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Correction: Wang et al. STING Restricts EV-A71 Infection by Regulating T Cell Development and Enhancing Immune Cell Effector Function. <i>Int. J. Mol. Sci.</i> 2025, <i>26</i>, 11441.

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STING Restricts EV-A71 Infection by Regulating T Cell Development and Enhancing Immune Cell Effector Function.

Huiqiang Wang1,2, Ya Wang1,2, Shuo Wu1,2,3

  • 1CAMS Key Laboratory of Antiviral Drug Research, Beijing Key Laboratory of Technology and Application for Anti-Infective New Drugs Research and Development, NHC Key Laboratory of Biotechnology of Antibiotics, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.

International Journal of Molecular Sciences
|December 11, 2025
PubMed
Summary

Activating STING inhibits Enterovirus A71 (EV-A71) replication in vivo, improving survival. STING knockout worsens EV-A71 infection, highlighting STING

Keywords:
EV-A71STINGdiABZIimmune regulationinflammation

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Enterovirus A71 (EV-A71) infection can activate STING signaling pathways in vitro.
  • The in vivo role of STING and its immune regulatory mechanisms in EV-A71 infection are not fully understood.

Purpose of the Study:

  • To investigate the role and mechanism of STING in regulating EV-A71 infection in vivo.
  • To explore STING's impact on immune responses during EV-A71 infection.

Main Methods:

  • Utilized STING-specific agonist diABZI to activate STING.
  • Employed STING-knockout mice to assess STING's function in EV-A71 infection.
  • Analyzed viral replication, clinical symptoms, survival rates, immune cell populations, and cytokine profiles.

Main Results:

  • STING activation inhibited EV-A71 replication, reduced symptoms, and increased survival in mice.
  • STING knockout exacerbated viral replication, lethality, and disease severity.
  • STING activation promoted interferon signaling, upregulated interferon-stimulated genes (ISGs), modulated cytokine profiles, and expanded immune cell populations (T cells, NK cells, myeloid cells).
  • STING knockout impaired T cell development and reduced CD8+ T cell and NK cell effector functions.

Conclusions:

  • STING activation effectively suppresses EV-A71 replication and alleviates infection symptoms by modulating immune and inflammatory responses.
  • Findings provide a framework for understanding STING's role in antiviral immunity.
  • Suggests potential for STING-targeted therapies against viral infections.