4th International AIDS Conference Stockholm, Sweden. — June 12-16, 1988

Int Conf AIDS. 1988 Jun 12-16;4:1.105 (abstract no. K3)

Robert C. Gallo
Laboratory of Tumor Cell Biology, National Institutes of Health, Bethesda, USA

1) Each of the human retroviruses, not just HIV-1, appear to be spreading by the same mode of transmission as HIV-1. HIV-2 appears to be spreading with far less efficiency and probably less pathogenicity than HIV-1. HTLV-I, which can cause T-cell leukemia and central nervous system disease, is far more prevalent than HIV-2. Testing of blood for HTLV-I prior to transfusion will soon be routine in the U.S. A new retrovirus (HTLV-V) may be linked to cutaneous T-cell lymphoma.

2) The pathogenesis of HIV-1 is clearly related to T4 and macrophage infection. There are exciting new indications that some small animals with CD4 negative cells may also be susceptible to infection. Antibody dependent cell killing of uninfected T4 cells may contribute to T4 depletion due to complex formation of CD4 and the gp120 envelope. Also, HBLV and HTLV-I can transactivate the HIV-1 LTR and infect the same T4 cell as HIV-1.

3) Use of the CD4 molecule in soluble form and dextran sulfate to block virus binding and systems for the study of inhibitors of viral reverse transcriptase, protease, and tat function have rapidly developed.

4) An international collaborative program (called HIVAC) to develop a vaccine against AIDS was initiated in 1984. Studies from members of this group have defined a neutralizing epitope (Putney et al.), and T cell epitopes (Berzofsky et al.). Other studies (Zagury et al.) have made the first attempts to define the immune response in man.

880612
K3

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