Induction and suppression of type I interferon responses by mink enteritis virus in CRFK cells

Xiaomei Zhang1, Jigui Wang1, Yaping Mao1

  • 1State Key Laboratory of Agrobiotechnology, Department of Biochemistry and Molecular Biology, College of Biological Sciences, China Agricultural University, Beijing 100193, PR China.

Veterinary Microbiology
|January 24, 2017
PubMed

Insights

Mink enteritis virus (MEV) evades the host immune system by suppressing interferon responses. The MEV nonstructural protein 1 (NS1) is key to this immune evasion.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Mink enteritis virus (MEV) causes significant disease in mink.
  • Type I interferon (IFN) is crucial for antiviral innate immunity.
  • Viruses often develop strategies to counteract IFN responses for successful infection.

Purpose of the Study:

  • To investigate MEV's interaction with the host immune system, specifically its effect on Type I interferon.
  • To identify the viral components responsible for immune evasion.

Main Methods:

  • MEV infection of feline kidney (CRFK) cells.
  • Analysis of IFN and interferon-stimulated genes (ISGs) expression.
  • Assessment of MEV replication in IFN-treated cells.
  • Investigation of the role of MEV nonstructural protein 1 (NS1).

Main Results:

  • MEV infection did not induce IFN or ISG responses in CRFK cells.
  • MEV suppressed IFN production in both stimulated and unstimulated cells.
  • Pre-exposure to IFN did not inhibit MEV infection or replication.
  • The MEV nonstructural protein 1 (NS1), particularly its ORI-binding domain, was identified as mediating this inhibition.

Conclusions:

  • MEV actively evades the host's antiviral defense mechanisms by inhibiting Type I interferon.
  • The MEV NS1 protein is a critical factor in this immune evasion strategy.
  • Targeting NS1 could be a potential therapeutic approach against MEV infections.