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Ifit2 deficiency restricts microglial activation and leukocyte migration following murine coronavirus (m-CoV) CNS

Jayasri Das Sarma1,2, Amy Burrows1, Patricia Rayman1

  • 1Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Ohio, United States of America.

Plos Pathogens
|November 30, 2020
PubMed

Insights

Interferon-induced tetratricopeptide repeat protein (Ifit2) is crucial for controlling neurotropic virus infections in mice. Its absence impairs microglial activation and T cell recruitment, hindering viral clearance.

Area of Science:

  • Immunology
  • Virology
  • Neuroscience

Background:

  • Interferon-induced tetratricopeptide repeat protein (Ifit2) is known to protect against viral infections.
  • Neurotropic viruses can cause severe neurological disease.

Purpose of the Study:

  • To investigate the role of Ifit2 in protection against neurotropic coronavirus MHV-RSA59 infection.
  • To elucidate the mechanisms underlying Ifit2-mediated immune protection in the brain.

Main Methods:

  • Infection of Ifit2 knockout (Ifit2-/-) mice and wild-type littermates with MHV-RSA59.
  • Analysis of viral replication, morbidity, mortality, cytokine/chemokine induction, microglial activation, and immune cell recruitment in the brain.
  • Assessment of CX3CR1 expression in microglia.

Main Results:

  • Ifit2-/- mice exhibited increased morbidity and mortality with widespread viral replication in the brain.
  • Despite similar cytokine/chemokine levels, Ifit2-/- mice showed impaired microglial activation and reduced T cell (NK1.1+ and CD4+) recruitment.
  • These deficits correlated with lower microglial CX3CR1 expression, the receptor for CX3CL1 (Fractalkine).

Conclusions:

  • Ifit2 plays a critical role in antiviral immunity within the central nervous system.
  • Ifit2 is essential for proper microglial activation and T cell infiltration, mediated partly through CX3CR1 signaling.
  • These findings reveal a novel function for Ifit2 in host defense against neurotropic viral infections.

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