensitivity for HIV can only be measured by the use of HIV isolation as a gold standard;(237) (b) There are no scientific reasons and indeed no commonsense reasons why reactions such as reverse transcription or antibody/antigen reactions, even if specific for retroviruses, can be considered proof for viral isolation. If these phenomena are considered proof for virus isolation then both the pregnancy test, (measurement of the protein ?CG in blood or urine using antibodies), or estimation of cardiac enzymes in suspected myocardial infarction, must also be considered proof for "isolation" of placenta or heart respectively.

8.2.2 To improve on the p24 assay, the DNA extracted from frozen uncultured PBMC of their seven "antibody-positive culture negative subjects" and "23 healthy heterosexual HIV-1 antibody negative, culture negative individuals" was assayed by PCR. In addition, "In order to compare the sensitivity and specificity" of the two tests, PCR and culture, the PBMC of 59 seropositive and 20 seronegative individuals were analysed by both tests. "Amplifications of HIV-1 were performed by using a primer pair, SK38-39, which amplifies a 115-base-pair conserved region of the gag gene (nucleotides 1551 to 1665 of HIV SF23: GenBank accession no. K02007). The amplified product was detected by oligomer hybridization, a technique in which a 32p-end-labeled probe (SK19) to the nucleotide 1595 to 1635 gag region hybridizes in solution to one strand of the amplified sequence. The probe-target duplex was then resolved by electrophoresis on a 10% polyacrylamide gel and autoradiographed". None ! of the seronegative individuals was reported to have a positive PCR test. "All initial DNA samples from the 7 HIV-1 antibody-positive, culture-negative patients" were reported positive. When the PCR and culture tests were compared, 57 of the 59 patients had a positive PCR and 57 of the 59 patients had a positive culture. The 2 PCR negative individuals had positive cultures and the two culture negative individuals had a positive PCR. The authors concluded, "We isolated HIV-1 or detected HIV-1 DNA sequences from the PBMC of all 409 HIV-1 antibody-positive individuals. None of 131 HIV-1 antibody-negative individuals were HIV-1 culture positive, nor were HIV-1 DNA sequences detected by PCR in the blood specimens of 43 seronegative individuals. In addition, HIV-1 PCR and HIV-1 culture were compared in testing the PBMC of 59 HIV-1 antibody positive and 20 HIV-1 antibody negative hemophiliacs. Both methods were found to have sensitivities and specificities of at least 97 and 100% r! espectively...Our ability to directly demonstrate HIV-1 infection in all HIV-1 antibody-positive individuals provides definite support that HIV-1 antibody positivity is associated with present HIV-1 infection".(52) In other words, Jackson et al used the antibody tests as a gold standard for both the culture and PCR tests and the PCR and culture tests as a gold standard for the antibody test.

Jackson et al's claims are not even confirmed by other laboratories. According to Jackson et al, up until 1990 only three small studies reported "100% isolation rates of HIV-1 from AIDS patients". In all the other studies, "HIV-1 was not isolated from 6 to 50% of HIV-1 seropositive AIDS cases reported. The culture recovery rate of HIV-1 from HIV-1 antibody positive asymptomatic patients has generally been even lower, only 20 to 42% in some studies". The most recent situation is best illustrated by a large WHO study published in 1994. Between 1992-93, 224 specimens were collected in Brazil, Rwanda, Thailand and Uganda from asymptomatic "HIV positive" individuals. Serostatus was first confirmed in the country of origin and then at the "centralized laboratories responsible for confirm‎ing serology, virus isolation, virus expression‎, and distribution of reagents (George-Speyer-Hans Chemotherapentisches Forschunginstitut (GSH) in Frankfurt, Germany; National Institute for Biolo! gical Standards and Control (NIBSC) in London, United Kingdom,; and DAIDS/NIAID in Bethesda, Maryland, United States". Using the method of Jackson et al, "of a total of 224 virus cultures, 83 were positive (Isolation rate=37%)".(238) Jackson et al's PCR results, like their culture results, are not reproducible in other laboratories. For example, in the study conducted by Defer and her colleagues, where the same samples were tested in "Seven French laboratories with extensive experience in PCR detection of HIV DNA", the data revealed that of 138 samples shown to contain "HIV DNA", 34 (25%) did not contain "HIV antibodies" while of 262 specimens that did not contain "HIV DNA", 17 (6%) did contain "HIV antibodies".197 In a paper published in 1994 by researchers from The Laboratory of Molecular Retrovirology Georgetown University, Chiron Corporation California, Retrovirology Section, US National Institutes of Health, Maryland, the authors noted that the PCR techniques are "excee! dingly labor intensive and suffer from laboratory-to-laboratory variation due to differences in technique and operations" and that "in some reported studies there is no correlation between p24 antigen levels and measurements of infectious virions. Similarly, a decrease in p24 antigen level is not necessarily associated with a positive clinical outcome". Because of this, to "Monitor Human Immunodeficiency Virus Type 1 Burden in Human Plasma", the authors used "the branched DNA signal amplification assay" which, "offers improved sensitivity" and compared it with the "two other standard assays for viral burden; end-point dilution plasma culture and immune complex-dissociated (ICD) serum p24 antigen". They reported that "HIV-1 DNA and ICD serum p24 antigen assays were done on serum samples from 102 seropositive (Western blot-confirmed) patients who were being screened for enrollment in clinical trials...of the 102 patients, 75 (74%) were positive for HIV RNA by the bDNA assay an! d 61 (60%) were positive by the ICD p24 assay. Only a subset of patients (n=56: CD4 cell range, 29-394; median 160) was tested for plasma viremia by viral culture; 34 (61%) were culture-positive, while 50 (89%) were positive by bDNA assay and 39 (70%) were positive by the ICD p24 assay".(239) How is it then possible to claim that "virtually all people who contain HIV DNA also contain antibodies against Montagnier's HIV strain" and "most, but certainly not all people who lack HIV DNA contain no such antibodies"?

CONCLUSION AND COMMENTS

Since Jackson et al did not test all 409 patients and all 131 antibody negative individuals for the presence of "HIV DNA" using PCR, but tested only 66 patients and a maximum of 43 "antibody- negative" individuals; did not sequence the amplified segments and did not determine the specificity of the PCR by using the only valid gold standard, HIV isolation, it was not possible for them to report "HIV specific DNA subsets...in 403 of the 409 antibody- positive, but none of the 131 antibody-negative people". Furthermore, Jackson et al acknowledged that their PCR method did not prove the existence of the full-length HIV genome but only "that AIDS patients as well as HIV-1 antibody-positive asymptomatic individuals harbor HIV-1 genetic material". In addition, for their PCR determinations, Jackson et al used a small fragment of the gag gene as a primer. But: (a) since the best known HIV experts agree that the gag genes of retroviruses are homologous, Jackson et al's negative PCR! results in all 43 "antibody-negative" individuals who must at least have had the retrovirus present "in all of us", remains unexplained; (b) finding a positive PCR result using a small fragment of the gag gene as primer is not proof for the existence of the "full-length HIV genome" or even for the existence of the "full-length HIV gag gene". As has been already mentioned, by 1989 researchers at the Pasteur Institute concluded that "the task of defining HIV infection in molecular terms will be difficult". In fact, as far back as 1973, retrovirologists were aware that the unusual nature of retroviruses "will prove a stumbling block to any genetic analysis of RNA tumor viruses".(240) Yet, at least some HIV experts, including Jackson et al insist on defining HIV infection in genetic terms. On the other hand, an analysis of the presently available data on retroviruses shows that all retrovirologists seem to agree that the single most decisive factor in proving the existence of a! unique retrovirus is the existence of specific antibodies, its importance well illustrated by the history of the discovery and subsequent demise of HL23V (see 5.4). As far as HIV is concerned, it is well known that the only evidence considered to prove the HIV theory of AIDS is a correlation between the clinical syndrome and a positive antibody test. Less well known is the fact that in the four papers published in Science in May 1984, Gallo and his colleagues claimed that in contradistinction to Montagnier and his colleagues, he and his colleagues achieved "true isolation". However, it is of pivotal significance that the only difference between the experiments performed by the two groups is that Gallo's group employed a leukaemic cell line from which they were able to obtain abundant "HIV antigens" and thus could perform significantly more antibody tests. Given the crucial status retrovirologists accord to specific antibodies proving the existence of a unique retrovirus, an! d its role in pathogenicity, proof of antibody specificity would appear to be mandatory. The specificity of the HIV antibody tests can be determined only by the use of HIV isolation as a gold standard. To date this has not been done and at present would seem impossible because nobody has fulfilled even the first step in the only scientifically valid method for retroviral isolation, that is, electron microscopic demonstration of particles with the morphological characteristics of retroviruses banding in sucrose density gradients at the density of 1.16 gm/ml. In addition, "HIV" can only be "isolated" from a minority of individuals who has a positive antibody test.

Furthermore, as in the case of HL23V, there is evidence that antibodies present in human sera which react with "HIV proteins" are also non-specific: (a) "One half of the molecular weight of gp120 is represented by oligomannosidic oligosaccharides...Polyclonal antibodies to mannan from yeast also recognize the carbohydrate structure of gp120 of the AIDS virus";(241) (b) "The immunochemical determinants of the antigenic factors of Candida albicans display a high identity with the glycoprotein (gp) 120 of HIV-1: they contain ?12) and ?13) linked mannose terminal residues";(242) (c) antibodies to the mannans of Candida albicans "block infection of H9 cells by HIV-1" as well as the binding of lectins to gp120;(242) (d) recognition of gp120 by antibodies to a synthetic peptide of the same antigen was "partially abolished if it was absorbed with the total polysaccharide fraction of C. albicans" while the antigen recognition by antibodies to "gp120 from human T cell lymphotropi! c virus type IIIB", "was totally blocked". From these data the authors concluded: "These results indicate that mannan residues of C. albicans can serve as antigens to raise neutralizing antibodies against HIV infection;(242) (e) "normal human serum contains antibodies capable of recognizing the carbohydrate moiety of HIV envelope glycoproteins...from 100ml of human serum approximately 200ug of MBIgG was recovered [MBIgG=mannan-binding IgG]...MBIgG bound to HIV envelope glycoproteins gp160, gp120 and gp41";(243) (f) researchers from the University of Rome infected healthy mice with an E. coli lipopolysaccharide (LPS) and reacted their sera with two synthetic peptides, one encompassing gp120 V3 loop of "HIV-1 MN" and the other "representing a gp41 immunodominant epitope". The "LPS-treated mice showed a significant antibody reactivity" with the two peptides. (V Colizzi et al., personal communication). (g) Kashala, Essex and their colleagues have shown that antibodies to carbohy! drate containing antigens such as lipoarabinomannan and phenolic glycolipid that constitute the cell wall of Mycobacterium leprae, a bacterium which "shares several antigenic determinants with other mycobacterial species" cause "significant cross- reactivities with HIV-1 pol and gag proteins". This led the authors to warn that among leprosy patients and their contacts there is a "very high rate of HIV-1 false-positive ELISA and WB results", that "ELISA and WB results should be interpreted with caution when screening individuals infected with M. tuberculosis or other mycobacterial species", and furthermore that "ELISA and WB may not be sufficient for HIV diagnosis in AIDS-endemic areas of Central Africa where the preval‎ence of mycobacterial diseases is quite high".(244)

Not only mycobacteria (M. leprae, M. tuberculosis, M. avium- intracellulare) but also the walls of all fungi (Candida albicans, Cryptococcus neoformans, Coccidioides immitis, Histoplasma capsulatum including Pneumocystis carinni),(245-247) contain carbohydrate (mannans). One hundred per cent of AIDS patients (even those with "No candida clinically") have Candida albicans antibodies leading researchers from St. Bartholomews and St. Stephen's Hospitals to state: "It is possible that candida may act as a cofactor in the development of overt AIDS in HIV infected individuals".(248) It may also be of interest to note that in gay men the only sexual act which is a risk factor for seroconversion is passive anal intercourse (exposure to semen) (249) that mannose is present in both sperm and seminal plasma.(250) Since antibodies to mannans react with the "HIV proteins" then, as Essex and his colleagues have pointed out for mycobacterial infection in Africa, one would expect the ser! a of all people infected with fungi and mycobacteria to cross-react with the "HIV-1 glycoproteins" as well as to cause "significant cross-reactivities with HIV-1 pol and gag proteins". Given the fact that individuals with fungal and mycobacterial infections have antibodies which may produce a positive "HIV" antibody test even in the absence of "HIV", how can one assert that: (a) PCP, candidiasis, cryptococcosis, coccidioidomycosis, histoplamosis, tuberculosis or Mycobacterium avium-intracellulare disease, that is, the vast majority of the opportunistic infections (88% of AIDS cases diagnosed between 1988 and 1992 had one or more fungal or mycobacterial infections251) which signify AIDS are caused by HIV on the basis of a positive antibody test? (b) that a positive antibody test in individuals with fungal and mycobacterial infections proves HIV infection?

Indeed, as in the case of HL23V, is it only a matter of time before HIV researchers accept that there may be no such entities as specific HIV antibodies? As a consequence, will the compilation of phenomena inferred as proof of the existence of the human immunodeficiency virus, pass into history as "non-viral material altogether"? *

>
>In addition, we have some more questions. According to anti-AIDS sources;
>1. HIV is a false virus and what has been presented as a picture of HIV is normal cellular particles.

SEE http://healtoronto.com/emphotos.html

BARRE-SINOUSSI AND MONTAGNIER "ISOLATION OF HIV" PAPER 1983

The second line "in the publications from the NIH (www.niaid.nih.gov/spotlight/hiv00/default.htm)" reads: "abundant evidence indicates that AIDS is caused by human immunodeficiency virus (HIV) [Fig. 5], which was discovered in 1983". Indeed, to have an HIV hypothesis one must first have proof for the existence of HIV, that is, one must isolate the virus and demonstrate that it is unique. If there is no such proof for HIV then there can be no HIV hypothesis. The only evidence published in 1983 claiming HIV isolation (purification) was that of Luc Montagnier and his colleagues. However, as we have already mentioned, the 1983 evidence of Montagnier et al is not considered sufficient proof by both Robert Gallo and Jaap Goudsmit . Here we give our interpretation of the evidence from this study and seek comments by other panelists.

To claim the discovery of a new retrovirus one must:

1. Present evidence that in cultures containing the putative infected tissue, retrovirus-like particles can be detected with the electron microscope.
2. Obtain the particles separate (isolated) from any other biological components.
3. Show that all particles are identical and possess:

1. all the morphological characteristics of retroviruses;
2. the enzyme reverse transcriptase;
3. RNA and not DNA.

1. Prove that the difference between the RNA obtained from particles originating from different cultures is about the same as the differences between the RNAs of other RNA viruses. Such proof is absolutely necessary because small genomic variations lead to large phenotypic variations. For example, the difference between the human and the chimpanzee genomes is no more than 2 per cent while even 1% sequence differences in RNA viruses are considered to represent "extreme variability".
2. Show that the particles proteins are unique and are coded by the particles RNA.
3. Prove that the particles are infectious.

The evidence that Luc Montagnier and his associates published in 1983 and said to prove isolation and thus the existence of HIV is as follows:

1. In the supernatant fluids of a mitogenically stimulated culture from lymphocytes originating from the lymph nodes of a gay man they detected reverse transcription of the template primer An.dT₁₅. This was interpreted as proof that the gay man뭩 lymphocytes were infected with a retrovirus.
2. The gay man뭩 lymphocytes were co-cultured with mitogenically stimulated lymphocytes from a healthy blood donor. The detection of reverse transcriptase (RT) activity in the co-culture was considered proof of virus transmission from the gay man뭩 to the blood donor뭩 lymphocytes.
3. Mitogenically stimulated umbilical cord lymphocytes were cultured with supernatant fluids from the co-culture. In this, the third culture, they also detected reverse transcriptase activity. The finding of RT activity was considered proof that the virus was isolated and "could be propagated on normal lymphocytes from either newborns or adults". In the umbilical cord lymphocyte culture using the electron microscope they reported retrovirus-like particles.

According to Montagnier and his associates "That this new isolate was a retrovirus was further indicated by its density in a sucrose gradient, which was 1.16 gm/ml". (Retroviruses are purified by banding in density gradients. In sucrose density gradients the Retroviridae particles band at the density of 1.16 gm/ml.)

At the 1.16 gm/ml band, which they claimed was "purified" retrovirus (now know as HIV), they reported:

1. RT activity;
2. Three proteins that reacted with antibodies present in the gay man뭩 serum. One of the proteins, a protein of molecular weight of 25,000 (now known as HIV p24), was claimed to be a retroviral protein, and the antibodies present in the gay man뭩 serum which reacted with it to be induced by HIV.

   The second protein which reacted with the patient뭩 serum it was said may be the cellular protein actin, an ubiquitous protein of a molecular weight of 41,000 (p41), which contaminated the "purified" virus. No comments were made about the third, a protein of molecular weight 80,000 (p80). The p25 (p24) protein did not react with antibodies to the p24 and p19 of HTLV-I. This was considered proof that HIV was a unique retrovirus.

Comments:

1. The detection of an enzymatic activity cannot be considered proof of isolation no matter in how many consecutive cultures it is detected. For example, the measurement of cardiac or liver enzymes in cases of myocardial infarction or hepatitis respectively cannot be considered as "isolation" of the heart or liver. Neither can this finding be considered a proof for transmission or even detection of a retrovirus. This is because the enzyme is not specific to retroviruses. Normal cells which are not infected with retroviruses as well as bacteria and viruses other than retroviruses have these enzymes. This fact has been proven (or accepted) by the researchers who first discovered such an enzyme, by Harold Varmus, the ex-director of the NIH as well as Barr?Sinoussi and Chermann . In fact the enzyme reverse transcriptase is no more specific for retroviruses than adenosine triphosphatase, a wide spread enzyme which, before the discovery of RT, was used to detect and even quantif! y retroviruses. It is also of interest that Montagnier et al did not prove the existence of the enzyme itself but reverse transcription of the template-primer An.dT₁₅. However An.dT₁₅ can be transcribed not only by An.dT₁₅ but also by the normal cellular DNA polymerases.
2. They did not publish an electron micrograph to prove that what they called "purified" virus contains purified retrovirus particles. It is not possible to prove that a protein is retroviral just because it bands in a sucrose density gradient at the density of 1.16 gm/ml and reacts with patient sera. It is a fact that many other constituents of the culture supernatant, including cellular fragments, (microvesicles), also band at the same density. Indeed, if two of the proteins (p41 and p80) which band at this density and react with the antibodies present in the patient뭩 serum were non-HIV, then why not the third, p24?
3. Even if the 1.16 gm/ml band contained nothing else but isolated retroviral particles, that is, a purified virus, the reaction between the protein and antibodies present in the serum is not proof that the antibodies were directed against the retroviral proteins, that is, that the patients are infected with the retrovirus. This is because:

1. Antibodies cross-react. Even monoclonal antibodies interact not only with the inducing antigen but also with other antigens. Indeed, there are instances where "cross-reactive antibodies may have higher affinity with antigens other than the inducing antigen. Even antigens that differ for most of their structure can share one determinant, and a monoclonal antibody recognising this site would then give a 100% cross-reaction. An example is the reaction of autoantibodies in lupus with both DNA and cardiolipin...It should be emphasised that sharing a "determinant" does not mean that the antigens contain identical chemical structures, but rather that they bear a chemical resemblance that may not be well understood, for example, a distribution of surface charges".
2. The sera of AIDS patients and those at risk contain a plethora of antibodies. They include circulating immune complexes, rheumatoid factor, anti-cardiolipin, anti-nuclear factor, anti-cellular, anti-platelet, anti-red cell, anti-actin, anti-DNA, anti-tubulin, anti-thyroglobulin, anti-albumin, anti-myosin, anti-trinitrophenyl and anti-thymosin antibodies .

   This means that even if the origin of one of the reactants is known, from an antibody-antigen reaction it is impossible to determine the other if no a priori evidence exists that the reaction is specific. Yet, from such a reaction, Montagnier and his colleagues concluded that p24 was an HIV protein and the antibody that reacted with it was synthetised as a response to HIV infection.

   Again, if the antibodies that reacted with actin and p80 were non-HIV, why not those that reacted with p24?

1. Even if Montagnier and his colleagues had proof that the material from the supernatant of the umbilical cord lymphocytes cultures which banded at 1.16 gm/ml contained nothing else but retroviral particles, the retrovirus could not have been HIV.

1. According to all HIV experts, including Montagnier, HIV is a Lentivirus. However, the retrovirus-like particles which Montagnier et al detected in the culture supernatant of the umbilical cord lymphocytes did not have the morphology of Lentiviruses: "Electron microscopy of the infected umbilical cord lymphocytes showed characteristic immature particles with dense crescent (C-type) budding at the plasma membrane꿚his virus is a typical type-C RNA tumour virus", that is, a retrovirus belonging to the subfamily of oncoviruses, not Lentiviruses.
2. Similar particles have been seen in non-"HIV"-infected umbilical cord lymphocytes.

1. Even if Montagnier et al had proof for the isolation of a retrovirus and the retroviral particles had the morphology of a Lentivirus, the virus could not have originated from the gay man. In Luc Montagnier뭩 book Virus, published last year, one reads: "Particles of HIV are shaped like little spheres, each with roughly eighty little rounded projections shaped like pegs (see the accompanying figure). Each peg contains three or four molecules of a large protein, gp120, which has a strong affinity for the receptors (now called CD4) of T4 lymphocytes". Elsewhere he and his colleagues wrote: "The gp120 is responsible for binding the CD4 receptor" .

   The view that gp120 is "crucial to HIV뭩 ability to infect new cells" is shared by all HIV experts. However, (i) gp120 is said to be present only on the particles pegs (knobs), (ii) to date nobody, not even Hans Gelderblom from the Robert Koch Institute, Berlin, and his colleagues who have conducted the most intense and thoroughly electron microscopy studies could prove that the cell-free particles, that is, the particles detected in the culture supernatant, had these projections.

   In a study published in 1992 by these researchers in collaboration with researchers from many institutions in the USA, including Los Alamos National Laboratory, National Cancer Institute and the Diamond AIDS Research Centre, they reported that immediately after release there is about half a knob per particle. But they added: "It is possible that structures resembling knobs might be observed even when there was no gp120 present, i.e. false positive".

   If:

1. Pegs or knobs are absolutely necessary for infectivity;
2. The cell-free particles do not have knobs;
3. Montagnier et al cultured their umbilical cord lymphocytes with cell-free fluids from the co-culture;

   it follows then, that the umbilical cord lymphocytes could not have been infected with HIV originating from the gay man.

   (6) The non-reactivity of their p24 with antibodies to the HTLV-I p24 and p19 cannot be considered proof that their "purified" virus was a new human retrovirus. In fact this may be considered as an indication that their p24 was not a retroviral protein. Since the HIV as well as the HTLV-I p24s and p19s are said to be coded by the gag gene, (group specific antigen gene), antibodies to HTLV-I p24 would be expected to react with the HIV p24.

   In 1997 in an interview which Luc Montagnier gave to the French journalist Djamel Tahi he was asked why, in 1983, he and his colleagues did not publish an electron microscopy picture of the 1.16 gm/ml band to prove that indeed what they had there was nothing else but isolated HIV particles, "purified" virus. His answer was because, even after "Roman effort", they could see no particles with "morphology typical of retroviruses" (http://www.virusmyth.com/aids/data/vtcorweiss.htm*). The fact that the 1.16gm/ml band, the "purified" HIV, did not have retrovirus-like particles means that:

   (i) the "purified" virus did not have HIV;

   (ii) the retrovirus-like particles seen with the electron microscope in the culture were not retroviruses;

   (iii) the enzyme present at 1.16gm/ml which transcribed An.dT₁₅ was not a retroviral enzyme;

   (iv) none of the proteins which banded at 1.16gm/ml, including p24 were retroviral.

Conclusion One has no choice but to agree with Robert Gallo and Jaap Goudsmit, that Montagnier et al뭩 evidence does not prove "true isolation" "{Popovic, 1984 #249; which in turn means that HIV was not "discovered in 1983".

*The French transcript of Mongagnier's reply to this question can be found in the Perth group email correspondence with Professor Robin Weiss debating the existence of HIV (www.virusmyth.com/aids/perthgroup/papers2.html).