Expression of MHC class II in T cells is associated with increased HIV-1 expression

Clin Exp Immunol. 2000 Aug;121(2):324-31. doi: 10.1046/j.1365-2249.2000.01290.x.

Abstract

HIV-1 replicates in activated T cells at significantly higher levels than in resting cells. Thus, certain molecules up-regulated during T cell activation appear to be important for HIV-1 replication. In this study, we present evidence suggesting that expression of MHC class II (class II) molecules on CD4+ T cells facilitate HIV-1 replication. T cells that expressed class II supported greater virus replication than T cells lacking class II. The class II+ cells, when either infected with HIV-1 or transfected with an env-minus HIV-1 provirus plasmid, produced 10-20-fold greater virus expression than class II- cells. Anti-class II antibody markedly inhibited virus expression in class II+ cells (but not class II- cells) and also decreased the nuclear binding activity of AP-1, an inducible transcription factor important in T cell activation and HIV-1 expression. Most importantly, the induction of class II expression by transfection of the MHC class II transactivator (CIITA) stimulated HIV-1 replication in Jurkat T cells. Taken together, these data suggest that expression of MHC class II molecules and/or CIITA in T cells enhances HIV-1 transcription.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / metabolism
  • CD4-Positive T-Lymphocytes / virology*
  • Cell Line
  • Chemokines / metabolism
  • Culture Media, Conditioned / chemistry
  • Cytokines / metabolism
  • Genes, Reporter
  • HIV-1 / genetics
  • HIV-1 / physiology*
  • HLA-DR Antigens / immunology*
  • Humans
  • Jurkat Cells / immunology
  • Jurkat Cells / virology
  • Lymphocyte Activation
  • Proviruses / genetics
  • Transcription Factor AP-1 / metabolism
  • Transfection
  • Virus Replication*

Substances

  • Chemokines
  • Culture Media, Conditioned
  • Cytokines
  • HLA-DR Antigens
  • Transcription Factor AP-1