The HIV-1 Tat protein modulates CD4 expression in human T cells through the induction of miR-222

RNA Biol. 2014;11(4):334-8. doi: 10.4161/rna.28372. Epub 2014 Mar 6.

Abstract

Several cellular microRNAs show substantial changes in expression during HIV-1 infection and their active role in the viral life cycle is progressively emerging. In the present study, we found that HIV-1 infection of Jurkat T cells significantly induces the expression of miR-222. We show that this induction depends on HIV-1 Tat protein, which is able to increase the transcriptional activity of NFkB on miR-222 promoter. Moreover, we demonstrate that miR-222 directly targets CD4, a key receptor for HIV-1, thus reducing its expression. We propose that Tat, by inducing miR-222 expression, complements the CD4 downregulation activity exerted by other viral proteins (i.e., Nef, Vpu, and Env), and we suggest that this represents a novel mechanism through which HIV-1 efficiently represses CD4 expression in infected cells.

Keywords: CD4; HIV-1; NFkB; microRNAs; post-transcriptional regulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD4 Antigens / genetics*
  • CD4 Antigens / metabolism
  • Cell Line
  • Gene Expression Regulation*
  • HIV Infections / genetics*
  • HIV Infections / immunology
  • HIV Infections / metabolism
  • HIV-1 / physiology*
  • Humans
  • MicroRNAs / genetics*
  • NF-kappa B / metabolism
  • RNA, Messenger / genetics
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / metabolism*
  • tat Gene Products, Human Immunodeficiency Virus / metabolism*

Substances

  • CD4 Antigens
  • MIRN222 microRNA, human
  • MicroRNAs
  • NF-kappa B
  • RNA, Messenger
  • tat Gene Products, Human Immunodeficiency Virus