Tuesday, January 14, 2014

Unfinished Blog-Post: "February 1983: Gallo proposes that AIDS is probably caused by a retrovirus, presumably a variant of HTLV-1 or II"

A long time ago I started some blog-posts, but never found the time nor energy to finish them. Now I have long lost interest in the matter and will publish them all "as is" – maybe someone will find these raw thoughts helpful.

Transcribed by OCR, some errors corrected manually – may still contain errors.
The chronology of AIDS research
Nature 326, 435 - 436 (08 April 1987); doi:10.1038/326435a0
(e.g., available here)

This statement from Gallo and Montagnier constitutes part of the agreement between the US and French AIDS research groups.

February 1983.

At the Cold Spring Harbor Workshop on AIDS, Gallo proposes that AIDS is probably caused by a retrovirus, presumably a variant of HTLV-1 or II.

May 1983.

Barro-Sinoussi, Chermann, Momagnier and co-workers (1983). publish:

(1) the isolation and identification of a non-transforming retrovirus (later called lymphadenopathy-associated vino (LAV)). different from HTLV-I and HTLV-II, in cultures of T lymphocytes derived from a patient with lymph-adenepathy syndrome;

(2) the continuous passage of the virus by its transient growth in cultures of T lymphocytes of normal blood donors;

(3) the identification of a major protein associated with this virus, p25, not immunologically cross-reactive with the p24 of HTLV-I; and

(4) the detection by immunoprecipita-tion of antibodies against this protein in two patients. Essex and co-workers (1983) detect antibodies cress-reactive with HTLV-I membrane protein in 25-30% of AIDS patients.

Gelman and co-workers (Gallo's group) (1983) find evidence for presence of the viral genume of HTLV-I or an HTLV-I variant in 2 of 33 AIDS patients.

September 1983.

At the Cold Spring Harbor meeting on human T-cell leukaemia-lymphoma viruses:
Montagnier and co-workers (1984) report:

(1) the identification of LAV-like viruses from 5 patients with lymphadenopathy and 3 patients with AIDS (homosexual, haemophiliac, Haitian);

(2) the selective affinity of LAV for CD4(T4) helper lymphocytes:

(3) the presence of antibodies (enzyme-linked immunosorbent assay, ELISA) against the main LAV antigens in patients with lymphadenopathy-associated syndrome (LAS) (63%) and AIDS (20%);

(4) that LAV is morphologically similar to equine infectious anaemia virus (EIAV) and different from HTLVs; and

(5) the antigenic cross-reactivity between core proteins of EIAV and LAV (virus isolates from LAS patients are called LAV, and from AIDS patients are called IDAV).

Gallo and co-workers (1984) report the presence of HTLV-I antibodies in 10% of AIDS patients and isolates of HTLV-I or HTLV-II or variants of it in fewer than 10% of such cases.

March-April 1984.

Montagnier et al. (1984) by using more sera of horses infected with EIAV confirm cross-reactivity of the core proteins of LAV with that of EIAV and identify a second viral protein, p18.

Vilmer, Chermann, Montagnier and co-workers (1984) confirm previous isolation of an LAV-like virus from one haemophiliac and isolate another one from his asymptomatic brother.

May 1984.

Gallo's group (1984) reports:

(1) mass and continuous production in a clone of a permanent cell line (H9) of HTLV-III from two AIDS patients and four additional isolates (SN, BK, CS, WI) also infectious for another clone (114) derived from the same parental cell line (Popovic, Sarngadharan, Gallo and co-workers).

(2) 48 virus isolations, that is, 18 of 21 patients with pre-AIDS, 3 of 4 clinically normal mothers of juveniles with AIDS, 26 of 72 juveniles and adults with AIDS, 1 of 22 healthy male homosexuals, and 0 of 115 heterosexual subjects (Gallo, Salahuddin, Popovic and colleagues). The use of anti-p24 hyperimmune sera proves that the 48 isolates belong to the same kind of virus;

(3) The introduction of the Western blot technique for clinical detection of antibodies in 88% of 48 patients with AIDS, 79% of 14 homosexuals with pre-AIDS and less than 1% of hundreds of heterosexuals. A gp41 is identified as a major viral antigen (Sarngadharan, Popovic, Gallo and co-workers). Later, it is demonstrated by Veronese, Sarngadharan and Gallo to be the HTLV-III viral transmembrane component of the envelope.

(4) Partial characterization of the immunologically reactive proteins by the Western blot technique. (Schupbach, Sarngad-haran, Popovic, Gallo and co-workers).

June 1984.

Safai, Gallo, Pupovic and Sarngailharan report 34 of 34 (100%) of AIDS patients positive for HTLV-III antibodies, 16 of 19 (84%) of LAS patients and 0 of 14 (0%) of controls (1984).

Brun-Vezinet, Barre-Sinoussi, Montagnier, Chermann arid co-workers (1984) publish detection of antibodies against LAI/ proteins by ELISA in 74,5% of the patients presenting with iymphadenopathy syndrome, 37,5% of patients with frank AIDS, 18% of healthy homosexuals, 1% of blood donors.

July 1984.

Kalyanarainan, Iviontagnier, Francis and co-workers (1984) report the detection of anti-p25 (LAV) antibodies in 51 of 125 (41%) of AIDS patients, 81 of 113 (72%) of LAS patients, and 0 of 70 of healthy individuals;

Montagnier and co-workers (1984) report the growth of LAV in continuous B-cell lines, most of them transformed by Epstein-Barr virus.

Kiatzmann, Gluckman., Chermann, Montagnier and co-workers (1984)42 publish:

(1) the selective isolation of LAU. from CD4+ (T4 4) lymphocytes of a healthy carrier of the virus;

(2) the inhibition of CD4 cell growth at the same time of in vitro virus production;

(3) the simultaneous disappearance of the CD4 antigen at the surface of the infected CD4 lymphocytes.

August 1984.

A third group, Levy et al., (1984) isolate virus antigenically and structurally related to LAV from San Francisco AIDS patients.

September 1984.

Cheinsong-Popov, Weiss and collaborators publish identical prevalence of antibodies against antigens of HTLV-III grown in H9 line and of LAV-1 grown in CEM line in UK patients with AIDS or at risk of AIDS (1984).

Goedert, Gallo and co-workers (1984) report that in a cohort of homosexual men at risk of AIDS, 53% were antibody-positive for HTLV-III. In HTLV-III antibody positive subjects, AIDS developed at 6.9% per year.

October 1984.

Brun-Vezinet, Montagnier, Dot. Quinn and co-workers (1984) publish the presence of antibody against LAV in 35 of 37 Zairean patients with AIDS.

Zagury, Gallo and co-workers (1984) isolate HTLV-III from cells cultured from semen of two patients with AIDS.

November 1984.

Hahn, Gallo and co-workers (1984) report the molecular cloning of HTLV-III virus.

Kitchen, Allan, Essex and co-workers (1984) (1985) identify the viral external glycoprotein gp120, a finding confirmed by Montagnier and co-workers (1985).

December 1984.

Alizon, Barre-Sinoussi, Wain-Hobson, Montagnier and co-workers (1984) report the molecular cloning of LAV-1.

Wong-Stool, Shaw, Gallo and co-workers (1984) discover genomic heterogeneity of HTLV-III.

Dagleish, Weiss and co-workers (1984) and independently Klatzmann, Gluckman, Montagnier and co-workers (1984) show the CD4 molecule is involved in the receptor to the virus.

Popovic, Read-Connole and Gallo (1984) publish a series of CD4-positive human neoplastic cell lines susceptible to and permissive for HTLV-III, including HUT78, Molt3 and CEM cell lines.

January 1985.

The nucleotide sequence of the AIDS virus genome is established independently at the Pasteur Institute (1985), at the NCI/NIH (1985), at Genentech, Inc. (1985) and at Chiron (1985), revealing the similarity of the various isolates.

Sodroski, Wong-Staal, Gallo, HeseMae and co-workers (1985) demonstrate transactivation of transcription in HTLV-III infected cells.

Shaw, Gallo and co-workers (1985) discover the presence of virus in the brain.

March 1985.

Redfield, Gallo and co-workers (1985) describe heterosexual transmission of HTLV-III.

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