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Enterovirus 71 2C Protein Inhibits NF-κB Activation by Binding to RelA(p65)

Haiwei Du1, Peiqi Yin1, Xiaojie Yang1

  • 1MOH Key Laboratory of Systems Biology of Pathogens, Institute of Pathogen Biology, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing 100176, PR China.

Scientific Reports
|September 24, 2015
PubMed

Insights

Enterovirus 71 (EV71) protein 2C binds to RelA(p65), inhibiting NF-κB immune signaling. This discovery reveals a new mechanism for how EV71 evades the host immune response.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Viruses employ diverse strategies to disrupt host immune signaling pathways.
  • Nuclear factor-kappa B (NF-κB) signaling is crucial for regulating innate and adaptive immunity.
  • Enterovirus 71 (EV71) is a significant pathogen responsible for hand-foot-mouth disease.

Purpose of the Study:

  • To identify novel viral proteins that interact with components of the NF-κB pathway.
  • To elucidate the mechanism by which EV71 antagonizes host immune responses.

Main Methods:

  • Yeast two-hybrid screening to identify protein-protein interactions.
  • Co-immunoprecipitation assays to confirm interactions between viral and host proteins.
  • Analysis of NF-κB activation and complex formation.

Main Results:

  • The EV71 2C protein was identified as a binding partner for RelA(p65).
  • EV71 2C interacts with the IPT domain of p65, hindering p65/p50 heterodimer formation.
  • Picornavirus 2C proteins were shown to inhibit NF-κB activation and interact with p65 and IKKβ.

Conclusions:

  • EV71 utilizes its 2C protein to directly interfere with NF-κB signaling.
  • This interaction represents a novel mechanism of viral immune evasion employed by EV71.
  • The findings offer insights into the broader strategies of picornavirus 2C proteins in subverting host immunity.

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