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Cellular receptors for enterovirus A71.

Kyousuke Kobayashi1, Satoshi Koike2

  • 1Neurovirology Project, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, 156-8506, Japan.

Journal of Biomedical Science
|January 12, 2020
PubMed
Summary

Enterovirus 71 (EV-A71) uses scavenger receptor class B, member 2 (SCARB2) to infect cells and cause severe disease. Other attachment receptors enhance EV-A71 infection but do not initiate viral uncoating.

Keywords:
Enterovirus 71Hand, foot, and mouth diseaseNeurological diseaseUncoating, SCARB2Viral receptor, attachment

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Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Enterovirus 71 (EV-A71) causes hand, foot, and mouth disease, sometimes leading to severe neurological complications.
  • Scavenger receptor class B, member 2 (SCARB2) is identified as a major receptor for EV-A71 entry.

Purpose of the Study:

  • To elucidate the structural basis of EV-A71 binding to its receptor SCARB2.
  • To investigate the roles of SCARB2 and other attachment receptors in EV-A71 infection and pathogenesis.

Main Methods:

  • Cryo-electron microscopy was used to determine the structure of the EV-A71-SCARB2 complex.
  • Expression of SCARB2 in transgenic mice was used to study EV-A71 susceptibility in vivo.
  • Analysis of various cell surface molecules involved in viral attachment.

Main Results:

  • The three-dimensional structure reveals specific binding interactions between SCARB2 and EV-A71 capsid proteins (VP1 and VP2).
  • SCARB2-mediated viral entry and RNA uncoating are dependent on SCARB2 and low pH.
  • Other molecules like heparan sulfate proteoglycans act as attachment receptors, enhancing but not initiating viral uncoating.

Conclusions:

  • SCARB2 is crucial for EV-A71 internalization and subsequent RNA release.
  • Attachment receptors contribute to viral binding but are distinct from the entry-mediating receptor SCARB2.
  • Further research is needed to fully understand the roles of these molecules in EV-A71 pathogenesis.