ICAM-1 is required for resistance to herpes simplex virus type 1 but not interferon-alpha1 transgene efficacy.

The purpose of this study was to determine the role of ICAM-1 in ocular herpes simplex virus type 1 (HSV-1) infection. Wild-type and ICAM-1 knockout mice were assessed for resistance to ocular HSV-1 infection in the presence of naked DNA plasmid vector or plasmid DNA encoding interferon-alpha1 topically applied to the cornea of the mice. Wild-type mice showed greater resistance to HSV-1 infection compared to ICAM-1 knockout mice as measured by cumulative survival. The absence of ICAM-1 did not affect the efficacy of the interferon-alpha1 transgene against ocular HSV-1. Both ICAM-1 and wild-type mice treated with the transgene showed a reduction in viral load and antigen expression in the trigeminal ganglion compared to the plasmid vector-treated counterparts. In contrast, the presence of the transgene reduced the number of infiltrating cells into the cornea in comparison to plasmid vector DNA controls in the wild-type mice but not in the ICAM-1 knockout mice. Collectively, these results suggest that the IFN-alpha1 transgene can restore resistance against HSV-1 infection in ICAM-1-deficient mice. Copyright 2001 Academic Press.