The role of herpesvirus type 1 thymidine kinase in experimental ocular infections.
Herpesvirus type 1 thymidine-kinase-negative mutants are readily selected for in tissue culture and in humans by acyclovir, a promising antiviral agent. We investigated the ocular pathogenicity of thymidine-kinase-negative mutants in the rabbit. The natural course of untreated keratitis induced by the herpesvirus type 1 thymidine-kinase-negative strain was characterized by superficial dendrites and geographic ulcers that healed spontaneously without loss of corneal clarity. We also studied the relationship between herpesvirus type 1 thymidine-kinase activity and virulence in the rabbit with three strains of herpesvirus type 1: NIH thymidine-kinase-positive (100% thymidine-kinase activity), NIH thymidine-kinase-intermediate (25% thymidine-kinase activity), and NIH thymidine-kinase-negative (0% thymidine-kinase activity). Despite comparable ocular titers, the NIH thymidine-kinase-positive strain proved to be the most virulent, causing significantly (P less than .002) more keratitis, encephalitis, and death than the other strains.
D000818:Animals; D006564:Herpesviridae / Q000201:enzymology / Q000472:pathogenicity*; D007635:Keratitis, Dendritic / Q000209:etiology / Q000382:microbiology*; D009154:Mutation; D011817:Rabbits; D013937:Thymidine Kinase / Q000378:metabolism; D014774:Virulence
D013937:Thymidine Kinase