Purpose: To determine the effect of ICAM-1 deficiency on viral infection of the cornea.
Materials and methods: Wild-type and intercellular adhesion molecule 1 (ICAM-1)-deficient mice were infected with the RE strain of herpes simplex virus type 1 (HSV-1). Corneal swabs and trigeminal ganglia were obtained and analyzed for infectious virus. Corneas and trigeminal ganglia were evaluated for signs of inflammation by immunohistochemical staining and for interferon-gamma (IFN-gamma)-producing cells by enzyme-linked immunospot assay (ELISPOT). Serum anti-HSV-1 antibody titers were determined by enzyme-linked immunosorbent assay (ELISA).
Results: Viral titers in corneal swabs from the wild-type and ICAM-1-deficient mice were not significantly different during the 21-day study. Infectious virus was present in the trigeminal ganglia of wild-type and ICAM-1-deficient mice through day 6 after infection. Serum anti-HSV-1 antibody titers were significantly higher in wild-type mice 6 days after infection, compared with ICAM-1-deficient mice; by day 8 and thereafter, however, antibody titers were not significantly different. Production of interferon gamma was greater in trigeminal ganglion cells from wild-type mice stimulated with interleukin 12 and interleukin 18 on days 4, 6, and 8 after infection compared with cells from ICAM-1-deficient mice. Histopathologic analysis of corneal and ganglion sections from wild-type and ICAM-1-deficient mice showed no significant differences in the time-course of appearance or the intensity of the inflammatory infiltrate. Immunohistochemical staining for CD3(+) T-lymphocytes and CD11b(+) neutrophils and macrophages demonstrated equivalent numbers of these cells in the corneas and trigeminal ganglia of wild-type and ICAM-1-deficient mice.
Conclusions: The results of these experiments indicate that ICAM-1 deficiency has only a modest effect on viral infection of the cornea and the development of an acquired immune response.