Related Experiment Video

Updated: Jun 24, 2026

Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis
10:23

Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis

Published on: April 17, 2017

Lipid droplet-mitochondria tethering releases MAVS inhibition to potentiate antiviral immunity

Qianwen Peng1, Wenbo Liang1, Wei Wang1

  • 1Key Laboratory of Infection and Immunity of Shandong Province, and Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China; State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, Shandong, China.

Cell Reports
|June 22, 2026
PubMed

Insights

Viral infection triggers lipid droplet formation, which aids mitochondrial antiviral signaling protein (MAVS) aggregation and innate immunity. Lipid metabolism, through lipid droplets, enhances antiviral defense, offering new therapeutic strategies.

Area of Science:

  • Immunology
  • Cell Biology
  • Metabolic Regulation

Background:

  • Mitochondrial antiviral signaling protein (MAVS) aggregates are crucial for innate immunity against RNA viruses.
  • The metabolic regulation governing MAVS activation remains largely unknown.

Purpose of the Study:

  • To investigate the role of metabolic regulation, specifically lipid droplets (LDs), in controlling MAVS-mediated antiviral immunity.

Main Methods:

  • Studied the physical interaction between LDs and mitochondria during viral infection.
  • Investigated the function of LD-resident protein PLIN3 and mitochondrial protein MFN2 in MAVS aggregation.
  • Analyzed the impact of fatty acid transfer at organelle contact sites on MAVS signaling.
  • Assessed the effects of oleic acid (OA)-enriched diets and Seipin deficiency on antiviral responses in vivo.

Main Results:

  • Viral infection induces LD formation, promoting MAVS prion-like aggregate assembly through interaction with mitochondria.
  • PLIN3 binds MFN2, releasing MFN2-mediated inhibition of MAVS oligomerization.
  • LD-mitochondria contact sites facilitate fatty acid transfer, maintaining mitochondrial membrane potential for MAVS signaling.
  • OA-enriched diets enhance LD formation and antiviral immunity; myeloid-specific Seipin deficiency impairs MAVS activation and increases viral susceptibility.

Conclusions:

  • Lipid droplets act as metabolic platforms that link lipid metabolism to innate antiviral defense via organelle crosstalk.
  • LD induction represents a potential therapeutic strategy for enhancing antiviral immunity.
Keywords:
CP: immunologyMAVSSeipinantiviral immunityinnate immunitylipid droplettype I interferon

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