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THE ISOLATION OF HIV:
HAS IT REALLY BEEN ACHIEVED? Part 5 Note: The information on this website is presented for
educational purposes and This document was provided by Previous: The Isolation Of Hiv: Has It Really Been Achieved? Part 4 8. "IDENTIFICATION OF HIV" 8.1 "The existence of HIV predicts that infected cells contain a unique, virus specific DNA of 9150 nucleotides that cannot be detected in DNA of uninfected cells". The genome of a retrovirus cannot be identified on the basis of the length of a RNA (cDNA) fragment and its presence in some but not other cells. 8.1.1 Using fragments of "HIV DNA" as hybridization probes or primers, positive results with both standard hybridization and PCR have been obtained from DNA of "uninfected" human cells and insects (see 6.4.4). It is a fact that: (a) hybridization of nucleic acids of "exogenous retroviruses" "from different species gives a pattern which is the same as the phylogenic relatedness among their natural hosts",228 a relationship which led retrovirologists including Gallo to conclude that exogenous retroviruses "are derived from cell genes"; (b) The existence of human retroviruses has been "shown" using hybridization probes derived from endogenous and exogenous animal retroviruses. If this is the case and if "HIV DNA" is the genome of an exogenous human retrovirus, the non-infected human genome should contain sequences which will hybridize with "HIV DNA" probes. There can be two reasons why such findings have not been reported more often: (a) Most HIV researchers ignore one of the most fundamental requirement of basic experimental research, that is, controls. In the rare instances where controls are used, they are not suitable (see 6.1). In the 1970s, Gallo, Gillespie and their colleagues were saying that the success of the "hybridization assay appears to depend on the biological history of the virus", and on the physiological state of the cells.125,228 In a large study published in 1975 entitled "Relationship between Components in Primate RNA Tumor Viruses and in the Cytoplasm of Human Leukemia Cells: Implications to Leukemogenesis", the aim was to show that human leukemia cells but not normal cells have properties associated with retroviruses including retroviral genomic sequences. It was reported that "The human leukemic blood cell cytoplasmic particle that contains reverse transcriptase activity is capable of synthesizing DNA in vitro, using endogenous RNA as both template and primer. This endogenous activity has been used to learn about the nature of the particle itself. Many intracellular cytoplasmic particles or organelles (described generally in Table 8) can carry out endogenous DNA synthesis in vitro. These include mitochondria, small ytoplasmic particles of low density, 1.10-1.16 g/cc in sucrose density gradients, and small cytoplasmic particles of higher density, 1.17-1.19 g/cc in sucrose density gradients...Small particles have been detected in the cytoplasmic fraction of phytohemagglutinin-stimulated lymphocytes from normal donors... These particles carried out endogenous DNA synthesis, and the resulting DNA population contained sequences related to genomes of RNA tumor viruses...Viral-related sequences were found in patients with several types of leukemia, including AML, CML, CML-A and CLL...Attempts to detect viral sequences in RNA of leukemic cells by hybridizing DNA synthesized by animal viruses to RNA isolated from cytoplasmic small particles (the reciprocal hybridization experiment) in our hands fails to find differences in sequences in RNA of leukemic and dividing normal [PHA stimulated] human peripheral white blood cells. It has been reported by others that radioactive DNA probes synthesized by MuLV R hybridize to cytoplasmic RNA from leukemic, but not normal white blood cells. A difference between our experiments and those previously reported is that the normal human cells used as a source of RNA are actively dividing while most of those used in previous studies were not"125 (italics ours); (b) The "HIV RNA" is not the genome of either an exogenous or an endogenous retrovirus or even the transcribed DNA fragment present in un-"shocked" cells. 8.1.2 Most of the positive results in "uninfected cells" have been found by using probes and primers for one or at most two genes or even gene fragments. The "great majority" of HIV studies, encompass "2% to 30% of the genome".163 However, finding fragment of a gene or even a gene is not proof for the existence of the HIV genome. 8.1.3 Montagnier and his colleagues reported the "HIV DNA" to be 9 ± 1.5 Kb91 whereas Gallo and his colleagues reported that "The over-all length of the HTLV-III provirus is approximately 10 kilobases". 96 In Levy and colleagues’ first study of the "HIV genome", the "broad band (>15 Kb) represents provirus integrated into host cell DNA".98 In 1995, Pasteur researchers reported that "The complete 9193- nucleotide sequence of the probable causative agent of AIDS, lymphadenopathy- associated virus (LAV), has been determined. The deduced genetic structure is unique; it shows, in addition to the retro-viral gag, pol, and env genes, two novel open reading frames we call Q and F".229 In the same year, Gallo and his colleagues reported their results on the "HIV" nucleotide sequences using clone BH10 but also added, "The sequence of the remaining 182 bp of the HTLV-III provirus not present in clone BH10 (including a portion of R, V5, tRNA primer binding site and a portion of the header sequence) was derived from clone HXB2...Of note is the presence of a fifth open reading frame (nucleotides 8, 344-8991) designated 3’ orf, present in clone BH8 but truncated in BH10". They concluded, "The complete nucleotide sequence of two human T-cell leukaemia type III (HTLV-III) proviral DNAs each have four long open reading frames, the first two corresponding to the gag and pol genes. The fourth open reading frame encodes two functional polypeptides, a large precursor of the major envelope glycoprotein and a smaller protein derived from the 3’ terminus long open reading frame analogous to the long open reading frame (lor) product of HTLV-I and -II...The HTLV-III provirus is 9,749 base pairs (bp) long".32 In 1990 the HIV genome was said to consist of ten genes.230 This year Montagnier reported that HIV possesses eight genes7 and Barré-Sinoussi,8 HIV has nine genes. To date, no two "HIV DNA" of the same length have been reported and moreover, it is accepted that most "HIV genomes" are defective. Even if all the genes can be amplified by PCR, it still does not mean that the "full-length HIV genome" is present. For example, in 1995 the nef gene of three of the blood recipient members of the Sydney "Bloodbank" cohort and of the donor were amplified by PCR. "The resulting amplified fragments for the three recipients ranged from 410 bp to 680 bp. One recipient yielded fragments of two sizes...The amplified fragment from the donor (D36) was 550 bp in length, indicating a deletion of 290 bp...compared with 840-bp fragment from the molecular clone pNL4-3".231 In 1995 David Ho and his colleagues "analyzed by polymerase chain reaction and direct sequencing 57 viral sequences from 47 individuals of North American, Australian and Haitian origin infected with human immunodeficiency virus type 1 (HIV-1), focussing on the V1 and V2 regions of gp120. There was extensive length polymorphism in the V1 region, which rendered sequence alignment difficult. The V2 hypervariable locus also displayed considerable length variations, whereas flanking regions were relatively conserved".232 As far as Gallo is concerned, it is not even a requirement that the "HIV" genome possess any genes whatsoever to be pathogenic, "This suggests that defective virions such as RNA-free particles and/or viral proteins expressed in the absence of particle formation contribute to AIDS pathogenesis".114 8.1.4 In searching the HIV literature it is striking that to date, not one single 9150 bp or any length of "full length HIV genome" from fresh uncultured cells has been sequenced. "The low abundance of HIV-1 proviral DNA in clinical samples is a barrier to full-genome analysis of HIV-1 provirus as it occurs in vivo". All the "full-length HIV genomes" sequenced so far have been from cultured cells; in fact "Completely sequenced full-length HIV-1 genomes in the current Los Alamos data base have been derived, almost without exception, from HIV-1 isolates adapted to growth in continuous [leukaemic or transformed] T-cell lines". As of late 1995 "only 19 sequences encompassing the full-length, 10-Kb HIV-1 genome have been reported, and most derive from HIV-1 isolates of genotype B expressed in continuous cell lines. Five of the eight most prevalent genetic subtypes of HIV are without a single, full-length, sequenced prototype". 193 At present it is also known that: (a) patients belonging to the AIDS risk groups are exposed to high doses of oxidizing agents and that these agents have profound effects on DNA and RNA;74,79 (b) in cultures "HIV" cannot be detected unless cultures are treated with chemical or physical oxidants including PHA; (c) there are structural and functional abnormalities in the lymphocyte genome of AIDS patients. "AIDS patients have shown increased levels of spontaneous DNA repair synthesis (three times higher),increased quantity of single-stranded DNA breaks (11-18%), decreased ability to restore DNA damage (2-2.5 times lower) compared to healthy persons";233 (d) according to Chermann and his colleagues, "Different populations of distinct HIV-1 DNA fragments of highly variable size ranging from 600 bp to full length provirus were present in PBMC from HIV-infected persons... Defective genomes tended to gradually disappear after activation of PBMC with phytohemagglutinin";234 (e) According to the HIV experts, the defective genomes are "rescued" by recombination and this recombination is one of the main causes of "HIV DNA" complexity. If this is the case one may ask:
As has been pointed out, HIV researchers seldom use controls and to date those that have, failed to use appropriate controls, that is, tissues or cultures derived from similarly sick, non-AIDS individuals in which experimental techniques and conditions employed are identical apart from the presence of putative retroviral material. However, if HIV researchers or others capable of mounting such experiments were encouraged to put as much effort as they put into studying "HIV" from lymphocytes of at risk patients into studying lymphocytes from patients not at risk but:
can one exclude the possibility that in another ten years time these researchers will not be able to report "19 full-length HIV genomes" in these individuals? 8.2 "For example, Jackson et al. have tested blood cells of 409 anti-body-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 anti-body-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 individuals) 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 background reactivity. In this context, even if there are "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 assays". 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 bHCG 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 analyzed 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 32 p-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 seven 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 two 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% respectively...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 anti-body 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 Biological 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 "exceedingly 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 and 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", remain unexplained; (b) finding a positive PCR result using a small fragment of the gag gene as a 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 sub-sequent 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 and its 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 have a positive antibody test. Furthermore, as in the case of HL23V, there is evidence that the 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 recognise 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 (a1->2) and (a1->3) 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 gp 120;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 lymphotrophic 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 neutralising 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 200mg of MBIgG was recovered [MBIgG=mannan-binding IgG]...MBIgG bound to HIV envelope glycoproteins gp 160, gp 120 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 gp 120 V3 loop of "HIV-1 MN" and the other "representing a gp41 immunodominant epitope". (V Colizzi et al., personal communication). (g) Kashala, Essex and their colleagues have shown that antibodies to carbohydrate 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 crossreactivities 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 carinii),245-247 contain carbohydrate (mannans). One hundred percent of AIDS patients (even those with "No candida clinically") have Candida albicans antibodies leading researchers from St. Bartholomew's 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 and 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 sera 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, coccidiodomycosis, histoplasmosis, 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"? ACKNOWLEDGMENTS We would like to thank all our colleagues and especially Bruce Hedland-Thomas, Richard Fox, Livio Mena, Alun Dufty, Barry Page, Andrew Campbell, Jennie Brooks, Gordana Pelemis, Daphne Peters, Gladys Powell, Ron Hirsch, David Dawson, June Rider-Jones, Christine Sibley, the staff of the Royal Perth Hospital Library and the clerical staff of the Department of Medical Physics. We also thank Todd Miller, Christine Johnson, Philip Johnson, Harvey Bialy, Charles Thomas, John Lauritsen, Neville Hodgkinson, Gordon Stewart, Huw Christie, Tony Tompsett, James Whitehead, Volker Gildemeister, Michael Baumgartner, Michael Verney Elliot, Joan Shenton, Stefan Lanka, Michael Ristow, Fabio Franchi, Djamel Tahi, Richard and Rosalind Chirimuuta, Udo Schuklenk, Brian Peachey, Philip Adams and Hiram Caton, as well as any others we may have unfortunately omitted. We especially thank Peter Duesberg for all his help and encouragement and for his inspiring example of scientific courage and integrity. References: The Isolation Of Hiv: Has It Really Been Achieved? References |