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Updated: Jul 17, 2025

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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MAVS integrates glucose metabolism and RIG-I-like receptor signaling

Qiao-Qiao He1, Yu Huang1, Longyu Nie1

  • 1State Key Laboratory of Virology, Modern Virology Research Center, Frontier Science Center for Immunology and Metabolism, College of Life Sciences, Wuhan University, Wuhan, 430072, China.

Nature Communications
|September 2, 2023
PubMed

Insights

Mitochondrial antiviral signaling (MAVS) protein regulates glucose metabolism by shifting pathways like glycolysis to the pentose phosphate pathway (PPP) and hexosamine biosynthesis pathway (HBP). Peroxisomal and MAMs-associated MAVS have distinct roles in this metabolic reprogramming and interferon signaling.

Area of Science:

  • Immunology
  • Cell Biology
  • Metabolic Pathways

Background:

  • Mitochondrial antiviral signaling (MAVS) protein is crucial for RIG-I-like receptor (RLR) signaling.
  • The precise roles of MAVS in glucose metabolism and its cross-regulation with RLR signaling across organelles remain unclear.
  • Understanding how these pathways are coordinated is essential for deciphering cellular defense mechanisms.

Purpose of the Study:

  • To investigate the role of MAVS in glucose metabolism.
  • To elucidate the cross-regulation between RLR signaling and glucose metabolism.
  • To define the organelle-specific functions of MAVS in coordinating these pathways.

Main Methods:

  • Investigated MAVS localization and function in peroxisomes and mitochondria-associated ER membranes (MAMs).
  • Analyzed glucose flux shifts using metabolic pathway tracing.
  • Identified protein-protein interactions within MAVS signalosomes using co-immunoprecipitation and Western blotting.

Main Results:

  • RLR activation via MAVS promotes a metabolic switch from glycolysis to the pentose phosphate pathway (PPP) and hexosamine biosynthesis pathway (HBP).
  • Peroxisomal MAVS directs glucose flux to PPP and induces type III interferon expression.
  • MAMs-associated MAVS directs glucose flux to HBP and induces type I interferon expression, involving specific protein interactions like G6PD and glutamine-fructose-6-phosphate transaminase.

Conclusions:

  • MAVS acts as a critical mediator linking RLR signaling with glucose metabolism.
  • Organelle-specific localization of MAVS dictates distinct metabolic and immune signaling outcomes.
  • This study reveals a novel mechanism of metabolic reprogramming orchestrated by MAVS during innate immune responses.

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