Resistance of AIDS virus at room temperature.
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Biomedical subjects
Publications and source records attributed to J C Chermann.
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The major envelope glycoprotein of the causative agent of Acquired Immune Deficiency Syndrome (AIDS) lymphadenopathy-associated virus (LAV) has been identified and characterized. The glycoprotein has an apparent molecular weight of 110,000-120,000 under denaturing conditions in polyacrylamide gel electrophoresis. Upon deglycosylation by a specific endoglycosydase, its size is reduced to 80,000. Cellular precursors of this glycoprotein have been detected with apparent molecular weight of 150,000 and 135,000. Nearly all AIDS and pre-AIDS patients have detectable antibodies against this viral glycoprotein.
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Lymphadenopathy associated virus is inactivated by heating at 56 degrees C for 30 min, and is not inactivated by 2 X 10(5) rad gamma irradiation or 5 X 10(3) J/m2 ultraviolet irradiation.
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49 french haemophiliacs (haemophilia A: 41 patients; haemophilia B: 8 patients) were serologicaly tested for LAV antibodies: 10 patients (20.4%) were seropositive including 9 (21.9%) with haemophilia A and 1 (12,5%) with haemophilia B. Between seronegative and seropositive patients total lymphocyte and T-lymphocyte sub-populations counts were not significantly different. The mean serum IgG level was higher and palpable lymphadenopathy more frequently encountered among seropositive patients.
49 French haemophiliacs (haemophilia A: 41 patients; haemophilia B: 8 patients) were serologically testes for lymphadenopathy-AIDS virus antibodies: 10 patients (20.4%) were seropositive including 9 (21.9%) with haemophilia A and 1 (12.5%) with haemophilia B. Among haemophiliacs A, seropositive patients received significantly larger amounts of factor VIII concentrate during the 2 years preceding the study.
We present evidence of transmission of lymphadenopathy-associated virus (LAV)/human T-lymphotropic virus type III (HTLV-III) from a man to his wife, and a return to a normal number of T-helper lymphocytes and loss of antibody after discontinuing sexual exposure to LAV/HTLV-III. The man had hemophilia A, and developed the lymphadenopathy syndrome, antibody to LAV, and a low number of T-helper lymphocytes. His wife, who had no risks for the acquired immunodeficiency syndrome other than sexual contact with him, developed LAV antibody (titer, 1:160) and a mildly decreased number of T-helper cells. The husband subsequently developed the syndrome and lost the LAV antibody. During 10 months of follow-up his wife remained clinically well, discontinued exposure to semen, and then lost the LAV antibody, and regained a normal number of T-helper cells.
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This study deals with the immunohistochemistry of a monoclonal antibody (Mab) raised against the p18 protein of the LAV virus in lymphnodes from 20 cases of persistent generalized lymphoadenopathy (PGL) (2) and 6 of acquired immunodeficiency syndrome (AIDS) (3). In all the PGL cases that have been studied, we observed a very important disruption of the follicular dendritic cell's (FDC) framework in the germinal centers which is associated with the presence of an increased number of Leu2a+ lymphocytes inside the germinal centers. This observation is consistent with the main morphological feature of the lymphnodes in the PGL syndrome which is mainly characterized by lesions of FD cells.
We investigated whether serologic evidence of lymphadenopathy-associated virus (LAV), an exogenous human T-cell lymphotropic and cytopathic retrovirus, correlated with the acquisition and transmission of the acquired immunodeficiency syndrome (AIDS). Serum from 17 of 25 patients with AIDS contained circulating IgG anti-LAV antibody (all of 5 adults with cancer and 6 of 12 adults and 6 of 8 children with opportunistic infections, with or without Kaposi's sarcoma). All of eight homosexual men with generalized lymphadenopathy or the AIDS-related complex and five homosexual men with AIDS prodromes who subsequently had AIDS were also seropositive. The anti-LAV antibody was not found in 99 of 100 healthy blood donors or in 23 patients with genetic immunodeficiencies, supporting the contention that LAV is unlikely to represent simply another opportunistic microorganism. An AIDS carrier state was indicated by the probable transfer of LAV from asymptomatic, immunologically competent mothers to their offspring. These data offer a basis for the hypotheses that LAV is a marker for AIDS, may be carried and transmitted in the absence of clinical findings or in vitro T-cell abnormalities, and is probably an etiologically important agent in AIDS and its prodromes.
The presence of antibodies to lymphadenopathy-associated retrovirus (LAV) was determined by a radioimmunoprecipitation assay and by an enzyme-linked immunosorbent solid assay of sera from Zairian patients with the acquired immune deficiency syndrome (AIDS) in 1983. Thirty-five of 37 patients (94 percent) and 32 of 36 patients (88 percent), respectively, were seropositive by the two tests. In a control group of 26 patients, six (23 percent) showed positive results in these tests. Of these six control patients, five had clinically demonstrable infectious diseases and a low ratio of T4 to T8 lymphocytes. In addition, sera collected from a control group of Zairian mothers in 1980 were positive for LAV in 5 of 100 cases. Other serologic data suggest that LAV was present as early as 1977 in Zaire.
Reverse transcriptase activity of lymphadenopathy associated virus was assayed after exposure to various standard chemical disinfectants. 25% ethanol or 1% glutaraldehyde should prove sufficient to disinfect medical instruments, and 0.2% sodium hypochlorite for cleaning floors and benches. 0.1% formalin is too slow to be recommended.