Consequences of CXCL10 and IL-6 induction by the murine IFN-alpha1 transgene in ocular herpes simplex virus type 1 infection.

Herpes simplex virus type 1 infection of the mouse eye results in an impressive inflammatory response culminating in the death of the animal or the establishment of a "latent" infection depending on a number of ill-defined variables that include components of the innate and adaptive immune system. The application of type I interferon transgenes has been found to antagonize viral replication and spread from the eye to the nervous system. Associated with the in situ transfection of the cornea is the upregulation of two inflammatory molecules, interleukin-6 and CXCL10. In this article, we will further examine the contribution these molecules may have in the host response to ocular infection with herpes simplex virus type 1.