Serum Vpr regulates productive infection and latency of human immunodeficiency virus type 1

David N. Levy, Yosef Refaeli, Rob Roy Macgregor, David B. Weiner

Research output: Contribution to journalArticlepeer-review

Abstract

In human immunodeficiency virus (HIV)-positive individuals, the vast majority of infected peripheral blood cells and lymph node cells may be latently or nonproductively infected. The vpr open reading frame of HIV-1 encodes a 15-kDa virion-associated protein, Vpr. The vpr gene has been shown to increase virus replication in T cells and monocyte/macrophages in vitro. We have previously reported that vpr expression in various tumor lines leads to growth inhibition and differentiation, indicating that Vpr may function as a regulator of cellular permissiveness to HIV replication. Here we show that Vpr protein is present in significant amounts in the serum of AIDS patients. Purified serum Vpr activated virus expression from five latently infected cell lines, U1, OM.10.1, ACH-2, J1.1, and LL58. Serum Vpr also activated virus expression from resting peripheral blood mononuclear cells of HIV- infected individuals. Together, these findings implicate serum Vpr in the activation of HIV replication in vivo and in the control of latency. Anti- Vpr antibodies inhibited Vpr activity, suggesting that humoral immunity modulates Vpr activity in vivo. These results have broad implications for the virus life cycle and for the prospective control of HIV replication and pathogenesis.

Original languageEnglish (US)
Pages (from-to)10873-10877
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume91
Issue number23
DOIs
StatePublished - Nov 8 1994

ASJC Scopus subject areas

  • General

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