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Encephalomyocarditis virus (EMCV) uses ADAM9 as a crucial factor for cell entry. This discovery enhances understanding of picornavirus infection mechanisms and viral myocarditis.

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Area of Science:

  • Virology
  • Molecular Biology
  • Pathogenesis

Background:

  • Picornaviruses are diverse pathogens causing various diseases.
  • Viral tropism drives picornavirus pathogenesis, with some infecting the heart causing myocarditis.
  • Encephalomyocarditis virus (EMCV) models myocarditis but its entry pathway is unclear.

Purpose of the Study:

  • To identify the host cell receptor and entry requirements for Encephalomyocarditis virus (EMCV).
  • To elucidate the molecular mechanisms underlying EMCV infection and pathogenesis.

Main Methods:

  • CRISPR knockout screening was performed in human cells susceptible to EMCV.
  • Infection assays were conducted to assess the role of identified factors.

Main Results:

  • ADAM9 was identified as an essential entry factor for EMCV in both mouse and human cells.
  • The extracellular domain of ADAM9, not its enzymatic activity or intracellular domain, is required for EMCV infection.
  • These findings suggest ADAM9 functions as an entry receptor or at an early stage of viral entry.

Conclusions:

  • ADAM9 is a critical host factor for EMCV entry into cells.
  • Understanding ADAM9's role provides insights into picornavirus tropism and myocarditis.
  • This research opens new avenues for studying EMCV pathogenesis and potential therapeutic targets.