These results are in line with literature reports describing genital infection with HSV-2 to be characterized by the expression of chemokines including CXCL9 and CXCL10, which interact with the chemokine receptor CXCR3, and that deficiency of these chemokines in the knockout animals rendered them to be more susceptible to infection with HSV [29,42]. This evidence concerns the gene CXCR3 and infection.