Differential regulation of human immunodeficiency viruses (HIVs): A specific regulatory element in HIV-2 responds to stimulation of the T-cell antigen receptor

D. M. Markovitz, M. Hannibal, V. L. Perez, C. Gauntt, T. M. Folks, G. J. Nabel

    Research output: Contribution to journalArticle

    47 Scopus citations

    Abstract

    The human immunodeficiency viruses (HIVs) types 1 and 2 have similar genetic organization but differ significantly in nucleic acid sequence. Although infection by either agent leads to symptoms of immunodeficiency, recent studies suggest potential differences in the time course and severity of these diseases. In this report, the transcriptional regulation and induction of these retroviruses were analyzed. We report that the regulation of HIV-2 differs from that of HIV-1: a distinct T-cell activation pathway, triggering of the CD3 component of the T-cell receptor complex, stimulates HIV-2 but not HIV-1 gene expression. The response to T-cell receptor stimulation in HIV-2 is mediated partly by an upstream regulatory element, termed CD3R, which is recognized by a sequence-specific DNA binding protein, NF-CD3R. Jurkat T leukemia cell lines containing HIV-2 provirus also showed increased viral replication after stimulation of the T-cell receptor complex, in contrast to HIV-1. These findings suggest that transcriptional regulation and induction of HIV-2 differ from HIV-1 and raise the possibility that different cofactors contribute to the activation of HIV-1 and HIV-2-associated AIDS.

    Original languageEnglish (US)
    Pages (from-to)9098-9102
    Number of pages5
    JournalProceedings of the National Academy of Sciences of the United States of America
    Volume87
    Issue number23
    DOIs
    StatePublished - Dec 1 1990

    Keywords

    • CD3
    • HIV-1
    • cofactors
    • viral gene expression

    ASJC Scopus subject areas

    • General

    Fingerprint Dive into the research topics of 'Differential regulation of human immunodeficiency viruses (HIVs): A specific regulatory element in HIV-2 responds to stimulation of the T-cell antigen receptor'. Together they form a unique fingerprint.

    Cite this