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HIV-1 Vpr suppresses the cytomegalovirus promoter in a CRL4(DCAF1) E3 ligase independent manner.

Abstract：

:Although the Vpr protein of human immunodeficiency virus type 1 (HIV-1) has been shown to act as a transcriptional activator of the HIV-1 LTR and certain host genes, the current study demonstrates that it can also function as a potent inhibitor of the cytomegalovirus (CMV) promoter. Previous studies have shown that the cell cycle arrest and apoptotic functions of Vpr required recruitment of the CRL4(DCAF1) E3 ligase, but this complex is shown not to be required for inhibition of the CMV promoter. We identified conserved sites (A30/V31) from diverse Vpr from HIV/SIV that were critical for blocking the CMV promoter activity. Interestingly, the Vpr mutant A30S/V31S protein also impaired the ability of Vpr to down-regulate transcription of the host UNG2 gene. Our findings shed light on the dual functions of Vpr on the transcription of HIV-1, other viruses and host genes which may contribute to viral replication and disease progression in vivo.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Liu X,Guo H,Wang H,Markham R,Wei W,Yu XF

doi

10.1016/j.bbrc.2015.02.060

subject

Has Abstract

pub_date

2015-04-03 00:00:00

pages

214-219

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(15)00288-0

journal_volume

459

pub_type

杂志文章

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