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J Virol, August 1998, p. 6911-6916, Vol. 72, No. 8
Department of Microbiology and Pediatrics,
New York University School of Medicine, New York, New York 10016
Received 29 January 1998/Accepted 16 May 1998
For productive replication of human immunodeficiency virus type 1 (HIV-1) in host cells, the viral genome-encoded transactivator Tat and
several cellular transcription factors are required for efficient viral
gene transcription. However, it remains unclear how the viral
genome initiates transcription before Tat is transcribed or when Tat is
at suboptimal levels. Here, we utilized the human T-cell leukemia type
1 Tax protein as a molecular tool to investigate the
mechanism of viral gene transcription that initiates the early phase of
infection of HIV-1. Tax alone does not significantly increase the
activity of HIV-1 long terminal repeat (LTR) in T lymphocytes, but it markedly enhanced the replication of an
infectious HIV-1 provirus with a truncated nef gene. This
enhancement is preferentially mediated by the cooperation of Tax and
Tat which is dependent on TAR and duplicated
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Human Immunodeficiency Virus Type 1 Genome Activation Induced by
Human T-Cell Leukemia Virus Type 1 Tax Protein Is through
Cooperation of NF-
B and Tat
B cis
elements of the HIV-1 LTR as well as the NF-
B activation domain of
Tax. Furthermore, phorbol myristate acetate and
membrane-targeted HIV-1 Nef also enhanced the LTR activity in the
presence of Tat in the TAR- and
B cis element-dependent
manner. These data suggest that activated NF-
B can functionally
interact with a suboptimal amount of Tat and the HIV-1 LTR for
efficient initiation of viral gene transcription.
*
Corresponding author. Mailing address: Department of
Pediatrics, New York University School of Medicine, 550 First Ave.,
Room H501A, New York, NY 10016. Phone: (212) 263-6425. Fax: (212)
263-8172. E-mail: PARKSW01{at}MCRCR.MED.NYU.EDU.
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