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Influenza virus uses mGluR2 as an endocytic receptor to enter cells

Zixin Ni1, Jinliang Wang1, Xiaofei Yu1

  • 1State Key Laboratory for Animal Disease Control, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, People's Republic of China.

Nature Microbiology
|June 7, 2024
PubMed

Insights

Influenza virus uses HA to bind host cells, triggering clathrin-mediated endocytosis (CME) via mGluR2 and KCa1.1. Blocking this interaction offers a novel antiviral strategy.

Area of Science:

  • Virology
  • Cell Biology
  • Neuroscience

Background:

  • Influenza virus initiates infection by HA binding to host cell sialic acids.
  • Viral entry predominantly occurs via clathrin-mediated endocytosis (CME).
  • Mechanisms linking viral binding to CME initiation remain unclear.

Purpose of the Study:

  • To identify host factors involved in influenza virus-induced CME.
  • To elucidate the role of mGluR2 and KCa1.1 in viral entry.
  • To explore potential host-directed antiviral targets.

Main Methods:

  • siRNA screening to identify host factors.
  • Co-immunoprecipitation to assess protein interactions.
  • Analysis of viral entry in knockout mice models.

Main Results:

  • Metabotropic glutamate receptor subtype 2 (mGluR2) and KCa1.1 are crucial for influenza virus CME.
  • Influenza HA directly interacts with mGluR2, utilizing it as an endocytic receptor.
  • mGluR2 activation of KCa1.1 facilitates F-actin polymerization and clathrin-coated pit maturation.
  • mGluR2-knockout mice exhibit enhanced resistance to influenza virus infection.

Conclusions:

  • Influenza virus HA hijacks the mGluR2/KCa1.1 pathway to mediate CME.
  • Targeting the HA-mGluR2 interaction presents a potential host-directed antiviral therapy.
  • mGluR2 is a key host factor for influenza virus entry and pathogenesis.

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