Inhibition of herpes simplex virus reactivation by dipyridamole

Antimicrobial Agents and Chemotherapy

Volumn 45, Issue 12, 2001, Pages 3657-3659

  Tenser, R B ^a   Gaydos, A ^a   Hay, K A ^a  

^a Division of Neurology   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANTIVIRUS AGENT; DIPYRIDAMOLE; THYMIDINE KINASE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CONTROLLED STUDY; HERPES SIMPLEX VIRUS; INOCULATION; LATENT PERIOD; MOUSE; NONHUMAN; NUCLEOSIDE TRANSPORT; PRIORITY JOURNAL; STRAIN DIFFERENCE; VIRUS REACTIVATION;

ANIMALS; DIPYRIDAMOLE; GANGLIA, SPINAL; HERPESVIRUS 1, HUMAN; HUMANS; MICE; PLATELET AGGREGATION INHIBITORS; THYMIDINE; THYMIDINE KINASE; TRIGEMINAL GANGLION; VIRUS LATENCY; VIRUS REPLICATION;

EID: 0035180517     PISSN: 00664804     EISSN: None     Source Type: Journal    
DOI: 10.1128/AAC.45.12.3657-3659.2001     Document Type: Article

References (18)

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13. Herpes simplex virus type 1 latency-associated transcription unit promotes anatomical site-dependent establishment and reactivation from latency
14. Dipyridamole potentiates the activity of various acyclic nucleoside phosphonates against varicella-zoster virus, herpes simplex virus and human cytomegalovirus
15. Dipyridamole potentiates the inhibition by 3′-azido-3′ deoxythymidine and other dideoxynucleosides of human immunodeficiency virus replication in monocyte-macrophages
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17. Reactivation of thymidine kinase-defective herpes simplex virus is enhanced by nucleoside
18. Antiviral activity of dipyridamole and its derivatives against influenza virus A