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.
- Bibliografia sull'AIDS
1. Ratner, L., Haseltine, W., Patarca, R.P. et al. 1985. Complete nucleotide sequence of the
AIDS virus, HTLV-III. Nature 313:277-284.
2. Hausmann, E.H.S., Gelderblom, H.R., Clapham, P.R. et al. 1987. Detection of HIV envelope
specific antibodies by immunoelectron microscopy and correlation with antibody titer and
virus neutralizing activity. J. Virol. Meth. 16:125-137.
3. Pinter, A., Honnen, W.J., Tilley, S.A. et al. 1989. Oligomeric Structure of gp41,the
Transmembrane Protein of Human Immunodeficiency Virus Type 1. J. Virol. 63:2674-2679.
4. BarrG-Sinoussi, F., Chermann, J.C., Rey,
F. et al. 1983. Isolation of a T-Lymphotrophic Retrovirus from a patient at Risk for
Acquired Immune Deficiency
(AIDS). Science 220:868-871.
5. SchEpbach, J., Popovic, M., Gilden, R.V. et al. 1984. Serological analysis of a Subgroup
of Human T-Lymphotrophic Retroviruses (HTLV-III) Associated with AIDS. Science
6. Damsky, C.H., Sheffield, J.B., Tuszynski, G.P. et al. 1977. Is there a role for Actin in
Virus Budding? J. Cell. Biol. 75:593-605.
7. Stanislawsky, L., Mongiat, F., Neto, V.M. et al 1984. Presence of Actin in
Oncornaviruses. Biochem. Biophys. Res. Com. 118:580-586.
8. Papadopulos-Eleopulos, E., Turner, V.F. and Papadimitriou, J.M. 1992. Oxidative stress,
HIV and AIDS. Res. Immunol. 143:145-148.
9. Hinshaw, D.B., Burger, J.M., Beals, T.F. et al. 1991. Actin polymerization in cellular
oxidant injury. Arch. Biochem. Biophys. 228:311-316.
10. Bach, M.A., Lewis, D.E., McClure, J.E. et al. 1986. Monoclonal Anti-actin Antibody
Recognizes a Surface Molecule on Normal and Transformed Human B Lymphocytes:Expression
Varies with Phase of Cell Cycle. Cell. Immunol. 98:364-374.
11. Stricker, R.B., Abrams, D.I., Corash, L. et al. 1985. Target Platelet Antigen in
Homosexual Men with Immune Thrombocytopenia. NEJM 313:1375-1380.
12. Henderson, L.E., Sowder, R., Copeland, T.D. et al. 1987. Direct Identification of Class II
Histocompatibility DR Proteins in Preparations of Human T-Cell Lymphotropic Virus Type
III. J. Virol. 61:629-632.
13. Wong-Staal, F. and Gallo, R.C. 1985. Human T-lymphotropic retroviruses. Nature
14. Genesca, J., Jett, B.W., Epstein, J.S. et al. 1989. What do Western Blot indeterminate
patterns for Human Immunodeficiency Virus mean in EIA-negative blood donors? Lancet
15. Ranki, A., Johansson, E. and Krohn, K. 1988. Interpretation of Antibodies Reacting Solely
with Human Retroviral Core Proteins. NEJM 318:448-449.
16. Delord, B., Ottmann, M., Schrive, M.H. et al. 1991. HIV-1 expression in 25 infected
patients:A comparison of RNA PCR, p24 EIA in Plasma and in situ Hybridization in
mononuclear cells, p113. In: Vol. I, Abstracts VII International Conference on
17. Todak, G., Klein, E., Lange, M. et al. 1991. A clinical appraisal of the p24 Antigen test,
p326. In:Vol. I, Abstracts VII International Conference on AIDS,Florence.
18. Courouce, A., Muller, J. and Richard, B. 1986. False-Positive Western Blot Reactions to
Human Immunodeficiency Virus in Blood Donors. Lancet II:921-922.
19. Stricker, R.B., McHugh, T.M., Moody, D.J. et al. 1987. An AIDS-related Cytotoxic
autoantibody reacts with a specific antigen on stimulated CD4+ T cells. Nature
20. Chassagne, J., Verelle, P., Fonck, Y. et al. 1986. Detection of the
Lymphadenopathy-Associated Virus p18 in cells of patients with Lymphoid Diseases using a
Monoclonal Antibody. Ann. Inst. Pasteur/Immunol. 137D:403-408.
21. Parravicini, C.L., Klatzmann, D., Jaffray, P. et al. 1988. Monoclonal Antibodies to the
human immunodeficiency virus p18 protein cross-react with normal human
22. Matsiota, P., Chamaret, S., Montagnier, L. et al. 1987. Detection of Natural
Autoantibodies in the serum of Anti-HIV Positive-Individuals. Ann. Inst.
23. Popovic, M., Sarngadharan, M.G., Read, E. et al 1984. Detection,
Production of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and
24. Wilber, J.C. 1991. New Developments in Diagnosing Infections, p.1-15. In:AIDS Clinical
Review, P. Volbering, M.A. Jacobson (Eds.). Marcel Dekker Inc. New York.
25. Lundberg, G.D. 1988. Serological Diagnosis of Human Immunodeficiency Virus Infection by
Western Blot Testing. JAMA 260:674-679.
26. Zolla-Pazner, S., Gorny, M.K. and Honnen, W.J. 1989. Reinterpretation of Human
Immunodeficiency Virus Western Blot Patterns. NEJM 320:1280-1281.
27. Burke, D.S. 1989. Laboratory Diagnosis of Human Immunodeficiency Virus
Lab. Med. 9:369-392.
28. Maskill, W.J. and Gust, I.D. 1992. HIV-1 Testing in Australia. Australian Prescriber
29. DeCock, K.M., Selik, R.M., Soro, B. et al. 1991. AIDS surveillance in Africa:a reappraisal
of case definitions. BMJ 303:1185-1189.
30. Voevodin, A. 1992. HIV screening in Russia. Lancet 339:1548.
Working Group on AIDS Case Definition 1990. Epidemiol. Bull. 4:9-11.
32. Edwards, V.M., Mosley, J.W. and the Transfusion Safety Study Group. 1991. Reproducibility
in Quality Control of Protein (Western) Immunoblot Assay for Antibodies to Human
Immunodeficiency Virus. Am. J. Clin. Pathol. 91:75-78.
33. CDC. 1989. Interpretation and Use of the Western Blot Assay for Serodiagnosis of Human
Immunodeficiency Virus Type 1 Infections. MMWR 38 No. S-7:1-7.
Weiss, S.H., Goedert, J.J., Sarngadharan, M.G. et al. 1985. Screening Test for HTLV-III
(AIDS Agent) Antibodies. JAMA 253:221-225.
35. Weiss, R. and Thier, S.O. 1988. HIV testing is the answer-what's the question? NEJM
D.S., Brundage, J.F., Redfield, R.R. et al. 1988. Measurement of the False Positive Rate
in a Screening Program for Human Immunodeficiency Virus Infections. NEJM 319:961-964.
Scarlatti, G.S., Lombardi, V., Plebani, A. et al. 1991. Polymerase chain reaction, virus
isolation and antigen assay in HIV-1-antibody-positive mothers and their children. AIDS
Griner, P.F., Mayewski, R.J., Mushlin, A.I. et al. 1981. Selection and Interpretation of
Diagnostic Tests and Procedures. Ann. Int. Med. 94 (Part 2):559-563.
39. CDC. 1987. Revision of the CDC
Surveillance Case Definition for Acquired
Syndrome. JAMA 258:1143-1145.
Conley, C.L. and Savarese, D. 1989. Biologic False-Positive Serologic Tests for Syphilis
and Other Serologic Abnormalities in Autoimmune Hemolytic Anemia and Thromobocytopenic
Purpura. Medicine 68:67-84.
Boue, F., Dreyfus, M., Bridley, F. et al. 1990. Lupus anticoagulant and HIV infection:a
prospective study. AIDS 4:467-471.
Jaffe, J.H., Moore, J.D., Cone, E.J. et al. 1986. HTLV-III Seropositivity in 1971-1972
Parenteral Drug Abusers-A case of false Positives or Evidence of Viral Exposure? NEJM
Biggar, R.J., Gigase, P.L., Melbye, M. et al. 1985. ELISA HTLV Retrovirus Antibody
Reactivity Associated with Malaria and Immune Complexes in Healthy Africans. Lancet
Ternynck, T. and Avrameas, S. 1986. Murine Natural Monoclonal Autoantibodies: A Study of
their Polyspecificities and their Affinities. Immunol. Rev. 94:99-112.
Pateraki, E., Kaklamani, E., Portocalas, K.R. et al. 1986. Autoantibodies in systemic
lupus erythematosus and normal subjects. Clin. Rheumatol. 5:338-345.
Morton, D.L. and Malmgren, R.A. 1968. Human Osteosarcomas:Immunologic Evidence suggesting
an associated agent. Science 162:1279-1281.
Hirshaut, Y., Pei, D.T., Marcove, R.C. et al. 1974. Seroepidemiology of Human Sarcoma
Antigen (S1). NEJM 291:1103-1107.
Kurth, R., Teich, N.M., Weiss, R. et al. 1977. Natural human antibodies reactive with
primate type-C viral antigens. Proc. Natl. Acad. Sci. 74:1237-1241.
Snyder, H.W. and Fleissner, E. 1980. Specificity of human antibodies to oncovirus
glycoproteins:Recognition of antigen by natural antibodies directed against carbohydrate
structures. Proc. Natl. Acad. Sci. 77:1622-1626.
Barbacid, M., Bolognesi, D. and Aaronson, S.A. 1980..Humans have antibodies capable of
recognizing oncoviral glycoproteins:Demonstration that these antibodies are formed in
response to cellular modification of glycoproteins rather than as consequence of exposure
to virus. Proc. Natl. Acad. Sci. 77:1617-1621.
Essex, M., McLane, M.F., Lee, T.H. et al. 1983. Antibodies to Cell Membrane Antigens
Associated with Human T-Cell Leukemia Virus in Patients with AIDS. Science 220:859-862.
Novick, D.M., Des Jarlais, D.C., Kreek, M.J. et al. 1988. Specificity of Antibody Tests
for Human Immunodeficiency Virus in Alcohol and Parenteral Drug Abusers with Chronic Liver
Disease. Alcoholism Clin Exp Res 12:687-690.
European Collaborative Study. 1991. Children born to women with HIV-1 infection:natural
history and risk of transmission. Lancet 337:253-260.
Beneviste, R.E., Ochs, H.D., Fischer, S.H. et al. 1986. Screening for antibodies to
LAV/HTLV-III in recipients of immunoglobulin preparations. Lancet I:1090-1092.
Burinsky, K.I., Chaplinskas, S.A., Syrtsev, V.A. et al. 1988. Reactivity to gag- and
env-related sequences in immunoblot assay is not necessarily indicative of HIV infection.
Calabrese, L.H. 1988. Autoimmune Manifestations of Human Immunodeficiency Virus (HIV)
Infection. Clin. Lab. Med. 8:269-279.
Bonara, P., Maggioni, L. and Colombo, G. 1991. Anti-Lymphocyte Antibodies and Progression
of Disease in HIV Infected Patients,p.149. In:Vol. II, VII International Conference on
Tumietto, F., Costigliola, P., Ricchi, E. et al. 1991. Anti-Lymphocyte
Auto-antibodies:Evaluation and correlation with different stages of HIV Infection,p149.
In:Vol. II, VII International Conference on AIDS,Florence.
Morozov, V.A., Ilyinskii, P.O., Uckert, W.A. et al. 1989. Antibodies to structural and
nonstructural gag-coded proteins of type-D retroviruses in human with lymphadenopathy and
AIDS. Int. J. Tiss. Reac. XI:1-5.
Lucey, D.R., Hendrix, C.W., Andrzejewski, C. et al. 1992. Comparison by Race of Total
Serum IgG,IgA,and IgM with CD4+ T-Cell Counts in North American Persons Infected with the
Human Immunodeficiency Virus Type 1. J. Acquir. Immun. Defic. Syndr. 5:325-332.
Papadopulos-Eleopulos, E. 1988. Reappraisal of AIDS:Is the oxidation induced by the risk
factors the primary cause? Med. Hypotheses 25:151-162
Papadopulos-Eleopulos, E., Turner, V.F. and Papadimitriou, J. 1992. Kaposi's sarcoma and
HIV. Med. Hypotheses 39:22-29.
Igel, H.J., Turner, H.C., Kotin, P. et al. 1969. Mouse Leukaemia Virus Activation by
Chemical Carcinogens. Science 166:624-1626.
C. 1988. Cocaine and HIV Seropositivity. Lancet I:1052-1053.
Kion, T.A. and Hoffmann, G.W. 1991. Anti-HIV and Anti-Anti-MHC Antibodies in Alloimmune
and Autoimmune Mice. Science 253:1138-1140.
Conley, L.J. and Holmerg, S.D. 1992. Transmission of AIDS from blood screened negative for
antibody to the human immunodeficiency virus. NEJM 326:1499.
Burgher, H., Weiser, B., Robinson, W.S. et al. 1985. Transient Antibody to
Lymphadenopathy-Associated/Human T-Lymphotrophic Virus Type III and T-Lymphocyte
Abnormalities in the Wife of a Man who Developed the Acquired Immunodeficiency Syndrome.
Ann. Int. Med. 103:545-547.
Esteva, M.H., Blasini, A.M., Ogly, D. and Rodriguez, M.A. 1992. False positive results
from antibody to HIV in two men with systemic lupus erythrematosus. Ann. Rhem. Dis.
Dummer, J.S., Erb, S., Breinig, M.K. et al. 1989. Infection with Human Immunodeficiency
Virus in the Pittsburgh Transplant Population. Transplantation 47:134-139.
Pitchenik, A.E., Burr, J., Suarez, M. et al. 1987. Human T-Cell Lymphotrophic Virus-III
(HTLV-III) Seropositivity and Related Disease Among 71 Consecutive Patients in Whom
Tuberculosis was Diagnosed. Am. Rev. Respir. Dis. 135:875-879.
Nzilambi, N., Mann, J.M., Francis, H. et al. 1986. Seroprevalence among tuberculosis
patients in Zaire. In:Abstracts II International AIDS Conference, Paris, No.105:S17b.
St.Louis, M.E., Rauch, K.J., Peterson, L.R. et al. 1990. Seroprevalence rates of Human
Immunodeficiency Virus Infection at Sentinel Hospitals in the United States. NEJM
Chamberland, M., Conley, L. and Dondero, T. 1988. Epidemiology of heterosexually acquired
AIDS-United States, p.264. In:Abstacts IV International AIDS Conference,Stockholm.
York City AIDS Surveillance Report, January-March 1992.
Rodriquez, L., Dewhurst, S., Sinangil, F. et al. 1985. Antibodies to HTLV-III/LAV among
Aboriginal Amazonian Indians in Venezuela. Lancet II:1098-1100.
Volsky, D.J., Wu, Y.T., Stevenson, M. et al 1986. Antibodies to HTLV-III/LAV in Venezuelan
patients with acute malarial syndromes. NEJM 314:647.
Rous, P. 1911. A Sarcoma of the Fowl transmissible by an agent separable from the Tumor
Cells. J. Exp. Med. 13:397-411.
Toplin, I. 1973. Tumor Virus Purification using Zonal Rotors. Spectra No. 4:225-235.
Temin, H.M. and Baltimore, D. 1972. RNA-Directed DNA Synthesis and RNA Tumor Viruses. Adv.
Vir. Res. 17:129-186.
RNA Tumor Viruses. 1982. R. Weiss, N. Teich, H. Varmus, J. Coffin (Eds.).Cold Spring
Harbor Laboratory. Cold Spring Harbor, New York.
Bader, J.P. 1975. Reproduction of RNA Tumor Viruses, p.253-331. In:Comprehensive Virology
Vol.4. H. Fraenkel-Conrat, R.R. Wagner (Eds.). Plenum Press, New York.
Sinoussi, F., Mendiola, L., Chermann, J.C. et al. 1973. Purification and partial
differentiation of the particles of murine sarcoma virus (M. MSV) according to their
sedimentation rates in sucrose density gradients. Spectra No. 4:237-243.
Amiesen, J.C. and Capron, A. 1991. Cell dysfunction and depletion in AIDS: the programmed
cell death hypothesis. Immunol. Today 12:102-105.
Wyllie, A.H., Kerr, J.F.R. and Currie, A.R. 1980. Cell Death:The Significance of
Apoptosis. Int. Rev. Cytol. 68:252-306.
Hoxie, J.A., Fitzharris, T.P., Youngbar, P.R. et al. 1987. Nonrandom Association of
Cellular Antigens with HTLV-III Virions. Hum. Immunol. 18:39-52.
McKeating, J.A. and Moore, J.P. 1991. HIV infectivity. Nature 349:660.
Masquelier, B., Combeau, T. and Poveda, J. 1991. In Vitro Assays Show a Dissociation of
Reverse Transcriptase Activity and Core Antigen (p24) Production in Two HIV-1 Isolates
from a Patient Receiving Long-Term Treatment with Zidovudine (ZDV). J. Acquir. Immun.
Defic. Syndr. 4:499-505.
Grunow, R., Valentin, A., Fenyo, E.M. et al. 1991. Release of HIV-1 core protein from
infected cells independent of infectious virus particles, p.157. In:Vol. I, Abstracts VII
International Conference on AIDS,Florence.
Tedder, R.S., Semple, M.G., Tenant-Flowers, M. et al. 1992. HIV, AIDS, and zidovudine.
Lemaetre, M., GuGtard, D., HGnin, Y. et al. 1990. Protective Activity of Tetracycline
Analogs against the Cytopathic effect of the Human Immunodeficiency Viruses in CEM Cells.
Res. Virol. 141:5-16.
Boulerice, F., Bour, S., Geleziunas, R. et al. 1990. High Frequency of Isolation of
Defective Human Immunodeficiency Virus Type 1 and Heterogeneity of Viral Gene Expression
in Clones of Infected U-937 Cells. J. Virol. 64:1745-1755.
Ehrnst, A., Sonnerborg, A., Bergdahl, S. and Strammegard, O. 1988. Efficient Isolation of
HIV From Plasma During Different Stages of HIV Infection. J. Med. Virol. 26:23-32.
Learmont, J., Tindall, B., Evans, L. et al. 1992. Long-term symptomless HIV-1 infection in
recipients of blood products from a single donor. Lancet 340:863-867.
Popovic, M., Sarngadharan, M.G., Read, E. et al. 1984. Detection, Isolation, and
Continuous Production of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and
Pre-AIDS. Science 224:497-500.
Gallo, R.C., Sarin, P.S. and Wu, A.M. 1973. On the nature of the Nucleic Acids and RNA
Dependent DNA Polymerase from RNA Tumor Viruses and Human Cells, p.13-34. In:Possible
Episomes in Eukaryotes. L.G. Silvestri (Ed.). North-Holland Publishing Company, Amsterdam.
Whitkin, S.S., Higgins, P.J. and Bendich, A. 1978. Inhibition of reverse transcriptase and
human sperm DNA polymerase by anti-sperm antibodies. Clin. Exp. Immunol. 33:244-251.
Tomley, F.M., Armstrong, S.J., Mahy, B.W.J. and Owen, L.N. 1983. Reverse transcriptase
activity and particles of retroviral density in cultured canine lymphosarcoma
supernatants. Br. J. Cancer 47:277-284.
Weissbach, A., Baltimore, D., Bollum, F. et al. 1975. Nomenclature of Eukaryotic DNA
Polymerases. Science 190:401-402.
Gallo, R.C., Wong-Staal, F., Reitz, M. et al. 1976. Some Evidence For Infectious Type-C
Virus in Humans, p.385-407. In:Animal Virology. D. Baltimore, A. S. Huang, C.F. Fox
(Eds.). Academic Press Inc., New York.
Panem, S., Prochownik, E.V., Reale, F.R. et al. 1975. Isolation of Type C Virions from a
Normal Human Fibroblast Strain. Science 189:297-299.
Panem, S., Prochownik, E.V., Knish, W.M. and Kirsten, W.H. 1977. Cell Generation and
Type-C Virus Expression in the Human Embryonic Cell Strain HEL-12. J. Gen. Virol.
Panem, S. 1979. C Type Virus Expression in the Placenta. Curr. Top. Pathol. 66:175-189.
Sarngadharan, M.G., Robert-Guroff, M. and Gallo, R.C. 1978. DNA Polymerases of Normal and
Neoplastic Mammalian Cells. Biochim. Biophys. Acta. 516:419-487.
Klatzmann, D., BarrG-Sinoussi, F., Nugeyre, M.T. et al. 1984. Selective Tropism of
Lymphadenopathy Associated Virus (LAV) for Helper-Inducer T Lymphocytes. Science
Montagnier, L. 1985. Lymphadenopathy-Associated Virus:From Molecular Biology to
Pathogenicity. Ann. Int. Med. 103:689-693.
Gendelman, H.E., Orenstein, J.M., Martin, M.A. et al 1988. Efficient Isolation and
Propagation of Human Immunodeficiency Virus on Recombinant Colony-Stimulating Factor
1-Treated Monocytes. J. Exp. Med. 167:1428-1441.
Gelderblom, H.R., Hausmann, E.H.S., tzel, M. et al. 1987. Fine Structure of Human
Immunodeficiency Virus (HIV) and Immunolocalization of Structural Proteins. Virol.
Gelderblom, H., Reupke, H., Winkel, T. et al. 1987. MHC-Antigens:Constituents of the
Envelopes of Human and Simian Immunodeficiency Viruses. Z. Naturforsch. 42C:1328-1334.
Gelderblom, H.R., Reupke, H. and Pauli, G. 1985. Loss of envelope antigens of
HTLV-III/LAV, a factor in AIDS pathogenesis? Lancet II:1016-1017.
Neidrig, M., Rabanus, J.P., L'Age Stehr, J. et al. 1988. Monoclonal Antibodies Directed
against Human Immunodeficiency Virus (HIV) gag Proteins with Specificity for Conserved
Epitopes in HIV-1, HIV-2 and Simian Immunodeficiency Virus. J. Gen. Virol. 69:2109-2114.
Gelderblom, H.R., tzel, M., Hausmann, E.H.S. et al. 1988. Fine Structure of Human
Immunodeficiency Virus (HIV),Immunolocalization of Structural Proteins and Virus-Cell
Relation. Micron Microsc. 19:41-60.
Meerloo, T., Parmentier, H.K., Osterhaus, A. et al. 1992. Modulation of cell surface
molecules during HIV-1 infection of H9 cells. An immunoelectron microscopic study. AIDS
Lecatsas, G. and Taylor, M.B. 1986. Pleomorphism in HTLV-III,the AIDS virus. S. Afr. Med.
Hockley, D.J., Wood, R.D., Jacobs, J.P. et al. 1988. Electron Microscopy of Human
Immunodeficiency Virus. J. Gen.
Dourmashkin, R.R., O'Toole, C.M., Bucher, D. and Oxford, J.S. 1991.The presence of budding
virus-like particles in human lymphoid cells used for HIV cultivation. p.122. In:Vol. I,
Abstracts VII International Conference on AIDS,Florence.
Brennan, J.K., Lichtman, M.A., Chamberlain, J.K. and Leblond, P. 1976. Isolation of
Variant Lymphoma Cells with Reduced Growth Requirements for Extracellular Calcium and
Magnesium and Enhanced Oncogenicity. Blood 47:447-459.
Garry, R.F., Fermin, C.D., Hart, D.J. et al. 1990. Detection of a Human Intracisternal
A-Type Retroviral Particle Antigenically Related to HIV. Science 250:1127-1129.
Armstrong, J.A. and Horne, R. 1984. Follicular Dendritic Cells and Virus-Like Particles in
AIDS-Related Lymphadenopathy. Lancet II:370-372.
Tenner-Racz, K., Racz, P., Bofill, M. et al. 1986. HTLV-III/LAV Viral Antigens in Lymph
Nodes of Homosexual Men With Persistent Generalized Lymphadenopathy and AIDS. Am. J.
Le Tourneau, A., Audouin, J.,Diebold, J. et al. 1986. LAV-like Viral Particles in Lymph
Node Germinal Centers in Patients with the Persistent Lymphadenopathy Syndrome and the
Acquired Immunodeficiency Syndrome-related Complex. Hum. Pathol. 17:1047-1053.
O'Hara, C.J., Groopmen, J.E. and Federman, M. 1988. The Ultrastructural and
Immunohistochemical Demonstration of Viral Particles in Lymph Nodes from Human
Immunodeficiency Virus-Related Lymphadenopathy Syndromes. Hum. Pathol. 19:545.
Culliton, B.J. 1992. The mysterious virus called "isn't". Nature 358:619.
Chiodi, F., Albert, J., Olausson, E. et al. 1988. Isolation Frequency of Human
Immunodeficiency Virus from Cerebrospinal Fluid and Blood of Patients with Varying
Severity of HIV Infection. AIDS Res. Hum. Retroviruses 4:351-358.
Salahuddin, S.Z., Groopman, J.E., Markham, P.D. et al. 1984. HTLV-III Symptom-Free
Seronegative Persons. Lancet II:1418-1420.
Boussin, F.,Rey, F., Dormont, D. et al. 1988. Isolation of HIV in a Seronegative Demented
Patient Without Symptoms of Immune Deficiency. Cancer Detect. Prev. 12:257-265.
Bayliss, G.J., Jesson, W.J., Evans, B.A. et al. 1989. Isolation of HIV-1 from small
volumes of heparinized whole blood. AIDS 3:45-49.
Fiore, J.R., Angarano, G., Fico, C. et al. 1990. Cell cultures from small amounts of
heparinized whole blood enhance HIV-1 isolation rate. AIDS 4:1295-1296.
SchEpbach, J., Jendis, J.B., Bron, C. et al. 1992. False-positive HIV-1 virus cultures
using whole blood. AIDS 6:1545-1546.
Hart, C., Spira, T., Moore, J. et al. 1988. Direct Detection of HIV RNA Expression in
Seropositive Subjects. Lancet II:596-599.
Aaronson, S.A., Todaro, G.J. and Scholnick, E.M. 1971. Induction of murine C-type viruses
from clonal lines of virus-free BALB/3T3 cells. Science 174:157-159.
Hirsch, M.S., Phillips, S.M., Solnik, C. et al. 1972. Activation of Leukemia Viruses by
Graft-Versus-Host and Mixed Lymphocyte Reactions In Vitro. Proc. Nat. Acad. Sci.
Toyoshima, K. and Vogt, P.K. 1969. Enhancement and Inhibition of Avian Sarcoma Viruses by
Polycations and Polyanions. Virol. 38:414-426.
Nakamura, N., Sugino, H., Takahara, K. et al. 1991. Endogenous retroviral LTR DNA
sequences as markers for individual human chromosomes. Cytogenet. Cell Genet. 57:18-22.
Varmus, H. and Brown, P. 1989. Retroviruses, p.53-108. In:Mobile DNA. D.E. Berg, M.M. Howe
(Eds.). American Society for Microbiology. Washington, D.C.
Weiss, R.A., Friis, R.R., Katz, E. et al. 1971. Induction of Avian Tumor Viruses in Normal
Cells by Physical and Chemical Carcinogens. Virol. 46:920-938.
Temin, H.M. 1974. On the origin of RNA Tumor Viruses. Harvey Lect. 69:173-197.
Wain-Hobson, S. and Myers, G. 1990. Too close for Comfort. Nature 347:18.
Genetics of RNA Tumour Viruses. 1973. p.656-699. In:The Molecular Biology of Tumour
Viruses. J. Tooze (Ed.). Cold Spring Harbor Laboratory, Cold Spring Harbor, New York.
Saag, M.S., Hahn, B.H., Gibbons, J. et al. 1988. Extensive Variation of Human
Immunodeficiency Virus Type-1 in vivo. Nature 334:440.
Marx, J.L. 1988. The AIDS Virus Can Take On Many Guises. Science 241:1039-1040.
von Briesen, H., Becker, W.B., Henco, K. et al. 1987. Isolation frequency and growth
properties of HIV-Variants:Multiple simultaneous variants in a patient demonstrated by
molecular cloning. J. Med. Virol. 23:51-66.
Bolton, V., Pedersen, N.C., Higgins, J. et al. 1987. Unique p24 Epitope Marker To Identify
Multiple Human Immunodeficiency Virus Variants in Blood from the Same Individuals. J.
Clin. Microbiol. 25:1411-1415.
Wain-Hobson, S. 1989. HIV genome variability in vivo. AIDS 3:S13-S18.
Innocenti, P., Ottmann, M., Morand, P. et al. 1992. HIV-1 Blood Monocytes: Frequency of
Detection of Proviral DNA Using PCR in Comparison with the Total CD4 Count. AIDS Res. Hum.
Meyerhans, A., Cheynier, R., Albert, J. et al. 1989. Temporal Fluctuations in HIV
quasispecies in vivo are not reflected by sequential HIV isolations.Cell 58:901-910.
Robey, W.G., Nara, P.L., Poore, C.M. et al. 1987. Rapid Assessment of Relationships Among
HIV Isolates by Oligopeptide Analyses of External Envelope Glycoproteins. AIDS Res. Hum.
Van Voorhis, B.J., Martinez, A., Mayer, K. and Anderson, D.J. 1991. Detection of human
immunodeficiency virus type 1 in semen from seropositive men using culture and polymerase
chain reaction deoxyribonucleic acid amplification techniques. Fertil. Steril. 55:588-594.
Shaw, G.M., Hahn, B.H., Suresh, K.A. et al. 1984. Molecular Characterization of Human
T-Cell Leukemia (Lymphotropic) Virus Type III in the Acquired Immune Deficiency Syndrome.
Simmonds, P., Balfe, P., Peutherer, J.F. et al.1990. Human Immunodeficiency Virus-Infected
Individuals Contain Provirus in Small Numbers of Peripheral Mononuclear Cells and at Low
Copy Numbers. J. Virol. 64:864-872.
Defer, C., Agut, H., and Garbarg-Chenon, A. 1992. Multicentre quality control of
polymerase chain reaction for detection of HIV DNA. AIDS 6:659-663.
Becker, J.L., Hazan, U., Nugeyre, M. T. et al. 1986. Infection of insect lines by HIV,
agent of AIDS, and evidence for HIV proviral DNA in insects from Central Africa. C. R.
Acad. Sci. Paris. 300:303-306.
Arya, S.K., Gallo, R.C., Hahn, B.H. et al. 1984. Homology of Genome of AIDS-Associated
Virus with Genomes of Human T-cell Leukemia Viruses. Science 225:927-930.
Mager, D.L. and Freeman, J.D..1987. Human Endogenous Retroviruslike Genome with Type C pol
Sequences and gag Sequences Related to Human T-Cell Lymphotropic Viruses. J. Virol.
154 Banki, K., Maceda, J., Hurley, E. et al. 1992. Human T-cell lymphotropic virus
(HTLV)-related endogenous sequence, HRES-1 encodes a 28-kDa
protein:A possible autoantigen
for HTLV-I gag-reactive autoantibodies. Proc. Natl. Acad. Sci. 89:1939-1943.
155. Webster, A.D.B., Dalgleish, A.G., Beattie, R. et al. 1986. Isolation of retroviruses from
two patients with "Common Variable" Hypogammaglobulinaemia. Lancet I:581-582.
156. Ciampolillo, A., Marini, V. and Buscema, M. 1989. Retrovirus-like Sequences in Graves'
Disease:Implications for Human Autoimmunity. Lancet I:1096-1100.
157. Horwitz, M.S., Boyce-Jacino, M.T. and Faras, A.J. 1992. Novel Human Endogenous Sequences
Related to Human Immunodeficiency Virus Type 1. J. Virol. 66:2170-2179.
158. Farzadegan, H., Polis, M., Wolinsky, S.M. et al. 1988. Loss of Human Immunodeficiency
Virus Type 1 (HIV-1) Antibodies with Evidence of Viral Infection in Asymptomatic
Homosexual Men. Ann. Int. Med. 108:785-790.
159. Horsburgh, C.R., Ou, C.Y., Holmberg, S.D. et al. 1989. Human Immunodeficiency Virus Type 1
Infection in Homosexual Men who remain Seronegative for prolonged periods. NEJM
160. Mikovits, J.A., Lohrey, N., Schuloff, R., Ruscetti, F. 1991. Immune Activation of latent
HIV-1 expression in monocyte/macrophages, p151. In:Vol. I, Abstracts VII International
Conference on AIDS,Florence.
161. Vartanian, J.P., Meyerhans, A., Henry, M. and Wain-Hobson, S. 1992. High-resolution
structure of an HIV-1 quasispecies:identification of novel coding sequences. AIDS