Inhibition of herpes simplex virus reactivation by dipyridamole

Richard Tenser, A. Gaydos, K. A. Hay

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

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

Original languageEnglish (US)
Pages (from-to)3657-3659
Number of pages3
JournalAntimicrobial agents and chemotherapy
Volume45
Issue number12
DOIs
StatePublished - Dec 13 2001

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Dipyridamole
Simplexvirus
Thymidine
Virus Latency
Nucleosides
Antiviral Agents

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Pharmacology (medical)
  • Infectious Diseases

Cite this

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Inhibition of herpes simplex virus reactivation by dipyridamole. / Tenser, Richard; Gaydos, A.; Hay, K. A.

In: Antimicrobial agents and chemotherapy, Vol. 45, No. 12, 13.12.2001, p. 3657-3659.

Research output: Contribution to journalArticle

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AU - Hay, K. A.

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