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COMMENTI sull'isolamento dello HIV
(English)
Bibliografia sull'Aids in fondo all'articolo
 

Nel gennaio 2009 pare sia stato sequenziato il cosiddetto virus HIV - vedi:
http://www.hiv.lanl.gov/content/sequence/HIV/COMPENDIUM/2008/frontmatter.pdf
http://www.hiv.lanl.gov/content/sequence/HIV/mainpage.html
Ma anche se lo hanno "trovato", anche perche nei corpi umani si trova di tutto...., questo NON significa ASSOLUTAMENTE che esso sia la CAUSA dell''AIDS, perche' come bene sappiamo, l'Aids e' una malattia MULTIFATTORIALE, come TUTTE le malattie !

"Il paziente malato di Aids NON muore a causa del virus dell'HIV ma per alterazioni dell'assorbimento intestinale  e quindi per ipoalimentazione  (malNutrizione), dovuta a una grave micosi." (By Dott. Gerhard Orth, Leuthkirch)

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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 oggettivo.
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 malattie.
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.
vedi anche: Le bugie sull'aids

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Comments on "isolation"  -   vedi: AIDS 2 + False le foto del virus HIV
+ L'altra storia dell'Aids
One 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)
The 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 leukaemia. 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.
Because 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.
A 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)
Conversely, 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)
As 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 vivo".(129)
Genomic Investigations
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 cancer.
In 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 proviruses".(80)
In 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).
At 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 with, those of infectious viruses".(80)
Depending 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 RNA, antigens and antibodies to them, is not proof of the presence of infectious particles.
Although 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)
Animal data also shows that new retroviruses may arise by phenotypic mixing, and genetic recombination and deletion.
When 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.
In 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)
According 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 disease.(135,136)
The time and appearance of the viral genome "may be millions of years in germ-line cells and days in somatic cells".(136)
In 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 variability".(137)
Hence, 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 retrovirus, HIV.
Some of these problems can be summarised as follows:
(I).No 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 isolation.(142,146)
(II) There is no correlation between "isolation" of HIV and detection of the HIV genome. Cultures positive for "infectious virus", may be "polymerase chain reaction-negative".(147)
(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 herein, 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 Kaposi's sarcoma 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 rarely, 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 researchers.
To improve detection, the polymerase chain reaction (PCR) method was introduced. However, "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 found, the "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.
Furthermore, 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 (blood donors).
The 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)
(IV) 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".
The "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 Grave's disease 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)
That 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 ConA-activated T-cells".(160)
As 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)
Conclusion
It 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 tests. 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. *
Acknowledgements
We 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.
Dedication
This work is dedicated to the memory of Methodios Papadopulos and Margaret Joan Turner.
Authors:
Eleni Papadopulos-Eleopulos, Physicist
Department of Medical Physics
Royal Perth Hospital
Valendar F. Turner, Staff Specialist
Department of Emergency Medicine
Royal Perth Hospital
John M. Papadimitriou Professor of Pathology
Department of Pathology
University of Western Australia
Correspondence to:
Eleni Papadopulos-Eleopulos
Department of Medical Physics
Royal Perth Hospital
Box X2213 GPO Perth
Captions for figures 0-4.
Figure 0.(left out with publication)
WB patterns with patient sera "and reaction with a strong, weak and non-reactive control". (Reproduced from Bio-Rad Laboratory Manual).
Figure 1.
(A): "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).
(B): 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).

Figure 2.
(A): "Lysates of HTLV-III producer" H4 clone cells, derived from the HUT78 cell line immunoprecipitated with various sera.
(B): "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) Lane 4).
(C): 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.
(D): "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.
Key to sera: (A) AIDS patient; (P) pre-AIDS patient; (h) healthy control; (U) drug user; (H) homosexual control; (Modified from Schubach et al 1984. Science Vol 224:p504).
Figure 3.
WB of one and the same serum specimen tested by 19 laboratories. (From Lundberg GD 1988. JAMA Vol 260:p676).
Figure 4.
Structural model of HIV. From reference 107.

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ù
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