Abstract

A significant restriction was demonstrated in the ability of herpes simplex virus type 1 virion host shutoff (vhs) mutant viruses to invade the corneal epithelium. Viral replication and invasion was confined to the areas of the cornea which were scarified prior to infection. Differences between wild-type andvhsmutant replication in corneasin vivowere 100- to 1000-fold at all timepoints postinfection. Smaller but still significant growth restrictions were observed in cultured corneal cells. This difference betweenin vitroandin vivois not likely to be due to differences in cell cycle status sincevhs-induced RNA degradation can occur in both cycling and noncycling cellsin vitro.The vhs function is therefore important for invasion of the cornea and secondarily the nervous system and is thereby required for efficient establishment of latency.

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