Enhanced resistance of CXCR3 deficient mice to ocular HSV-1 infection is due to control of replication in the brain ependyma.

Abstract

CXCR3 deficient (CXCR3(-/-)) mice are resistant to ocular HSV-1 infection in that less mice develop encephalitis and succumb to infection in comparison to wild type (WT) animals. A region of the brain previously identified to be crucial for development of encephalitis was evaluated in HSV-1-infected CXCR3(-/-) and WT mice. In this region, known as the ependyma, viral titer, infiltrating leukocyte populations, and key anti-viral cytokine message levels were evaluated. We found that CXCR3(-/-) mice possessed significantly less HSV-1 and expressed significantly more IFN-β mRNA in the brain ependyma compared to WT animals during the development of encephalitis.