An endogenous inhibitor of human immunodeficiency virus in human lymphocytes is overcome by the viral Vif protein

N. Madani, David Kabat

Research output: Contribution to journalArticle

206 Citations (Scopus)

Abstract

The vif gene of human immunodeficiency virus type 1 (HIV-1) encodes a basic M(r) 23,000 protein that is necessary for production of infectious virions by nonpermissive cells (human lymphocytes and macrophages) but not by permissive cells such as HeLa-CD4. It had been proposed that permissive cells may contain an unidentified factor that functions like the viral Vif protein. To test this hypothesis, we produced pseudotyped wild-type and vif-deleted HIV gpt virions (which contain the HIV-1 genome with the bacterial mycophenolic acid resistance gene gpt in place of the viral env gene) in permissive cells, and we used them to generate nonpermissive H9 leukemic T cells that express these proviruses. We then fused these H9 cells with permissive HeLa cells that express the HIV-1 envelope glycoprotein gp120- gp41, and we asked whether the heterokaryons would release infectious HIV gpt virions. The results clearly showed that the vif-deleted virions released by the heterokaryons were noninfectious whereas the wild-type virions were highly infectious. This strongly suggests that nonpermissive cells, the natural targets of HIV-1, contain a potent endogenous inhibitor of HIV-1 replication that is overcome by Vif.

Original languageEnglish (US)
Pages (from-to)10251-10255
Number of pages5
JournalJournal of Virology
Volume72
Issue number12
StatePublished - 1998

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vif Gene Products
viral proteins
Human immunodeficiency virus
Viral Proteins
Virion
lymphocytes
Human immunodeficiency virus 1
HIV-1
HIV
Lymphocytes
virion
heterokaryon
cells
vif Genes
Mycophenolic Acid
env Genes
Bacterial Genomes
Proviruses
Viral Genes
proviruses

ASJC Scopus subject areas

  • Immunology

Cite this

An endogenous inhibitor of human immunodeficiency virus in human lymphocytes is overcome by the viral Vif protein. / Madani, N.; Kabat, David.

In: Journal of Virology, Vol. 72, No. 12, 1998, p. 10251-10255.

Research output: Contribution to journalArticle

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