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Foot-and-mouth disease virus non-structural protein 3A inhibits the interferon-β signaling pathway

Dan Li1, Caoqi Lei2, Zhisheng Xu2

  • 1State Key Laboratory of Veterinary Etiological Biology, National Foot and Mouth Diseases Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, China.

Scientific Reports
|February 18, 2016
PubMed

Insights

Foot-and-mouth disease virus (FMDV) protein 3A inhibits the host

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Foot-and-mouth disease virus (FMDV) causes significant economic losses in cloven-hoofed animals.
  • The mechanisms of FMDV pathogenesis and host immune evasion remain incompletely understood.

Purpose of the Study:

  • To investigate the role of FMDV non-structural protein 3A in the host innate immune response.
  • To elucidate the molecular mechanisms by which FMDV evades the host interferon-beta (IFN-β) signaling pathway.

Main Methods:

  • Overexpression of FMDV 3A protein.
  • Analysis of virus-triggered IFN-β signaling pathway activation.
  • Transient transfection and co-immunoprecipitation assays.
  • Investigation of RIG-I, MDA5, and VISA mRNA levels.

Main Results:

  • FMDV 3A protein was identified as a negative regulator of virus-induced IFN-β signaling.
  • FMDV 3A inhibited Sendai virus-triggered activation of IRF3 and expression of RIG-I/MDA5.
  • FMDV 3A directly interacts with RIG-I, MDA5, and VISA via its N-terminal 51 amino acids.
  • FMDV 3A suppressed RIG-I, MDA5, and VISA expression by disrupting their mRNA levels.

Conclusions:

  • FMDV 3A protein inhibits the RIG-I-like receptor (RLR)-mediated IFN-β induction.
  • This study uncovers a novel mechanism of FMDV immune evasion through protein 3A targeting the RLR signaling pathway.

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