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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