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Related Experiment Video

Updated: Feb 27, 2026

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Venezuelan Equine Encephalitis Virus Antagonizes the cGAS-STING Pathway.

Brittany N Heath1,2, Maryna Akhrymuk1, Abdullahi T Jamiu1,2

  • 1Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA.

Cells
|February 26, 2026
PubMed
Summary

Venezuelan equine encephalitis virus (VEEV) antagonizes the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway. Priming STING before infection limits VEEV replication, but post-infection targeting is ineffective.

Keywords:
EEEVType I interferonVEEValphaviruscGAS-STING

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Venezuelan equine encephalitis virus (VEEV) causes significant human morbidity, including neurological complications.
  • The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway is crucial for antiviral immunity, responding to viral pathogens.
  • While cGAS-STING limits some RNA viruses, its role in New World alphavirus infections like VEEV is poorly understood.

Purpose of the Study:

  • To investigate the impact of STING activation on VEEV infection.
  • To explore STING activation as a potential prophylactic and therapeutic strategy against VEEV.
  • To determine if VEEV antagonizes the cGAS-STING signaling pathway.

Main Methods:

  • Studied STING phosphorylation (Ser366) and interferon-stimulated gene (ISG) upregulation during VEEV infection.
  • Utilized siRNA to assess STING dependency in VEEV infection.
  • Investigated the effects of STING pathway priming before and targeting after VEEV infection.
  • Examined STING phosphorylation inhibition at various multiplicities of infection (MOI).

Main Results:

  • VEEV infection alone did not induce STING phosphorylation, but ISGs were upregulated late in infection.
  • STING loss partially impaired ISG transcription, suggesting noncanonical STING activation.
  • Priming the STING pathway before infection was critical for limiting VEEV replication.
  • Post-infection STING activation targeting abrogated dsDNA antiviral effects.
  • VEEV suppressed STING phosphorylation in an MOI-dependent manner, with significant inhibition at MOI 10.

Conclusions:

  • VEEV infection does not canonically activate the cGAS-STING pathway.
  • VEEV actively antagonizes canonical STING activation in a dose-dependent manner.
  • STING pathway priming shows potential as a prophylactic measure against VEEV, but post-infection targeting is ineffective.