Document 3153
 DOCN  M94A3153
 TI    Superantigen TSST-1 enhances the replication of HIV-1 in PBMCs through
       selective activation of CD4+ T-cell and induction of TNF-alpha.
 DT    9412
 AU    Hashimoto K; Baba M; Shigeta S; Department of Microbiology, Fukushima
       Medical College, Japan.
 SO    Int Conf AIDS. 1994 Aug 7-12;10(1):140 (abstract no. PA0179). Unique
       Identifier : AIDSLINE ICA10/94369422
 AB    OBJECTIVE: Staphylococcal superantigens bind to the class II molecules
       expressed on the surface of peripheral blood mononuclear cells (PBMCs)
       and potently activate them. Tumor necrosis factor alpha (TNF-alpha)
       plays an essential role in human immunodeficiency virus type 1(HIV-1)
       infection. In addition, the superantigen has recently been reported to
       activate the gene expression of TNF-alpha and induce its secretion in
       PBMCs. We investigated the effect of the superantigen toxic shock
       syndrome toxin-1(TSST-1) on HIV-1 replication in PBMCs. METHODS: PBMCs
       were obtained from healthy donors, infected with HIV-1, and cultured in
       the presence of various concentrations of TSST-1. To some cultures,
       various diluted anti-TNF-alpha antibodies were added. After cultivation
       under various conditions, the culture supernatants were collected and
       examined for their p24 antigen and TNF-alpha levels.
       Fluorescent-activated cell sorter analysis and DNA synthesis were also
       determined. RESULTS: The p24 antigen level in the culture supernatant
       markedly increased in the presence of TSST-1 at a concentration of 1
       pg/ml or higher. TSST-1 specifically activated CD4+ T lymphocytes.
       Significant production of TNF-alpha was observed in HIV-1-infected PBMCs
       at 96h after incubation with TSST-1. Furthermore, addition of
       anti-TNF-alpha antibody in culture medium resulted in dramatical
       decrease of HIV-1 replication. CONCLUSIONS: The enhanced production of
       HIV-1 by TSST-1 in PBMCs is in part attributed to both the activation of
       CD4+ T lymphocytes and induction of TNF-alpha.
 DE    Cells, Cultured  Comparative Study  Dose-Response Relationship, Drug
       DNA/BIOSYNTHESIS  Enterotoxins/*PHARMACOLOGY  Flow Cytometry/METHODS
       Human  HIV Core Protein p24/ANALYSIS/BIOSYNTHESIS  HIV-1/DRUG
       EFFECTS/*PHYSIOLOGY  Kinetics  Lymphocyte Transformation/*DRUG EFFECTS
       Lymphocytes/DRUG EFFECTS/IMMUNOLOGY/*MICROBIOLOGY  Staphylococcus aureus
       Superantigens/*PHARMACOLOGY  Time Factors  Tumor Necrosis
       Factor/*BIOSYNTHESIS  T4 Lymphocytes/DRUG
       EFFECTS/IMMUNOLOGY/*MICROBIOLOGY  Virus Replication/*DRUG EFFECTS
       MEETING ABSTRACT

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).