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J Virol, April 1998, p. 3161-3168, Vol. 72, No. 4
Department of Pathology and Laboratory
Medicine,1
Division of
Hematology-Oncology,
Received 24 October 1997/Accepted 22 December 1997
Successful infection by human immunodeficiency virus type 1 (HIV-1)
requires the activation of target cells. Infection of quiescent
peripheral CD4 lymphocytes by HIV-1 results in incomplete, labile,
reverse transcripts. In the present study, we isolated highly purified
quiescent T cells and utilized the CD3/CD28 activation pathways as well
as cell cycle inhibitors to further define the role of costimulation
and cell cycle progression in HIV-1 reverse transcription. Activation
with
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Progression to the G1b Phase of the
Cell Cycle Is Required for Completion of Human Immunodeficiency
Virus Type 1 Reverse Transcription in T Cells
CD3 alone resulted in cell cycle progression into only
G1a and incomplete HIV-1 reverse transcription. Costimulation through the CD28 receptor and transition into
G1b was required to efficiently complete the reverse
transcription process. These findings have relevance to immune
activation in vivo, since lymphocytes rendered anergic by a single
activation signal would be nonpermissive for productive infection with
HIV-1. Importantly, these data also suggest that HIV vector-based
genetic transduction strategies might be successful only in target
cells that transition into the G1b phase of the cell cycle.
*
Corresponding author. Mailing address: Department of
Medicine, Division of Hematology-Oncology, and Department of
Microbiology and Molecular Genetics, 11-934 Factor Bldg., 10833 Le
Conte Ave., Los Angeles, CA 90095. Phone: (310) 794-7765. Fax: (310)
825-6192. E-mail: JZACK{at}UCLA.edu.
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