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EMCV VP2 degrades IFI16 through Caspase-dependent apoptosis to evade IFI16-STING pathway

Ruofei Feng1,2, Dianyu Li1,3, Zhenfang Yan1,3

  • 1Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, China.

Virology Journal
|November 17, 2024
PubMed

Insights

Interferon-gamma inducible protein 16 (IFI16) fights EMCV infection. However, EMCV VP2 protein degrades IFI16, suppressing antiviral immunity via apoptosis.

Area of Science:

  • Innate immunity
  • Molecular virology
  • Cellular signaling

Background:

  • Interferon-gamma inducible protein 16 (IFI16) is a DNA sensor crucial for initiating antiviral responses through the STING-dependent type I interferon (IFN-I) pathway.
  • The precise regulation of the IFI16-STING signaling pathway during Enterovirus species C (EMCV) infection remains incompletely understood.

Purpose of the Study:

  • To investigate the interaction between IFI16 and EMCV.
  • To elucidate the mechanism by which EMCV modulates the IFI16-STING antiviral pathway.

Main Methods:

  • Investigated IFI16 expression in EMCV-infected A549 cells.
  • Screened EMCV viral proteins for interaction with IFI16.
  • Analyzed the role of the caspase-dependent apoptosis pathway in IFI16 degradation.

Main Results:

  • EMCV infection was found to suppress IFI16 expression in A549 cells.
  • The EMCV VP2 protein was identified as a factor that hinders the IFI16-mediated antiviral response.
  • VP2 induces degradation of IFI16 through a caspase-dependent apoptosis pathway.

Conclusions:

  • IFI16 plays an active role in combating EMCV infection.
  • The EMCV VP2 protein employs a novel mechanism to counteract IFI16-STING innate immune signaling by promoting IFI16 degradation.
  • Understanding this interaction is key to developing strategies against EMCV infections.
Keywords:
Caspase-dependent apoptosisEMCVIFI16Viral protein VP2

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