Host control of HIV-1 parasitism in T cells by the nuclear factor of activated T cells

Cell. 1998 Nov 25;95(5):595-604. doi: 10.1016/s0092-8674(00)81630-x.


Post HIV-1 entry, productive HIV-1 infection of primary T cells requires overcoming several cellular blocks to provirus establishment and replication. Activation of unknown host intracellular events overcomes such inhibitory steps and is concomitant with HIV-1 replication. We show that the transcription factor NFATc was sufficient as a cellular factor to induce a highly permissive state for HIV-1 replication in primary CD4+ T cells. NFATc overcame a blockade at reverse transcription and permitted active HIV-1 replication. Pharmacologic blockade of endogenous NFAT activity by FK506 or CsA inhibited synthesis of reverse transcription and also potently blocked HIV-1 replication. T cells therefore can become competent for HIV-1 replication by control of regulated host factors such as the NFATc transcription factor. The host mechanisms regulated by such permissivity factors are potential targets for anti-HIV-1 therapy.

Publication types

  • 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 / virology
  • Cell Division
  • Cells, Cultured
  • Cyclosporine / pharmacology
  • DNA-Binding Proteins / physiology*
  • HIV Infections / immunology*
  • HIV Reverse Transcriptase / antagonists & inhibitors
  • HIV-1 / pathogenicity*
  • HIV-1 / physiology
  • Humans
  • Immunosuppressive Agents / pharmacology
  • Lymphocyte Activation*
  • NFATC Transcription Factors
  • Nuclear Proteins / physiology*
  • Phytohemagglutinins / pharmacology
  • T-Lymphocytes / immunology
  • T-Lymphocytes / virology*
  • Transcription Factors / physiology*
  • Virus Replication


  • DNA-Binding Proteins
  • Immunosuppressive Agents
  • NFATC Transcription Factors
  • Nuclear Proteins
  • Phytohemagglutinins
  • Transcription Factors
  • Cyclosporine
  • HIV Reverse Transcriptase