These results correlate with the observation of a small-plaque phenotype exhibited by the UL13-deficient HSV-1 mutants (Fig 2) and corroborate the viral DNA accumulation data (Fig 3), suggesting that the HSV-1 ΔUL13 mutants are deficient in their ability to spread from one host cell to another and that the activity of viral protein kinases is crucial at the late phase of viral infection. This evidence concerns the gene RPL13A and viral infectious disease.