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Related Experiment Video

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LL-37 Inhibits EV71 Infection by Upregulating STAC via the EGFR-ERK Signaling Pathway.

Jiaqi Zhang1,2, Hanlin Zhang3, Yi Chen1,2

  • 1Medical School of Chinese People's Liberation Army, Beijing 100853, China.

Viruses
|April 27, 2026
PubMed
Summary
This summary is machine-generated.

The human antimicrobial peptide LL-37 inhibits Enterovirus 71 (EV71) by upregulating the host protein Stac via the EGFR-ERK pathway. This suggests LL-37 as a potential therapy for non-enveloped viral infections.

Keywords:
EV71STACcathelicidinhost defense peptide

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Human antimicrobial peptide LL-37 previously shortened SARS-CoV-2 Omicron variant conversion time.
  • Enterovirus 71 (EV71) is a non-enveloped virus causing significant human disease.

Purpose of the Study:

  • To investigate the broad antiviral mechanism of LL-37 against the non-enveloped virus EV71.
  • To elucidate the host-directed pathways involved in LL-37's antiviral activity.

Main Methods:

  • LL-37 treatment of EV71-infected cells.
  • Viral RNA and protein quantification.
  • Infectious titer assays.
  • Transcriptomic analysis (RNA sequencing).
  • Gene silencing (shRNA) and overexpression studies for Stac.
  • EGFR-ERK signaling pathway analysis.

Main Results:

  • LL-37 dose-dependently reduced EV71 RNA, protein expression, and infectious titers.
  • LL-37's antiviral effect occurred post-viral entry.
  • SH3 and cysteine-rich domain protein (Stac) was uniquely upregulated by LL-37.
  • Stac silencing enhanced EV71 infection; Stac overexpression reduced it.
  • LL-37 activated the EGFR-ERK pathway, leading to Stac upregulation.

Conclusions:

  • LL-37 exhibits broad-spectrum antiviral activity against non-enveloped viruses like EV71.
  • LL-37 employs a host-directed mechanism involving Stac upregulation via EGFR-ERK signaling.
  • LL-37 represents a potential therapeutic candidate for treating non-enveloped viral diseases.