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Abstract
The role of pseudorabies virus (PRV) thymidine kinase (TK) expression in the pathogenesis of PRV infection of mice was studied with TK-negative (TK-) mutants. Thymidine phosphorylation and arabinosylthymine inhibition of PRV replication and efficiency of plating were used to characterize TK+ and TK- PRV. In addition, a plaque autoradiography procedure was utilized to determine the TK phenotype of individual plaques. TK+ and TK- PRV replicated well in ocular tissues, while TK+ but not TK- did so in ganglion tissue. Mortality was absent after TK- PRV inoculation and widespread after inoculation of similar amounts of TK+ PRV. Latent infection in mice was not detected with either TK+ or TK- PRV. This study indicated the probable importance of PRV TK expression in acute trigeminal ganglion infection.
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