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Receptors for enterovirus 71.

Seiya Yamayoshi1, Ken Fujii2, Satoshi Koike2

  • 1Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, The University of Tokyo , Tokyo 108-8639, Japan.

Emerging Microbes & Infections
|June 4, 2015
PubMed
Summary

Enterovirus 71 (EV71), a cause of hand, foot, and mouth disease, utilizes scavenger receptor B2 (SCARB2) for cell entry and infection. Understanding SCARB2

Keywords:
SCARB2enterovirus 71hand, foot and mouth diseaseneurological disease

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Area of Science:

  • Virology and Molecular Biology
  • Infectious Diseases
  • Neuroscience

Background:

  • Enterovirus 71 (EV71) is a primary cause of hand, foot, and mouth disease (HFMD), occasionally leading to severe neurological complications like encephalitis and paralysis.
  • Multiple cell surface molecules, including scavenger receptor B2 (SCARB2), P-selectin glycoprotein ligand-1 (PSGL-1), sialylated glycan, heparan sulfate, and annexin II (Anx2), facilitate EV71 infection.
  • SCARB2 is crucial for EV71 attachment, entry, and uncoating, significantly enhancing viral infectivity.

Purpose of the Study:

  • To elucidate the structural basis of EV71-SCARB2 interactions and understand the early steps of viral infection.
  • To investigate the role of SCARB2 in the in vivo pathogenesis of EV71-associated neurological diseases.
  • To explore the contribution of other attachment receptors (PSGL-1, sialylated glycan, heparan sulfate, Anx2) to EV71 infection, both independently and in cooperation with SCARB2.

Main Methods:

  • Structural biology techniques to determine the three-dimensional structures of EV71 virions, procapsids, empty capsids, and the SCARB2 exofacial domain.
  • Utilized transgenic mice expressing human SCARB2 to model EV71 susceptibility and neurological disease development in vivo.
  • In vitro studies to assess the roles of various attachment receptors in viral infection, individually and in combination with SCARB2.

Main Results:

  • Elucidation of the structural basis for EV71 infection, providing insights into viral entry mechanisms.
  • Demonstrated that human SCARB2 expression in transgenic mice confers susceptibility to EV71 infection and leads to neurodegenerative disease, mirroring human pathology.
  • Identified PSGL-1, sialylated glycan, heparan sulfate, and Anx2 as attachment receptors that enhance EV71 infection in vitro, with potential synergistic roles with SCARB2.

Conclusions:

  • SCARB2 is a critical determinant of EV71 tropism and pathogenesis, playing essential roles in viral entry and the development of severe neurological disease.
  • The developed transgenic mouse model expressing human SCARB2 is valuable for in vivo studies of EV71 infection and disease.
  • Further research is needed to fully understand the cooperative mechanisms of multiple EV71 receptors and their combined impact on viral pathogenicity in vivo.