Abstract
Inoculation of the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the central nervous system (CNS) of susceptible strains of mice results in wide-spread replication within glial cells accompanied by infiltration of virus-specific T lymphocytes that control virus through cytokine secretion and cytolytic activity. Virus persists within white matter tracts of surviving mice resulting in demyelination that is amplified by inflammatory T cells and macrophages. In response to infection, numerous cytokines/chemokines are secreted by resident cells of the CNS and inflammatory leukocytes that participate in both host defense and disease. Among these are the ELR-positive chemokines that are able to signal through CXC chemokine receptors including CXCR2. Early following JHMV infection, ELR-positive chemokines contribute to host defense by attracting CXCR2-expressing cells including polymorphonuclear cells to the CNS that aid in host defense through increasing the permeability the blood-brain-barrier (BBB). During chronic disease, CXCR2 signaling on oligodendroglia protects these cells from apoptosis and restricts the severity of demyelination. This review covers aspects related to host defense and disease in response to JHMV infection and highlights the different roles of CXCR2 signaling in these processes.
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