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Updated: Jun 23, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
08:32

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

MAVS-mediated apoptosis and its inhibition by viral proteins

Yu Lei1, Chris B Moore, Rachael M Liesman

  • 1Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina, USA.

Plos One
|May 1, 2009
PubMed
Abstract

Insights

The mitochondrial antiviral signaling adaptor MAVS induces apoptosis during viral infection, independent of interferon production. Viral proteins inhibit this MAVS-mediated cell death, suggesting a novel immune evasion strategy.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Host antiviral responses involve immune activation and programmed cell death.
  • The mitochondrial antiviral signaling adaptor MAVS is crucial for inducing type-1 interferons (IFN-I) against viral infections.

Purpose of the Study:

  • To elucidate the role of MAVS in virus-induced apoptotic responses.
  • To identify viral mechanisms that may evade MAVS-mediated apoptosis.

Main Methods:

  • Investigated MAVS-induced apoptosis in fibroblasts.
  • Utilized MAVS knockout (MAVS-/-) fibroblasts for viral challenge.
  • Conducted a functional screen to identify viral protein inhibitors of MAVS-induced apoptosis.

Main Results:

  • MAVS induces apoptosis independently of IFN-I production, requiring mitochondrial localization and caspase activity.
  • MAVS-/- fibroblasts exhibit resistance to Sendai virus-induced apoptosis.
  • Hepatitis C virus NS3/4A and SARS-CoV NSP15 were identified as inhibitors of MAVS-induced apoptosis.

Conclusions:

  • MAVS plays a novel role in controlling viral infections by inducing apoptosis.
  • Specific viral proteins have evolved to inhibit MAVS-mediated apoptosis as an immune evasion tactic.

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