Eleni Papadopulos-Eleopulos (1) Valendar F. Turner (2) John M. Papadimitriou (3) & David Causer (1)

(1) Department of Medical Physics, (2) Department of Emergency Medicine, Royal Perth Hospital, Perth, Western Australia; (3) Department of Pathology, University of Western Australia.

The challenge by Continuum to produce proof of the isolation of HIV particles to enable their characterisation has drawn a response in an article published in the National AIDS Manual Treatment Update. Although this article makes several points which are claimed to answer the challenge they do not unambiguously satisfy the requirements of proof.

1. "...there is no standard 'set of rules' for isolating retroviruses".

It is impossible to make scientific claims unless one is guided by scientific principles. In fact, as far back as 1957, J. W. Beard, a leading retrovirologist of the day, discussing the isolation and analysis of particles wrote: "Although this has resulted in considerable success in some instances, there remain numerous unresolved problems in the general field, as well as outstanding omissions in the systematic use of the principles and procedures of well-recognised applicability. Fundamentally, the scheme of approach, as well illustrated by that devised and rigorously tested in investigations of viral agents, is relatively simple. This consists in (1) isolation of the particles of interest: (2) recovery (purification) of the particles in a given preparation that are homogeneous with respect to particle kind; (3) identification of the particles, and (4) analysis and characterisation of the particles for the physical, chemical, or biological properties desired" [1]. The "rules" employed by HIV/AIDS researchers, that is, detection of a protein, p24, OR an enzyme, reverse transcriptase, do not satisfy any scientific principle proving isolation of a viral particle and indeed defy common sense. If detection of p24 by an antibody is "HIV isolation" then why is the detection of the protein á-HCG in blood or urine (pregnancy test) not proof of placental isolation? The same argument can be advanced for reporting the measurement of cardiac enzymes in cases of suspected myocardial infarction as "isolation" of heart.

2. "...while some of Continuum's proposed seven steps (involving the propagation, purification and characterisation of the virus from a tissue sample) can easily be demonstrated for HIV..."

It may be possible but to date the fact is to date nobody has purified the "HIV particles" and propagation and characterisation are impossible without purification.

3. "Contrary to the implication by Continuum, the Pasteur Institute did not draw up such guidelines in 1973".

At the 1973 meeting at the Pasteur Institute [2, 3] the steps which one has to follow to isolate retroviruses were thoroughly discussed and indeed are straightforward commonsense and are not dissimilar from those enumerated earlier by Beard. In the first of the two papers from the Pasteur Institute meeting published in Spectra entitled "RNA tumor viruses purification using zonal rotors [RNA tumor viruses=retroviruses]", figure 1 is a "Flow chart for purification of RNA viruses by double sucrose density gradient zonal centrifugation". The flow chart is:

RNA Tumor Virus Purification:

VIRUS FLUID [80 litres]
CLARIFICATION [4000G X 10 min.]
K-3 ROTOR [RNAse-free sucrose 20-55% 12 litres/hour]
K-3 VIRUS ZONE [500 ml., 30-38%]
B-29 ROTOR [RNAase-free sucrose 30-45% 25,000 rpm X 180']
B-29 VIRUS ZONE [150 ml., 32-37%]

The particles thus obtained are then characterised by performing a number of assays. The flow chart for these assays is given in Table 3 and is as follows:

Assays for RNA Tumor Viruses:


Electron Microscopy (neg stain and thin sect.)
Virus count


Reverse transcriptase
60-70S RNA, total RNA
Total protein
Gel analysis of viral and host proteins and nucleic acids


Gel diffusion
Complement fixation

(The latter two for with specific reagents for enveloped and internal antigens gs and env).


Infectivity in vivo
Infectivity in vitro

Toplin, the author of this paper, pointed out it is much easier to isolate retroviruses than other viruses. Nonetheless, "The RNA tumor viruses also have buoyant densities that coincide with those of certain cellular constituents. Therefore, if the cell cultures used for virus propagation are not maintained at maximum viability, purification problems can also be encountered with these viruses in relation to contaminating microsomal and membrane fragments...". Because of this Toplin regards double banding as a necessity. It is worthwhile noting that "HIV" cell cultures are not maintained at maximal viability and in fact, unlike all other retroviruses, HIV is said to kill cells. Thus, unlike the supernatants (cell free culture fluids) from other retroviral cultures, in "HIV" cultures one would expect to find subcellar material, at least "cellular fragments", microsomes from disrupted cells and "membraneous vesicles which may enclose other cellular constituents including nucleic acids" [2, 4-6].

4. "...but did not themselves meet the seven steps Continuum was now requesting for HIV".

This is true but they did not have to meet these steps. Toplin's aim was to discuss in general terms the stages one has to follow in order to isolate and characterise retrovirus-like particles. Nonetheless, he does give electron micrographs (EM) of double banded particles. In his figure 6 there is an "electron micrograph (thin section of Rauscher murine leukaemia virus from cell culture fluid after double sucrose zonal centrifugation".

In the second paper "Purification an partial differentiation of the particles of murine [mouse] virus (M.MSV) according to their sedimentation rates in sucrose density gradients", Sinoussi, Chermann and their colleagues aimed to obtain a purified particle preparation and not to fully characterise the MSV. In double banding sucrose density gradients they obtained particles "banding in the region of the gradient corresponding to a density of 1.14-1.15 gm/ml". "No apparent differences in physical appearances could be discovered among the viral particles in these regions. There was no sign of aggregation of particles". They also showed that "The viral particles separated by zonal centrifugation are able to cause focus formation in murine embryonic fibroblast tissue cultures" and that reverse transcriptase (RT) "activity was found in the region of the gradient where particles were found".

5. "But if one put together three or four papers, all the data are there and have been published for years".

Where are these three or four papers? Where is even one paper where there is electron micrographic evidence revealing particles of any shape or form at the density of 1.16 gm/ml, the density that defines retroviral particles, let alone retrovirus-like particles with "No apparent differences in physical appearances" as Sinoussi and Chermann wrote in 1973 or, as Beard much earlier wrote, "homogeneous with respect to particle kind"?

6. "...purification by this method is no problem..."

If purification of HIV particles by density gradient centrifugation is no problem why has it not been reported?

7. "...[HIV] loses most of its infectivity during this laboratory process".

Given the fact there is no electron microscopic evidence for the existence of HIV particles at the density of 1.16 gm/ml, how may one have evidence that the particles lose their infectivity during density gradient centrifugation? If the infectivity of HIV particles is so labile how do they retain their infectivity during the processing of plasma into the factor VIII clotting concentrates which are administered to individuals with haemophilia? (This procedure involves collection of blood, separation of plasma by centrifugation, cool storage followed by freezing, transport to a facility for pooling with donation of similarly obtained plasma, thawing, further freezing and thawing, filtration, lyophilisation and storage as a dry powder for weeks to months before use [7]).

8. "HIV particles look different" from "naturally existing viruses".

In the scientific literature there is no data which permits one to distinguish on the basis of appearances between endogenous (natural) and exogenous retroviruses. "Retroviruses are enveloped viruses with a diameter of 100-120 nm budding at cellular membranes. Cell released virions [individual virus particles] contain condensed inner bodies (cores) and are studded with projections (spikes, knobs)" [8]. The particles are further categorised according to "site of core assembly (preformed in the cytoplasm or formed during the budding process at the plasma [cell] membrane); shape and size of surface protrusions (spike- or knob-like); presence or absence of electron -lucent space between envelope and core in immature particles, and shape and position of cores in mature particles". There are three Subfamilies of retroviruses (Oncovirinae, Lentivirinae, and Spumavirinae). The particles of the Subfamily Oncovirinae are in turn subdivided into four genera, type A intracisternal and intracytoplasmic particles, and type B, type C and type D particles [9].

As far as "HIV particles look different" is concerned, in cultures of tissues from AIDS patients one can see a "zoo" of particles with varying morphologies. For example:

(a) Hockley and his colleagues from the Electron Microscopy and Photography Section and Division of Virology at the National Institute for Biological Standards and Control in the United Kingdom describe a profusion of particles which they divide broadly into three groups, mature, ring-like and small with spikes. The mature particles "were approximately spherical in shape and 100 to 150 nm in diameter. The outer lipid membrane was frequently broken or absent in places and there was no evidence of surface spikes...A few mature particles were found that were larger than average and appeared to contain a double the preparation of HIV there were always many vesicles with granular contents in which it was not possible to recognize a distinct nucleoid".

Also, "The ring-like particles had a more consistently spherical shape and were larger (140 nm in diameter)" and the small particles "were usually spherical but sometimes slightly angular in shape and 65 to 90 nm in diameter" and had spike-like projections on their surface [10].

(b) Gelderblom who has done most of the EM studies in HIV/AIDS research reported that although HIV is considered to have a cone shaped core he and his colleagues found centrosymmetric and tubular cores as well. The caption to one of the many photographs reads: "Virions can be seen having either elongated, 'baton-like' tubular cores 30-35 nm in diameter or containing more than one core. Tubular and regular cone-shaped cores can coexist within one virion". The text states:

"Rarely, tubular core structures reminiscent of batons with a diameter of 30 35 nm and a length of 150-250 nm are observed" [8]. (If cores are of such dimensions then some of the particles must exceed twice the diameter of retroviral particles).

(c) Lekatsas and other virologists from Pretoria and Johannesburg: "We used the characteristic cylindrical structure in the core as an identifying characteristic for the virus to distinguish it form cellular debris and also noted that it may vary considerably in its dimensions and morphological features. Fig. 1 depicts a variety of such features encountered in our preparations. We have found two basic virus particle sizes, 90nm and 120 nm, both present in large numbers. The larger particle bears no surface projections while the smaller particle is rarely 'naked' and usually bears projections. We have seen no particles with partial loss of projections, suggesting that small particles retain these structures while large particles lose them soon after liberation" [11].

(d) The US CDC: HIV particles are "usually round and have a diameter of about 85-95 nm...Virus with bar-shaped nucleoids and particles with a tear-drop shape are commonly seen in HTLV-III/LAV infected lymphocytes, sometimes ring-shaped particles without dense nucleoids are also seen" [12].

Particles of the smaller dimension have also been found in both the non-infected H9 cell line and in another cell line called CEM. Both cell lines are used extensively in HIV/AIDS research and they are the cell lines from which practically all the EM studies have been reported. Particles have also been found in other cell lines such as C8166, EBV transformed B-cells, and cord blood lymphocytes [13].

Although all HIV/AIDS researchers report the finding of "HIV" particles in the cultures of tissues originating from AIDS patients or those at risk, there is no agreement as to which Genus or even Subfamily of retroviruses such "HIV" particles belong. For example:

  • (a) Montagnier and his colleagues reported HIV initially as a type C particle, then as a type D particle and then as a Lentivirus [14-16];
  • (b) in 1984 Gallo and his colleagues reported HIV as a type C particle. However, in 1985 he wrote: "A possible unique feature of the virions is the cylindrical core observed in many presumably mature virions. Virions having this type of core have been frequently reported for certain type D retroviruses, and in some instances, for type C retroviruses" [17];
  • (c) Jay Levy, reported HIV as a type D particle [18];
  • (d) Others at the University of California wrote that "AIDS virus isolated show morphologic characteristics of type C, type D and Lentiviruses" [19];
  • (e) Dr. Anthony Fauci and others: "T-cells and macrophages handle the virus very differently. In the T-cell, the virus buds out of the external plasma membrane of the cell. In the monocyte/macrophage cultures it buds into membrane-bound vesicles inside the cells" [20]. The latter is a description of a type A, retroviral particle [9].
  • Thus, although HIV has been described as a member of two Subfamilies of retroviruses including three different Genera of one of these Subfamilies, by consensus at present HIV is regarded as a Lentivirus. However, it is of pivotal significance that in cultures of tissues from AIDS patients although there are particles with the diameter of 100-120 nM these particles do not have spikes or knobs. The particles which possess spikes and knobs have diameters smaller than 100-120 nM In other words, there are no particles which fulfil the two principal morphological characteristics of retroviruses, that is, particles which have BOTH "a diameter of 100-120 nM" AND surfaces which "are studded with projections (spikes, knobs)".

    In view of the above the question then arises if the particles with the "unique" morphology considered to be HIV represent an exogenous retrovirus originating from tissues of AIDS patient or those at risk then what is the origin and role of the many non-HIV particles and which if any of these particles or the "HIV particle" band at 1.16 gm/ml?

    9. "The relationship between infection with HIV (indicated by the antibodies produced by the body in response) and risk of developing AIDS is clear; among groups of drug users, haemophiliacs or gay men, it is only those that are HIV-positive who are at risk of developing AIDS".

    One cannot talk about "HIV antibodies" as being synonymous with "HIV infection" unless one has proof that the antibodies present in sera are specific to HIV. The only way to obtain such scientific proof is to use HIV isolation as a gold standard. To date, since HIV has not been isolated, no such proof exists [21, 22]. However, as far back as 1934, Andrews, addressing the Royal College of Physicians in London on the subject of the Rous sarcoma retrovirus presented data that anti-retroviral antibodies are non-specific:

    "Most viruses evoke the production of antibodies which are demonstrated by their power of neutralising the virus in question when mixed with it in vitro...Normal fowls, particularly as they grow older, may develop in their sera varying amounts of similar neutralising properties...It is likely, therefore, that the antibodies in the birds with chronic tumours represent only an enhancement of a property occurring to a varying degree in normal birds" [23].

    The main immunogenic (antibody generating) retroviral proteins are said to be coded by two genes, gag and env. From the beginning it was known that the gag gene of retroviruses is present in all cells, including those that do not have retroviral particles and in fact this observation forms the basis of the oncogenic theory of cancer. In 1970, Huebner, one of the originators of this theory wrote: "Natural history studies of the prevalence of the gs [gag] antigen [protein] in virus-free laboratory mice revealed gs antigens in high titers in the hematopoietic tissues of individuals of most mice strains" [24]. One year later Robin Weiss wrote: "The idea that normal cells of chickens might contain avian tumor virus genomes first arose from the observation that normal embryonic tissues of some "leukosis-free" chicken strains possessed an antigen which was indistinguishable from the group-specific (gs) antigen of avian tumor viruses" [25]. The p17/18 and p24 proteins of "HIV" are said to be coded by its gag gene. The evidence that the p18 and p24 proteins (and antibodies) are non-specific is overwhelming and can be illustrated by a few examples:

    (a) Genesca et al conducted WB assays in 100 ELISA negative samples of healthy blood donors; 20 were found to have HIV bands (antibodies) which did not fulfil the then (1989) criteria used by the blood banks for a positive WB. These were considered as indeterminate WB, (WBI), with p24 being the predominant band, (70% of cases). Among the recipients of WBI blood, 36% were WBI 6 months after transfusion, but so were 42% of individuals who received WB-negative samples. Both donors and recipients of blood remained healthy. They concluded that WBI patterns "are exceedingly common in randomly selected donors and recipients and such patterns do not correlate with the presence of HIV-1 or the transmission of HIV-1", "most such reactions represent false-positive results" [26];

    (b) According to researchers from Germany and the United Kingdom (Wellcome Research Laboratories), "Western blotting should not be used as a screening assay because rates of up to 20% indeterminate results are found in blood donors" [27];

    (c) In most cases, by "HIV isolation" is meant detection of p24 in cultures. However, in cultures with whole unfractionated blood, positive results have been reported in 49/60 (82%) of "presumably uninfected, but serologically indeterminate" individuals and in 5/5 "seronegative blood donors" [28];

    (d) detection of p24 has been also reported in organ transplant recipients. In one kidney recipient (the donor was negative for p24 antigen) who, 3 days following transplantation developed fever, weakness, myalgias, cough and diarrhoea, all "Bacteriological, parasitological and virological samples remained negative [including HIV PCR]. The only positive result was antigenaemia p24, positive with Abbot antigen kits in very high titers of 1000pg/ml for polyclonal and 41pg/ml for monoclonal assays. This antigenaemia was totally neutalizable with Abbot antiserum anti-p24...2 months after transplantation, all assays for p24-antigen became negative, without appearance of antibodies against HIV. Five months after transplantation our patient remains asymptomatic, renal function is excellent, p24 antigenaemia still negative and HIV antibodies still negative" [29]. Using two kits, the Abbot and Diagnostic Pasteur, in one study, p24 was detected transiently in 12/14 kidney recipients. Peak titres ranged from 850 to 200 000 pg/ml 7-27 days post-transplantation. Two heart and 5/7 bone marrow recipients were also positive, although the titres were lower and ranged from 140-750 pg/ml. Disappearance of p24 took longer in kidney (approximately 6 months) than in bone-marrow (approximately 4-6 weeks) recipients. According to the authors: "This may be related to differences in immunosuppression therapy". Discussing their findings they wrote: "The observation of a 25-30kD protein [the French researchers report p24 as p25] binding to polyclonal anti-HIV human sera after immunoblots with reactive sera raises several questions. This protein could be related to a host immune response to grafts or transplants...Its early detection after transplantation might indicate the implications of immunosuppression therapy...The 25-30kD protein could therefore be compared with the p28 antigen recently described with human T-cell-related virus lymphotropic-endogenous sequence...The characterization of this 25-30kD protein may represent an important contribution to the detection of HIV-1-related endogenous retroviruses" [30];

    (e) In addition to the WB p24 band, the p17/18 band is the most often detected band in WB of healthy blood donors [31]. Also, sera from AIDS patients bind to a p18 protein in mitogenically stimulated HIV infected T-cells, but not to non-infected, unstimulated lymphocytes. However, when the lymphocytes are mitogenically stimulated, but non-infected, the AIDS sera bind to a p18 protein in these non-infected lymphocytes [32]. Similarly, a monoclonal antibody to HIV p18, reacts with dendritic cells in the lymphatic tissues of a variety of patients with a number of non-AIDS related diseases and the "same pattern of reactivity was present in normal tissue taken from uninfected individuals as in those taken from HIV positive subjects" [33];

    (f) Strandstrom and colleagues reported that 72/144 (50%) of dog blood samples "obtained from the Veterinary Medical Teaching Hospital, University of California, Davis" tested in commercial Western blot assays, "reacted with one or more HIV recombinant proteins [gp120--21.5%, gp41--23%, p31--22%, p24--43%]" [34].

    (g) According to 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" [35].

    Regarding antibodies found in human sera which react with the envelope proteins (p41, p120, p160), in 1981 Gallo accepted the evidence that the antibodies which reacted with retroviral glycoproteins were directed not against the proteins "but against the carbohydrate moieties on the molecule that are introduced by the host cell as a post-transcriptional event, and which are therefore cell-specific and not virus-specific" [36]. This is amply confirmed today for the HIV envelope glycoproteins by many HIV researchers including the 1994 studies of Essex and his colleagues [37].

    10. "...many pictures of HIV have been published..."

    What has been published is pictures of virus-like particles present in cell cultures where several types of particles are present and some are arbitrarily said to be HIV. There are no published EMs of material banding in sucrose density gradients.

    11. " next to impossible to remove all other debris from the culture..."

    It may not be possible for "HIV" but animal retroviruses have been isolated by banding in density gradients (see EM in Pasteur/Spectra publications).

    12. "'s like saying that it is impossible to identify a German Shepherd dog by its unique appearance, if it happens to be surrounded by a pack of poodles".

    How does one look at a zoo and know one has a German Shepherd or a poodle? The differentiation between a German Shepherd and the remainder of the universe including poodles is possible only because German Shepherds are obtained separate from all other objects in the universe and shown to possess unique morphology, constituents and behaviour such as walking, barking and biting. The analogy with HIV is more like someone who does not know what a German Shepherd is but who looks at an aerial photograph of a zoo, expects to see dogs (retroviruses) but all he sees is many objects some of which look like animals (viruses) and decides that one of the objects is a dog, in fact a dog with unique composition and behaviour without first showing the object is:

  • (a) an animal;
  • (b) the animal is a dog;
  • (c) the dog is unique.
  • Perusing the analogy, is it possible to mince up all the objects in the zoo, before there is ever proof of the existence of the Family Canidae (the Family Retroviridae) let alone dogs known as German Shepherds and poodles, centrifuge them in density gradients and then proclaim that the material which bands at 1.16 gm/ml (proteins and nucleic acids) belongs to the German Shepherd (HIV)?

    If the virus-like particles seen in cultures of tissues of AIDS patients and those at risk are HIV, what then are the particles seen by Weiss and his colleagues in cultures of patients with common variable hypogammaglobulinaemia "which on electron microscopy showed a retrovirus morphologically indistinguishable from HTLV-III/LAV [HIV] and animal lentiviruses. Supernatant from this co-culture was positive by reverse transcriptase, and the cells were positive by immunofluorescence with serum from a patient with AIDS and with the anti-HTLV-III monoclonal antibodies à-p24 and à-à-p19 (from Dr. R. C. Gallo). Southern blots of restricted DNA from infected cells were probed with yBH-10 (from Dr. R. C. Gallo) indicated that the viral genome showed homology to HTLV-III/LAV" [38]. According to Weiss, "It has long been known from electron microscope and immunofluorescent studies (24) that HIV is found in massive amounts in the lymph nodes, even in the asymptomatic phase of infection" [25]. Firstly, the authors of reference 24 [39] did not claim to have proven the existence of HIV particles or even retroviral particles but only "retrovirus-like particles". If the virus-like particles seen in the lymph nodes of AIDS patients and those at risk are HIV, then what are the particles with identical morphology seen with the same frequency in the enlarged lymph nodes of patients who do not have AIDS and who are not at risk of developing AIDS? In a study conducted by O'Hara and colleagues from Harvard, "HIV particles" were found in 18/20 (90%) of patients with enlarged lymph nodes attributed to AIDS. However, the identical particle was also found in 13/15 (87%) of patients with enlarged lymph nodes not attributed to AIDS leading the authors to conclude, "The presence of such particles does not, by themselves indicate infection with HIV" [40].

    13. "...the insistence that the experiment must start with pure particles makes this unattainable".

    If the proof of the existence of pure particles is unattainable then:

    (a) how can one claim virus purification or isolation? Isolation means obtaining an object separate from everything else that is not that object;

    (b) how can one know that the "HIV" proteins and nucleic acids belong to this virus and not to the impurities such as other viruses or non-viral material?

    (c) how can one claim that the effects, if any of "HIV" are caused by "HIV" and not by impurities?

    (d) since no EM has been published showing virus-like particles in the material which bands at 1.16 gm/ml, how can one know that such particles, pure or impure, are present at the retroviral density?

    14. "...grow HIV isolates..."

    How can one grow HIV isolates when the virus has not been isolated?

    15. "HIV's genetic material, on the other hand, can be purified.

    A critical analysis of the HIV literature shows that by "HIV genome" is meant nothing more than the selection of part of the RNA which from cultures which bands at a density of 1.16 gm/ml. Since no evidence exists for the presence of retroviral particles at this density, it is impossible to say that such RNA belongs to HIV or even to a virus-like particle.

    16. "Gene cloning techniques allow researchers to extract the viral genes found in HIV-infected cells".

    This cannot be the case unless one first has nucleic acids which have been proven to belong to a unique retroviral particle, which can be done only by isolating the particle.

    17. "When the complete set of genes is re-introduced into healthy human cells in culture, the cells produce HIV particles".

    In the vast HIV literature there is not one paper with such evidence.

    18. "It would clearly be unethical to inject these particles into humans to see if they caused AIDS".

    If it is impossible to obtain such evidence, or to have an animal model, how can the claim that the cause of AIDS is HIV be justified?

    19. "However, experiments with purified SIV, the monkey equivalent of HIV, have proved that the pure retrovirus causes the selective loss of CD4 cells resulting in an AIDS-like disease".

    (a) the evidence for SIV isolation and "purified" SIV is no better than that for HIV;

    (b) In most cases SIV, like HIV, has been "isolated" from cultures with the human leukaemic cell line H9 (HUT78) a cell line which Gallo claims to have shown contains the HTLV-I genome, a "human retrovirus" [41].

    (c) the effects obtained when animals are injected with "SIV" have nothing to do with the AIDS diseases. In fact, in many cases, they may represent nothing more than graft vs host effects.

    (d) even if the diseases were similar or identical to AIDS they may be the result of impurities in the "SIV preparations" and not to SIV.

    20. "Moreover, three American laboratory workers have been infected with purified HIV..."

    How is it possible to prove this when the "insistence that the experiment start with pure particles" is "unobtainable"?

    21. "By 1993, all three had developed low CD4 counts and one had been diagnosed with PCP, proving the link between HIV, immune suppression and AIDS".

    Even if these individuals were proven to have repeatedly low CD4 counts and to have PCP diagnosed by lung biopsy and not by the non-specific methods presently used, it does not mean that these abnormalities are caused by HIV. The existence of low CD4 counts and the AIDS like diseases are nothing new and are not specific to HIV. Furthermore, a superficial glance at the AIDS literature shows that no relationship exists between CD4 cell counts and the syndrome [42]. Indeed, in those at risk, low T4 cell counts frequently antedate "infection" with HIV which can be interpreted as low T4 cells counts being the "cause of HIV" and not vice versa.


    Retrovirus-like particles including particles with morphologies attributed to HIV are ubiquitous. The first absolutely necessary but not sufficient step in proving that the particles represent a retrovirus is to show that in sucrose gradients the particles band at the retroviral density of 1.16 gm/ml. The first absolutely necessary but not sufficient step in claiming the existence of a retroviral proteins and genome is to prove that each belongs to one and the same type of retrovirus-like particles such as type C, type D or Lentiviruses. No such evidence exists for the "HIV" particles, proteins or nucleic acids.


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