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Related Experiment Video

Updated: Feb 28, 2026

Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A16
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SHFL Post-Transcriptionally Restricts Coxsackievirus A16 In Vitro and In Vivo.

Huijie Li1,2,3,4, Rui Wang1,2,3,4, Jichen Li1,2,3,4

  • 1National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases (NITFID), National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing 102206, China.

Viruses
|February 27, 2026
PubMed
Summary

The shiftless (SHFL) gene restricts Coxsackievirus A16 (CVA16) replication, a cause of hand, foot, and mouth disease. SHFL deficiency worsens CVA16 infection severity and neurological complications in mice.

Keywords:
coxsackievirus A16enterovirus replicationinnate antiviral immunityneurotropismpost-transcriptional restrictionviral RNA stability

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Area of Science:

  • Virology
  • Immunology
  • Genetics

Background:

  • Coxsackievirus A16 (CVA16) causes hand, foot, and mouth disease, with increasing neurological complications.
  • No specific vaccines or antivirals are currently available for CVA16.
  • Interferon-stimulated genes are crucial in antiviral defense.

Purpose of the Study:

  • To investigate the role of the interferon-stimulated gene shiftless (SHFL) in restricting CVA16 infection.
  • To identify host factors that limit CVA16 replication and pathogenesis.

Main Methods:

  • CRISPR-Cas9 was used to generate SHFL knockout rhabdomyosarcoma cells.
  • Viral replication, cytopathic effects, and disease progression in neonatal mice were assessed.
  • Transcriptomic analysis was performed to understand SHFL-dependent pathways.

Main Results:

  • SHFL expression was induced by CVA16 infection and interferon-beta.
  • SHFL deficiency increased infectious virus production, accelerated replication, and caused severe cytopathic effects.
  • In vivo, SHFL deficiency led to rapid weight loss, neurological signs, increased viral burden, and mortality, with significant tissue damage.

Conclusions:

  • SHFL is a key host factor conferring resistance to CVA16.
  • SHFL acts post-transcriptionally to limit viral spread and tissue injury.
  • SHFL-associated pathways represent potential host-directed antiviral targets.