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Interferon regulatory factor 3 attenuates reovirus myocarditis and contributes to viral clearance

Geoffrey H Holm1, Andrea J Pruijssers, Lianna Li

  • 1Lamb Center for Pediatric Research, D7235 MCN, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. terry.dermody@vanderbilt.edu

Journal of Virology
|May 14, 2010
PubMed

Insights

Interferon regulatory factor 3 (IRF-3) is crucial for clearing reovirus infections in mice. Its absence leads to higher viral loads and severe tissue damage, particularly myocarditis, indicating IRF-3

Area of Science:

  • Virology
  • Immunology
  • Pathology

Background:

  • Apoptosis is a key feature of reovirus-induced encephalitis and myocarditis in newborn mice.
  • The antiviral transcription factor IRF-3 (interferon regulatory factor 3) promotes reovirus-induced apoptosis in cell culture.

Purpose of the Study:

  • To investigate the role of IRF-3 in reovirus disease pathogenesis and clearance in vivo.

Main Methods:

  • Newborn IRF-3(+/+) (wild-type) and IRF-3(-/-) (knockout) mice were infected orally with reovirus strains T1L (mild) and T3SA+ (virulent).
  • Survival rates, viral titers in various organs, and pathological changes were monitored.
  • Cellular and humoral immune responses were compared between wild-type and knockout mice.

Main Results:

  • IRF-3 deficiency did not affect survival following infection with the virulent T3SA+ strain.
  • Absence of IRF-3 significantly decreased survival rates and increased viral titers in all organs examined following infection with the mild T1L strain.
  • IRF-3(-/-) mice exhibited severe myocarditis and marked pathological changes, despite equivalent immune responses compared to wild-type mice.

Conclusions:

  • IRF-3 plays a critical role in facilitating reovirus clearance and preventing tissue damage, particularly myocarditis, in a strain-dependent manner.
  • IRF-3 functions independently of the adaptive immune response in controlling reovirus infection.

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