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  • Title: Lymphadenopathy associated virus and its etiological role in AIDS.
    Author: Montagnier L, Chermann JC, Barré-Sinoussi F, Klatzmann D, Wain-Hobson S, Alizon M, Clavel F, Brun-Vezinet F, Vilmer E, Rouzioux C.
    Journal: Princess Takamatsu Symp; 1984; 15():319-31. PubMed ID: 6100650.
    Abstract:
    Lymphadenopathy associated virus (LAV) is a novel human retrovirus first reported in 1983. It was isolated from the lymph node lymphocytes of a French homosexual patient with generalized hyperplasic lymphadenopathy. Subsequently LAV was isolated from patients with frank acquired immune deficiency syndrome (AIDS) coming from all the different high-risk groups, while anti-LAV antibodies were detected equally in individuals from all "at-risk" groups. Such a profile is consistent with the virus being the major etiological agent of AIDS. Furthermore its biological properties, namely its cytopathic effect in vitro, its T4-cell tropism as well as the role of the T4 molecule in virus infection explain, at least in part, the pathophysiology of AIDS. The major core (gag) proteins are p18, p25, and p13 which are products of a Pr55 precursor. The major envelope (env) glycoprotein is unusually large (gp110) for a retrovirus and comparable to those of the lentiviruses. Recently the virus has been molecularly cloned. The genome is 9.2 kb long, longer than any other known replication competent retrovirus apart from the lentiviruses. The absence of molecular hybridization between cloned LAV and human T-cell leukemia/lymphoma virus (HTLV) genomes compounds the original and extensive differences noted between these viruses and demonstrates that LAV is a prototype of a new class of human retrovirus.
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