Inhibition of apoptosis in human immunodeficiency virus-infected cells enhances virus production and facilitates persistent infection. (original) (raw)

J Virol. 1995 Apr; 69(4): 2384–2392.

Laboratory of Viral Pathogenesis, Center for Advanced Biotechnology and Medicine, Piscataway, New Jersey.

Abstract

Apoptosis is one of several mechanisms by which human immunodeficiency virus type 1 (HIV-1) exerts its cytopathic effects. CD4+ Jurkat T-cell lines overexpressing the adenovirus E1B 19K protein, a potent inhibitor of apoptosis, were used to examine the consequences of inhibition of apoptosis during acute and chronic HIV-1 infections. E1B 19K protein expression inhibited HIV-induced apoptosis, enhanced virus production, and established high levels of persistent viral infection. One E1B 19K-expressing line appeared to undergo HIV-induced death via a nonapoptotic mechanism, illustrating that HIV infection results in lymphocyte depletion through multiple pathways. Increased virus production associated with sustained cell viability suggests that therapeutic approaches involving inhibition of HIV-induced programmed cell death may be problematic.

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