MiR-155-5p modulates HSV-1 replication via the epigenetic regulation of SRSF2 gene expression

Epigenetics. 2019 May;14(5):494-503. doi: 10.1080/15592294.2019.1600388. Epub 2019 Apr 5.

Abstract

A previous study reported that miR-155-5p knockout mice were more resistant to herpes simplex virus type I (HSV-1) infection. However, the exact underlying molecular mechanism remains to be elucidated. Here, we demonstrated that HSV-1 infection upregulates miR-155-5p expression. By binding to the promoter of serine/arginine-rich splicing factor 2 (SRSF2), which is an important transcriptional activator of HSV-1 genes that was previously reported by our group, and altering the histone modification located near the transcription start site (TSS) of the SRSF2 gene, miR-155-5p promotes the transcription of the SRSF2 gene, ultimately increasing viral replication and viral gene expression. Our results provide insight for an understanding of the roles and molecular mechanism of miR-155-5p in HSV-1 replication and the epigenetic control of SRSF2 gene expression.

Keywords: HSV-1; Mir-155-5p; SRSF2; epigenetic regulation; gene transcription.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Epigenesis, Genetic*
  • HeLa Cells
  • Herpes Simplex / genetics
  • Herpes Simplex / virology*
  • Herpesvirus 1, Human / physiology*
  • Humans
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Promoter Regions, Genetic
  • Serine-Arginine Splicing Factors / genetics*
  • Serine-Arginine Splicing Factors / metabolism
  • Virus Replication

Substances

  • MIRN155 microRNA, human
  • MicroRNAs
  • SRSF2 protein, human
  • Serine-Arginine Splicing Factors

Grants and funding

This work was supported by the China Postdoctoral Research Foundation of China [2018M633216].