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CXCR2 signaling and host defense following coronavirus-induced encephalomyelitis

Brett S Marro1, Martin P Hosking, Thomas E Lane

  • 1Department of Molecular Biology & Biochemistry, University of California, Irvine 92697-3900.

Future Virology
|May 15, 2012
PubMed

Insights

Mouse hepatitis virus (JHMV) infection of the central nervous system (CNS) triggers immune responses. CXCR2 signaling plays a dual role, aiding initial defense and later protecting against demyelination.

Area of Science:

  • Neurovirology
  • Immunology
  • Cell Biology

Background:

  • Mouse hepatitis virus (JHMV) infection causes central nervous system (CNS) demyelination.
  • Cytokines and chemokines, including ELR-positive chemokines, are crucial in host defense and disease pathogenesis.
  • CXCR2 is a chemokine receptor involved in inflammatory responses.

Purpose of the Study:

  • To review the roles of CXCR2 signaling in host defense and disease during JHMV infection.
  • To highlight the dual functions of CXCR2 in the CNS during viral infection.

Main Methods:

  • Review of existing literature on JHMV infection, CNS inflammation, and chemokine signaling.
  • Analysis of the roles of ELR-positive chemokines and CXCR2 in glial cells and inflammatory cells.

Main Results:

  • Early JHMV infection involves CXCR2 signaling attracting polymorphonuclear cells to the CNS, aiding host defense.
  • During chronic JHMV infection, CXCR2 signaling on oligodendroglia protects against apoptosis and reduces demyelination severity.

Conclusions:

  • CXCR2 signaling has distinct roles in the acute and chronic phases of JHMV-induced CNS disease.
  • Targeting CXCR2 may offer therapeutic strategies for viral encephalitis and demyelinating diseases.

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