Repression of human immunodeficiency virus type 1 through the novel cooperation of human factors YY1 and LSF.

Important note: Information in this article was accurate in 1998. The state of the art may have changed since the publication date.

Repression of human immunodeficiency virus type 1 through the novel cooperation of human factors YY1 and LSF.

J Virol. 1997 Dec;71(12):9375-82. Unique Identifier : AIDSLINE MED/98037648
Romerio F; Gabriel MN; Margolis DM; Institute of Human Virology, Medical Biotechnology Center, University; of Maryland Biotechnology Institute, Baltimore 21201, USA.

Abstract: A subpopulation of stably infected CD4+ cells capable of producing virus upon stimulation has been identified in human immunodeficiency virus (HIV)-positive individuals (T.-W. Chun, D. Finzi, J. Margolick, K. Chadwick, D. Schwartz, and R. F. Siliciano, Nat. Med. 1:1284-1290, 1995). Few host factors that directly limit HIV-1 transcription and could support this state of nonproductive HIV-1 infection have been described. YY1, a widely distributed human transcription factor, is known to inhibit HIV-1 long terminal repeat (LTR) transcription and virus production. LSF (also known as LBP-1, UBP, and CP-2) has been shown to repress LTR transcription in vitro, but transient expression of LSF has no effect on LTR activity in vivo. We report that both YY1 and LSF participate in the formation of a complex that recognizes the initiation region of the HIV-1 LTR. Further, we have found that these factors cooperate in the repression of LTR expression and viral replication. This cooperative function may account for the divergent effects of LSF previously observed in vitro and in vivo. Thus, the cooperation of two general cellular transcription factors may allow for the selective downregulation of HIV transcription. Through this mechanism of gene regulation, YY1 and LSF could contribute to the establishment and maintenance of a population of cells stably but nonproductively infected with HIV-1.

Keywords: *DNA-Binding Proteins/METABOLISM *Gene Expression Regulation, Viral *HIV Long Terminal Repeat *HIV-1/GENETICS *Repressor Proteins/METABOLISM *Transcription Factors/METABOLISM
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