Reversal of HIV-1 latency with anti-microRNA inhibitors

Int J Biochem Cell Biol. 2009 Mar;41(3):451-4. doi: 10.1016/j.biocel.2008.07.016. Epub 2008 Aug 8.


Human immunodeficiency virus type 1 (HIV-1) latency is achieved when host cells contain integrated proviral DNA but do not produce viral particles. The virus remains in resting CD4 T-lymphocytes, evading host immune surveillance and antiviral drugs. When resting cells are activated, infectious viral particles are produced. Latency is critical for the survival of all HIV-1 strains in vivo. Recently, it has been reported that a cluster of cellular microRNAs (miRNAs) enriched specifically in resting CD4+ T-cells suppresses translation of most HIV-1-encoded proteins in the cytoplasm, sustaining HIV-1 escape from the host immune response. Complementary antisense miRNA inhibitors block the inhibitory effect of miRNAs and drive viral production from the resting T-lymphocytes without activating the cells. Therefore, inhibition of these HIV-1-specific cellular miRNAs is of great therapeutic significance for eliminating the HIV-1 reservoir in HIV-1-infected individuals receiving suppressive highly active antiretroviral therapy (HAART).

Publication types

  • Review

MeSH terms

  • Antiretroviral Therapy, Highly Active / trends
  • CD4-Positive T-Lymphocytes / physiology
  • CD4-Positive T-Lymphocytes / virology*
  • Gene Expression Regulation, Viral
  • Gene Silencing
  • HIV Infections / enzymology
  • HIV Infections / genetics*
  • HIV Infections / prevention & control
  • HIV-1 / physiology*
  • Humans
  • Immunologic Memory
  • Lymphocyte Activation
  • MicroRNAs / genetics*
  • T-Lymphocyte Subsets / physiology
  • T-Lymphocyte Subsets / virology*
  • Virus Latency
  • Virus Replication / genetics
  • p300-CBP Transcription Factors / antagonists & inhibitors
  • p300-CBP Transcription Factors / biosynthesis


  • MIRN17 microRNA, human
  • MIRN20a microRNA, human
  • MicroRNAs
  • p300-CBP Transcription Factors