Inhibition of apoptosis in human immunodeficiency virus-infected cells enhances virus production and facilitates persistent infection.
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.
Antoni
B A
BA
Laboratory of Viral Pathogenesis, Center for Advanced Biotechnology and Medicine, Piscataway, New Jersey.
Sabbatini
P
P
Rabson
A B
AB
White
E
E
D017501:Adenovirus E1B Proteins / Q000378:metabolism; D017209:Apoptosis; D002460:Cell Line; D006678:HIV / Q000502:physiology*; D006801:Humans; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2; D014779:Virus Replication
D017501:Adenovirus E1B Proteins; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2