HIV-1 infection increases microRNAs that inhibit Dicer1, HRB and HIV-EP2, thereby reducing viral replication

PLoS One. 2019 Jan 25;14(1):e0211111. doi: 10.1371/journal.pone.0211111. eCollection 2019.


HIV-1 is the causative agent of AIDS (Autoimmune Deficiency Syndrome). HIV-1 infection results in systemic CD4+ T cell depletion, thereby impairing cell-mediated immunity. MicroRNAs are short (~22 nucleotides long), endogenous single-stranded RNA molecules that regulate gene expression by binding to the 3' untranslated regions (3' UTR) of mRNA transcripts. The relation between HIV-1 infection and human miRNA expression profile has been previously investigated, and studies have shown that the virus can alter miRNA expression and vice versa. Here, we broaden the understanding of the HIV-1 infection process, and show that miRNA-186, 210 and 222 are up-regulated following HIV-1 infection of human Sup-T1 cells. As a result, the host miRNA target genes: Dicer1 (Double-Stranded RNA-Specific Endoribonuclease), HRB (HIV-1 Rev-binding protein) and HIV-EP2 (Human Immunodeficiency Virus Type I Enhancer Binding Protein 2), are down-regulated. Moreover, testing the miRNA-gene anti- correlation on the Jurkat and the HeLa-MAGI cell lines demonstrated the ability of the miRNAs to down-regulate viral expression as well. To conclude, we found that human miR-186, 210 and 222 directly regulate the human genes Dicer1, HRB and HIV-EP2, thus may be filling key roles during HIV-1 replication and miRNA biogenesis. This finding may contribute to the development of new therapeutic strategies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • DEAD-box RNA Helicases / biosynthesis*
  • DNA-Binding Proteins / biosynthesis*
  • Down-Regulation*
  • HIV Infections / metabolism*
  • HIV-1 / physiology*
  • HeLa Cells
  • Humans
  • Jurkat Cells
  • MCF-7 Cells
  • MicroRNAs / metabolism*
  • Nuclear Pore Complex Proteins / biosynthesis*
  • RNA-Binding Proteins / biosynthesis*
  • Ribonuclease III / biosynthesis*
  • Transcription Factors / biosynthesis*
  • Virus Replication / physiology*


  • AGFG1 protein, human
  • DNA-Binding Proteins
  • MicroRNAs
  • Nuclear Pore Complex Proteins
  • RNA-Binding Proteins
  • Transcription Factors
  • HIVEP2 protein, human
  • DICER1 protein, human
  • Ribonuclease III
  • DEAD-box RNA Helicases

Grant support

The authors received no specific funding for this work.