Hepatitis E virus infection activates signal regulator protein α to down-regulate type I interferon

Immunol Res. 2016 Feb;64(1):115-22. doi: 10.1007/s12026-015-8729-y.

Abstract

Hepatitis E virus (HEV) is a major cause of enterically transmitted acute hepatitis worldwide. However, the mechanism of HEV replication is unclear. Type I interferon is the first defense line of host against viral infection. Signal regulator protein α (SIRP-α) plays an important role in negative regulation of innate immunity. In the present study, HEV infection significantly activated the expression of SIRP-α and down-regulated phosphorylation of IRF3, consequently resulted in suppression of type I interferon (IFN-β). In conclusion, HEV exploited SIRP-α to negative regulated IFN-β of the host innate immune system to promote viral infection. It suggested that interfering with the functions of SIRP-α should be considered as a potential therapeutic approach to the prevention and treatment of HEV infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, Differentiation / genetics
  • Antigens, Differentiation / metabolism*
  • Gene Expression Regulation
  • HEK293 Cells
  • Hepatitis E / drug therapy
  • Hepatitis E / immunology*
  • Hepatitis E virus / physiology*
  • Host-Pathogen Interactions
  • Humans
  • Immune Evasion
  • Immunity, Innate / genetics
  • Interferon Regulatory Factor-3 / genetics
  • Interferon Regulatory Factor-3 / metabolism
  • Interferon-beta / metabolism
  • Molecular Targeted Therapy
  • Phosphorylation / genetics
  • RNA, Small Interfering / genetics
  • Receptors, Immunologic / genetics
  • Receptors, Immunologic / metabolism*
  • Virus Replication

Substances

  • Antigens, Differentiation
  • IRF3 protein, human
  • Interferon Regulatory Factor-3
  • RNA, Small Interfering
  • Receptors, Immunologic
  • SIRPA protein, human
  • Interferon-beta