VIRUSMYTH HOMEPAGE
ISOLATED FACTS ABOUT HIV - A REPLY
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%]
|
DIALYSIS OR
ULTRAFILTRATION
|
FINAL CONCENTRATE [150-200 ml.]
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:
Physical:
Electron Microscopy (neg stain and thin
sect.)
|
Virus count
|
Morphology
|
Purity
Biochemical:
Reverse transcriptase
|
60-70S RNA, total RNA
|
Total protein
|
Gel
analysis of viral and host proteins and nucleic acids
Immunological:
Gel diffusion
|
Complement fixation
|
Immunofluoroescence
(The latter two for with specific
reagents for enveloped and internal antigens gs and env).
Biological:
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
nucleoid...in 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:
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. "...is 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. "...it'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.
CONCLUSION
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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