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Antimicrobial Agents and Chemotherapy, December 2001, p. 3657-3659, Vol. 45, No. 12
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.12.3657-3659.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Inhibition of Herpes Simplex Virus Reactivation by Dipyridamole

Richard B. Tenser,* Andrew Gaydos, and Kathleen A. Hay

Division of Neurology and Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033

Received 16 April 2001/Returned for modification 12 July 2001/Accepted 27 August 2001

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.

* Corresponding author. Mailing address: Division of Neurology, 500 University Dr., Hershey, PA 17033. Phone: (717) 531-8692. Fax: (717) 531-4694. E-mail: rtenser{at}psu.edu.

Antimicrobial Agents and Chemotherapy, December 2001, p. 3657-3659, Vol. 45, No. 12
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.12.3657-3659.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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Copyright © 2001 by the American Society for Microbiology. All rights reserved.