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

• CXCR3 deficient mice are resistant to herpes simplex encephalitis.
• Brain ependymal tissue of CXCR3–/– mice contain less virus compared to wild type animals.
• IFN-β mRNA expression in the brain ependyma is correlative to resistance to HSV-1 in CXCR3–/– mice.

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.