Nel gennaio 2009 pare sia stato sequenziato il
cosiddetto virus HIV - vedi:
Ma anche se
lo hanno "trovato", anche perche nei corpi umani si
trova di tutto...., questo NON significa
ASSOLUTAMENTE che esso sia la
perche' come bene sappiamo, l'Aids e' una malattia
le malattie !
"Il paziente malato di
Aids NON muore a causa del virus
per alterazioni dell'assorbimento intestinale
quindi per ipoalimentazione (malNutrizione),
dovuta a una grave
micosi." (By Dott.
Gerhard Orth, Leuthkirch)
L’HIV NON ESISTE
– CENNI di ISOLAMENTO e PURIFICAZIONE RETROVIRALE
Quando si cerca la verità, il miglior metodo di indagine
è senza dubbio quello utilizzato dagli investigatori,
ovvero cercare le prove e attenersi ad esse:
1 - E’ fondamentale non lasciarsi ingannare dalle
apparenze, che sono spesso fuorvianti.
2 - Non fidarsi delle testimonianze di persone implicate
più o meno da vicino nella questione, soprattutto se ci
sono interessi economici o emotivi che rendono
soggettiva la valutazione di qualcosa che deve rimanere
3 - Cercare chi trae vantaggio dal crimine.
4 - Verificare gli alibi delle persone coinvolte.
5 - E soprattutto controllare punto per punto la
presunta veridicità dei fatti. Come verrà mostrato in
questo articolo, applicando questo metodo per andare
alla ricerca del “criminale misterioso” battezzato Hiv,
le sorprese non mancano certo.
Le APPARENZE INGANNANO
La miriade di scienziati che lavorano quotidianamente
sull’Hiv, così come le migliaia di articoli scientifici
pubblicati sull’argomento, hanno portato la reale prova
dell’esistenza del virus ?
La risposta è: NO !
In effetti, se si dedica il
tempo necessario (e ne serve davvero molto) per
consultare la letteratura scientifica relativa al virus
propriamente detto, si rimane sorpresi dal fatto che
nessuna di queste ricerche sia mai riuscita a mettere
direttamente in evidenza la presenza anche solo di una
minima particella virale, e in particolar modo
retrovirale, in un malato di Aids.
Tuttavia le tecniche necessarie a tal fine sono
classiche e semplici e sono state messe a punto
molto prima delle tecniche di biologia o di genetica
molecolare. Queste tecniche comportano l’isolamento
diretto a partire dal malato e l’infezione delle
cellule coltivate in laboratorio che sono suscettibili
di essere infettate da un particolare virus.
La concentrazione dei virus tramite centrifugazione ad
alta velocità, l’eliminazione dei batteri e dei detriti
cellulari tramite ultrafiltrazione, e l’osservazione
diretta delle particelle virali al microscopio
elettronico sono alla base della virologia classica e
della dimostrazione dell’origine virale di numerose
Visti al microscopio elettronico, tutti i virus sono uno
diverso dall’altro. Le loro differenti famiglie (vaiolo,
herpes, influenza, polio, ecc…) hanno tutte morfologie
proprie e specifiche. La classificazione delle
differenti famiglie di virus è infatti basata
principalmente sulla morfologia delle particelle virali.
Per contro, in una stessa famiglia di virus, le
particelle virali hanno dimensioni e morfologia stabile
e che quindi non lascia spazio ad alcun dubbio né ad
alcuna confusione. Al microscopio elettronico è
impossibile confondere un virus dell’herpes con quello
del vaiolo, ad esempio. i retrovirus sono stati isolati,
purificati e fotografati al microscopio elettronico con
estrema facilità fin dagli anni 60. Com’è possibile,
dunque, che tali prove non esistano per quanto concerne
il presunto Hiv ?
La SCOPERTA del VIRUS
E’ un’équipe dell’Istituto Pasteur diretta da Luc
Montagnier la prima ad aver annunciato la scoperta di
un’attività virale, nel 1983, a partire da prelievi
effettuati su un malato di Aids.
L’anno successivo, l’équipe di Robert Gallo negli USA
fece un annuncio simile. Si scoprirà inseguito che Gallo
aveva utilizzato un campione di colture cellulari
ricevute da Luc Montagnier mesi prima. Stranamente la
stessa cosa è successa a Robin Weiss, il grande
specialista dell’Aids britannico, che fu obbligato ad
ammettere che anche lui aveva usato un campione delle
colture cellulari di Montagnier. Possiamo quindi
constatare che da una parte all’altra dell’Oceano, le
tre équipe più specializzate sul tema, dopo più di due
anni di ricerca, non sono riuscite ad annunciare
nient’altro che una vaga supposizione a partire da
colture cellulari derivanti da uno stesso paziente.
Attenendosi ai dati
oggettivi, nessuna di queste équipe ha mai annunciato di
aver isolato un nuovo virus causa dell’Aids.
Non esiste in tutta la letteratura mondiale un solo
articolo che concluda che un tale retrovirus sia stato
isolato e che questo sia la causa dell’Aids.
Le bugie sull'aids
Visionare questa pagina che
riassume tutto su:
La FRODE SCIENTIFICA del SECOLO: HIV=AIDS - DOCUMENTI
Reportage e documenti aggiornati anno 2015:
False le foto del virus HIV
L'altra storia dell'Aids +
can conclude then that neither the antigen/antibody reaction, nor the particles nor RT can
be considered specific for retroviruses. Even if they were, their finding cannot be
considered as synonymous with the detection of an externally acquired
retrovirus, as is
claimed to be the case for HIV. Such findings may represent the expression of endogenous
retrovirus (vide infra) or other exogenous retrovirus. Lately, "several laboratories
reported retroviral activity [RT, particles] in cells of patients who appear not to be
infected by HIV", an activity said to be "from endogenous retrovirus".(122)
cell line most often used in AIDS research is the leukaemic cell line H9. It is known that
H9 is a clone of HUT78, which was derived from a patient with adult T-cell
Since the causative agent of this leukaemia is accepted to be HTLV-I, another exogenous
retrovirus, the H9 cultures should have both RT and retroviral particles even in the
absence of HIV.
about 25% of AIDS patients have antibodies to HTLV-I, about 25% of cultures should have in
addition to particles and RT, a positive WB to HTLV-I. However, since the proteins from
HIV and HTLV-I share the same molecular weights, the HTLV-I WB bands will appear to be
positive for HIV.
more direct problem associated with the use of "HIV isolation" as a gold
standard is the fact that, irrespective of the various phenomena accepted by AIDS
researchers as representing "HIV isolation", and despite the fact that no effort
has been spared, it is not possible to "isolate HIV" from all antibody positive
patients. The success rate varies between 17% and 80%.(92,93,123)
when the same effort is made, HIV can be isolated from some non-AIDS seronegative
patients, and even from normal seronegative individuals at no risk for HIV
infection.(124,125) With a more recent method used for "HIV isolation",
detection of p24 in cultures with whole unfractionated blood, (126,127) positive results
have been reported in 49/60 (82%) of "presumably uninfected, but serologically
indeterminate" individuals and in 5/5 "seronegative blood donors".(128)
far back as 1988, researchers at the CDC in the USA realised that no correlation exists
between "HIV isolation" and a positive antibody test (which they call documented
infection), and more importantly, between "HIV isolation" in vitro and its
presence in vivo-"correlation between these two methods is limited; they are
inconsistent, in that virus cannot be detected in every person with a documented
infection. Furthermore, the culture technique determines the ability of infected cells to
produce virus in vitro but does not necessarily indicate the status of virus expression in
the decades following Rous' experiments, Rous as well as other researchers performed
similar investigations with several animal species. However, although neoplasia could be
induced by injection of filtrates from tumour tissues, (infectious
retroviruses, exogenous retroviruses), no epidemiological evidence existed to suggest an infectious origin of
1939 Andrews "speculated on the possible activation of latent viral infectious
particles in cancerous tissues", and in 1948 Darlington postulated "that such
viruses [endogenous viruses] could arise from cellular genetic elements which he named
the 1950s and 1960s the following experimental evidence was considered proof of the
proviral hypothesis: (a) healthy animals in which no complete virus could be detected had
viral antigens similar to those of exogenous virus; (b) DNA genomes or partial genomes of
the infectious retroviruses were found to be integrated into the genomes of normal
non-virus producing cells; (c ) "Final proof came with the isolation of infectious
viruses from uninfected cells". Healthy non-virus producing cells when cultured were
found to spontaneously produce viruses.(80) Their appearance and yield could be increased
a millionfold by (i) mitogenic stimulation;(130) (ii) co-cultivation
techniques;(131) (iii) cultivation of cells with supernatant from non-viral producing
cultures.(132) (Note:For HIV isolation, mitogenic stimulation is an absolute
requirement, and in fact, in
most cases, all of the above are employed).
present it is generally accepted that "one of the most striking features that
distinguishes retroviruses from all other animal viruses is the presence, in the
chromosomes of normal uninfected cells, of genomes closely related to, or identical
those of infectious viruses".(80)
on conditions, the provirus genome remains unexpressed or part or all of it may be
expressed. The latter may or may not lead to the assembly of viral particles
(endogenous retrovirus). (80) In other words, the finding of a viral genome (DNA) or even of
antigens and antibodies to them, is not proof of the presence of infectious
most of the above findings are from animal experiments, at present, evidence exists that
"The human genome carries DNA sequences related to endogenous retroviral genomes that
are subdivided into families according to sequence homology. Some are present in only a
few copies, whereas others are present in hundreds to thousands of copies".(133)
data also shows that new retroviruses may arise by phenotypic mixing, and genetic
recombination and deletion.
a cell contains two proviruses, progeny may be found that possess the genome of one but
the structural proteins of either or both viruses present. Conversely, the RNA may be
viral but at least some of the proteins may be cellular.
other instances, the particles do not have a genome at all, or one or more genes are
missing (genetically defective viruses). The genetic mixing can be between viral genomes
or between viral and cellular genes.(80,134)
to distinguished retrovirologists such as Weiss and Temin, new retroviral genomes may
arise by rearrangement of cellular DNA caused by many factors including pathogenic
processes, a view that proposes retroviruses as an effect and not the cause of
time and appearance of the viral genome "may be millions of years in germ-line cells
and days in somatic cells".(136)
addition to the above, the retroviral replicative cycle "involves three distinct
steps: reverse transcription, DNA polymerization, and the synthesis of RNA from a DNA
template (transcription). Any errors made by the polymerase enzyme during the first and
the third steps are not subjected to proof reading, the result being pronounced sequence
as long ago as 1973, it was concluded that the above phenomena "will prove a
stumbling block to any genetic analysis of RNA tumour viruses" (138) (RNA tumour
viruses=retrovirus). To date, the data on the HIV genome has not altered the above
prediction and shows that many problems may exist with the use of the genomic studies in
efforts to prove infection of AIDS patients with a unique exogenous
of these problems can be summarised as follows:
two HIV genomes are the same.(a) No two identical HIV have been isolated even from the
same person. In one case where two sequential isolates were made 16 months
apart, none of
the provirus in the first isolate was found in the second (139) leading one HIV researcher
to conclude "The data imply that there is no such thing as an [AIDS virus]
isolate" (140); (b) from the same person at a given time more than one HIV can be
isolated (141,142); (c ) many, if not all of the proviruses detected in vivo and in vitro
are defective; (143) (d) In one and the same patient, the genomic data in monocytes
differs from that in T-lymphocytes; (144) (e) the genetic data obtained in vitro does not
correlate with the data obtained in vivo-"To culture is to disturb" (145); (f)
The type of virus isolated is determined by the cell types used for HIV
There is no correlation between "isolation" of HIV and detection of the HIV
genome. Cultures positive for "infectious virus", may be "polymerase chain
(III) HIV sequences cannot be found in all
AIDS patients. Gallo and his colleagues, summarising the first hybridisation studies with
fresh tissue concluded: "We have previously been able to isolate HTLV-III from
peripheral blood or lymph node tissue from most patients with AIDS or ARC"
[approximately 50% of patients referred to by Gallo]. "However, as shown
HTLV-III DNA is usually not detected by standard Southern Blotting hybridization of these
same tissues and, when it is, the bands are often faint...the lymph node enlargement
commonly found in ARC and AIDS patients cannot be due directly to the proliferation of
HTLV-III-infected cells...the absence of detectable HTLV-III sequences in
tissue of AIDS patients suggests that this tumor is not directly induced by infection of
each tumor cell with HTLV-III...the observation that HTLV-III sequences are found
if at all, in peripheral blood mononuclear cells, bone marrow, and spleen provides the
first direct evidence that these tissues are not heavily or widely infected with HTLV-III
in either AIDS or ARC".(148) These studies were confirmed by many other
improve detection, the polymerase chain reaction (PCR) method was introduced.
"a striking feature of the results obtained so far" with this
method, as with
the standard hybridisation technique, "is the scarcity or apparent absence of viral
DNA in a proportion of patients"(149) and, when viral RNA or DNA is
"signal" is very low.
For example, HIV is thought to be transmitted primarily by sexual intercourse yet with the PCR
the "HIV genome" can be detected in a minority of semen samples (1/25).(147) It
must be pointed out that a positive PCR, even if found in all patients as is claimed in
some publications, (149) cannot be regarded as signifying the presence of the whole HIV
genome. With the PCR "only small regions may be amplified, a gene at best" (143)
that is, one does not detect the whole viral genome, and, since most HIV
"isolates" to date are defective, detection of part of or a whole gene, or even
several genes, cannot be considered synonymous with the whole HIV genome.
the PCR is not standardised and to date, there has been only one study in which the
reproducibility, sensitivity and specificity of PCR were examined. In this
study, the gold
standard used was serological status. Specificity was determined by measuring the
percentage of negative PCR results in seronegative (ELISA), healthy, low risk individuals
PCR was found not to be reproducible and "false-positive and false negatives results
were observed in all laboratories (concordance with serology ranged from 40% to 100%). In
addition, the number of positive PCR results did not differ significantly between high-
and low-risk seronegatives".(150)
The positive hybridisation results may not be HIV specific. In 1984 when Gallo and his
associates conducted their first hybridisation studies, they found that when the results
were positive, the hybridisation bands were "faint", "low signal".
"low signal" was interpreted as proof that HIV infected individuals contain
provirus in small numbers of peripheral blood mononuclear cells and at low copy
numbers. However, according to Gallo and his associates, "theoretically this low signal
intensity could also be explained by presence of a virus distantly homologous to HTLV-III
in these cells".(148) Data which has come to light since then suggest this
theoretical possibility may be a fact: (a) Although it is no longer accepted that HIV is
transmitted by insects, in 1986 researchers from the Pasteur Institute found HIV DNA
sequences in tsetse flies, black beetles and ant lions in Zaire and the Central African
Republic.(151) (b) In 1984 Gallo's group reported that the genome of HIV hybridises with
the "structural genes (gag, pol, and env) of both HTLV-I and HTLV-II".(152)
Presently available evidence shows that normal human DNA contains retroviral genomic
sequences related to HTLV-I and II.(153,154) (c ) In 1985 Weiss and his colleagues
reported the isolation, from the mitogenically stimulated T-cell cultures of two patients
with common variable hypogammaglobulinaemia, a retrovirus which "was clearly related
to HTLV-III/LAV"; evidence included positive WB with AIDS sera and hybridisation with
HIV probes.(155) (d) DNA extracted from thyroid glands from patients with
hybridises with "the entire gag p24 coding region" of HIV.(156) (e) Horowitz et
al, "describe the first report of the presence of nucleotide sequences related to
HIV-1 in human, chimpanzee and Rhesus monkey DNAs from normal uninfected
individuals". They have "demonstrated the presence of a complex family of HIV-1
related sequences" in the above species, and concluded that "Further analysis of
members of this family will help determine whether such endogenous sequences contributed
to the evolution of HIV-1 via recombination events or whether these elements either
directly or through protein products, influence HIV pathogenesis".(157)
the positive hybridisation signals may be due to such events induced by the oxidative
agents (mutagens and mitogens) to which the AIDS risk groups and the cultures are exposed
is suggested by the following: A positive PCR reverts to negative when exposure to risk
factors is discontinued (158,159), and monocytes from HIV+ patients in which no HIV DNA
can be detected, even by PCR, become positive for HIV RNA after cocultivation with normal
far back as 1989 researchers at the Pasteur Institute concluded that "the task of
defining HIV infection in molecular terms will be difficult".(145) They confirmed
their conclusion in a recent study where they "described the enormous heterogeneity
found in vivo within HIV-1 populations" and the possibility "that an HIV carrier
may harbour easily in excess of 1010 proviruses, most of which will be genetically
unique". They conclude: "It is therefore possible that the sheer size of
variants within an infected individual will allow HIV to explore totally new genetic
possibilities". The appearance of "radically different genetic" retroviral
structures may be the result of "rearrangement, duplication, deletion or
hypermutation. The transduction of host cell DNA represents possibly the most startling
genetic trait of retroviruses".(161)
is axiomatic that the use of antibody tests must be verified against a gold standard. The
presently available data fail to provide such a gold standard for the HIV antibody
The inescapable conclusion from the above discussion is that the use of HIV antibody tests
as predictive, diagnostic and epidemiological tools for HIV infection needs to be
carefully reappraised. *
wish to thank all our colleagues and especially Udo SchEklenk, Barry Page, Bruce
Hedland-Thomas, David Causer, Richard Fox, John Peacock, David
Prentice, Ronald Hirsch,
Patricia Shalala, Keith Jones, Alun Dufty, June Rider Jones, Coronary Barrow, Dorothy
Davis, Julian Smith, Mark Strahan, Vincent Turner, Wallace Turner and Graham Drabble for
their continued support and assistance.
work is dedicated to the memory of Methodios Papadopulos and Margaret Joan
Eleni Papadopulos-Eleopulos, Physicist
Department of Medical Physics
Royal Perth Hospital
F. Turner, Staff Specialist
Department of Emergency Medicine
Royal Perth Hospital
M. Papadimitriou Professor of Pathology
Department of Pathology
University of Western Australia
Department of Medical Physics
Royal Perth Hospital
Box X2213 GPO Perth
for figures 0-4.
0.(left out with publication)
patterns with patient sera "and reaction with a strong, weak and non-reactive
control". (Reproduced from Bio-Rad Laboratory Manual).
"Cord blood T-lymphocytes infected with virus" (HIV-1) were lysed and the
supernatant of a 10,000g centrifugation of the cell lysate was immunoprecpitated with sera
from patients with lymphadenopathy (P); a healthy donor (h); goat antiserum to HTLV-I p24
(G); normal goat serum (g).
As 1A but cells infected with HTLV-I instead of HIV-1. 2C: The cell free supernatant from
the cultures of "cord blood T-lymphocytes infected with virus" (HIV-1) was
ultracentrifuged for one hour at 50,000 rev/min.The pellett was banded in sucrose density
gradients. Material which banded at 1.16gm/ml (the complete virus) was immunoprecipitated
with the above sera but instead of normal goat serum, serum from another healthy donor (h)
was used. Although in the published strips it is hard if not impossible to distinguish any
bands, in the text, it is stated that "three major proteins could be
seen: the p25
protein and proteins with molecular weights of 80,000 and 45,000" (Modifed from
BarrG-Sinoussi et al. Science Vol 220:p870).
"Lysates of HTLV-III producer" H4 clone cells, derived from the HUT78 cell line
immunoprecipitated with various sera.
"Lysates of HTLV-III producer" H17 clone cells also derived from the HUT78 cell
line, immunoprecipitated with various sera; (the serum in B lane 2 is identical to (A)
Lysates of H17 and H4 clones (b) "before" and (a) "after infection",
immunoprecipitated with serum from a male heterosexual drug user with lymphandenopathy and
thrombocytopenia (pre-AIDS). This is the same serum as (B) Lane 5.
"Lysates of H4/HTLV-III... cells" (C), or "virus purified from the cells
culture fluids", (V), using (I)-same serum as (B) Lane 5; (II)-serum from a patient
with pre-AIDS; (III) serum from a patient with AIDS. This is the same serum as (B) Lane 4.
to sera: (A) AIDS patient; (P) pre-AIDS patient; (h) healthy control; (U) drug
homosexual control; (Modified from Schubach et al 1984. Science Vol 224:p504).
of one and the same serum specimen tested by 19 laboratories. (From Lundberg GD 1988. JAMA
model of HIV. From reference 107.
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