Inhibition of Herpes Simplex Virus Reactivation by Dipyridamole

AUTOR(ES)

Tenser, Richard B.

FONTE

American Society for Microbiology

RESUMO

Herpes simplex virus (HSV) reactivation from latency was investigated. Reactivation of thymidine kinase-negative HSV, which is defective for reactivation, was greatly enhanced by thymidine (TdR). The reactivation-enhancing effect of TdR was blocked by dipyridamole (DPM), a known nucleoside transport inhibitor. DPM also inhibited wild-type HSV reactivation, suggesting potential antiviral use.

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