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Mammalian cells use the autophagy process to restrict avian influenza virus replication

Siwen Liu1, Bobo Wing-Yee Mok1, Shaofeng Deng1

  • 1State Key Laboratory for Emerging Infectious Diseases, InnoHK Centre for Virology, Vaccinology, and Therapeutics, and Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.

Cell Reports
|June 9, 2021
PubMed

Insights

Avian influenza A virus (IAV) with avian PB2 proteins forms aggregates in mammalian cells. This selective autophagy mechanism restricts avian-IAV replication, impacting host adaptation.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Host adaptive mutations in influenza A virus (IAV) PB2 protein are crucial for human infection.
  • The precise molecular mechanisms by which PB2 facilitates host adaptation remain incompletely understood.
  • IAV PB2 protein plays a significant role in viral replication and host range determination.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying host restriction of avian-IAV in mammalian cells.
  • To investigate the role of PB2 protein in viral ribonucleoprotein (vRNP) aggregation and cellular responses.
  • To determine the contribution of autophagy to the host restriction of avian-PB2 IAV.

Main Methods:

  • Observation of vRNP aggregation in mammalian cells infected with avian-PB2 IAV.
  • Analysis of vRNP aggregates using electron microscopy and immunofluorescence.
  • Assessment of autophagic flux and p62-mediated vRNP sequestration.

Main Results:

  • Avian-PB2 IAV infection induces vRNP aggregation at the microtubule-organizing center (MTOC) in mammalian cells.
  • These aggregates exhibit aggresome-like properties and are associated with autophagic vacuoles.
  • Avian-PB2 IAV increases autophagic flux, and p62 is essential for vRNP aggregate formation via interaction with PB2.

Conclusions:

  • Selective autophagic sequestration of vRNPs is a host restriction strategy against avian-PB2 IAV.
  • The PB2 protein's interaction with p62 mediates vRNP sequestration into autophagosomes.
  • This mechanism contributes to limiting avian-IAV replication in mammalian hosts.
Keywords:
M2PB2adaptationautophagyavian influenzacross species transmissionhost restrictioninfluenzap62

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