Shiraki K, Matsui S, Aiba N
Department of Virology, Toyama Medical and Pharmaceutical University, Japan.
Vaccine. 1993 Nov;11(14):1380-2. doi: 10.1016/0264-410x(93)90164-s.
Susceptibility of Oka varicella vaccine virus to antiherpetic drugs was determined by the effective dose for 50% plaque reduction (ED50) using cell-free virus preparation. ED50 values were 3.02 microM for acyclovir, 3.72 microM for vidarabine, 0.0035 microM for sorivudine, and 4.67 microM for penciclovir. Oka varicella vaccine virus was as susceptible to these drugs as wild-type viruses. Sensitivity of thymidine kinase (TK)-deficient virus to penciclovir and of some DNA polymerase (DPase) mutants to sorivudine suggested that these drugs might be used for the treatment of vaccine recipients, even if Oka varicella vaccine became acyclovir-resistant by mutations in the TK or DPase genes, respectively. This result encourages the wider use of Oka varicella vaccine even for immunocompromised hosts because of its attenuation and susceptibility to chemotherapeutic drugs.
