Fate of the human immunodeficiency virus type 1 provirus in infected cells: a role for vpr.
We investigated the fate of human immunodeficiency virus type 1 (HIV-1) viral DNA in infected peripheral blood lymphocytes and immortalized T-cell lines by using a replication-defective HIV-1. We observed that integrated HIV-1 DNA and viral gene expression decrease over time. A frameshift mutation in vpr resulted in maintenance of the HIV-1 provirus and stable persistence of viral expression. Transfection of vpr together with the neomycin resistance gene in the absence of other viral genes decreased the formation of geneticin-resistant colonies, indicating either a cytotoxic or a cytostatic effect upon cells. Therefore, maintenance of HIV-1 infection within an infected proliferating population is due to two competing processes, the rate of viral spread and the degree of cell growth inhibition and/or death induced by Vpr.
Planelles
V
V
Department of Microbiology and Immunology, UCLA School of Medicine 90094-1678, USA.
Bachelerie
F
F
Jowett
J B
JB
Haislip
A
A
Xie
Y
Y
Banooni
P
P
Masuda
T
T
Chen
I S
IS
D000818:Animals; D002478:Cells, Cultured; D004279:DNA, Viral / Q000235:genetics / Q000378:metabolism; D003673:Defective Viruses / Q000235:genetics / Q000502:physiology; D016368:Frameshift Mutation; D015870:Gene Expression; D016334:Genes, vpr; D015497:HIV-1 / Q000235:genetics / Q000502:physiology*; D006801:Humans; D007700:Kinetics; D008156:Luciferases / Q000032:analysis / Q000096:biosynthesis; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000276:immunology / Q000821:virology; D051379:Mice; D010957:Plasmids; D011533:Proviruses / Q000235:genetics / Q000502:physiology*; D013997:Time Factors; D014162:Transfection; D016662:Virus Integration; D014779:Virus Replication
D004279:DNA, Viral; D008156:Luciferases