Inhibition of herpes simplex virus reactivation by dipyridamole.
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.
Tenser
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RB
Division of Neurology and Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA. rtenser@psu.edu
Gaydos
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A
Hay
K A
KA
D000818:Animals; D004176:Dipyridamole / Q000494:pharmacology*; D005727:Ganglia, Spinal / Q000821:virology; D018259:Herpesvirus 1, Human / Q000187:drug effects*; D006801:Humans; D051379:Mice; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D013936:Thymidine / Q000494:pharmacology; D013937:Thymidine Kinase / Q000032:analysis / Q000378:metabolism; D012668:Trigeminal Ganglion / Q000821:virology; D017735:Virus Latency / Q000187:drug effects*; D014779:Virus Replication / Q000187:drug effects
D010975:Platelet Aggregation Inhibitors; D004176:Dipyridamole; D013937:Thymidine Kinase; D013936:Thymidine