Inhibition of herpes simplex virus replication by purine deoxyribonucleosides

T. W. North

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The inhibition of herpes simplex virus (HSV) replication by 2'-deoxyadenosine (dAdo) is greatly potentiated by the presence of the inhibitor of adenosine deaminase, erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA). HSV replication is inhibited by dAdo [in the presence of EHNA] or by 2'-deoxyguanosine (dGuo) at concentrations slightly lower than are necessary to inhibit growth of uninfected HeLa cells. Under conditions where virus replication is inhibited by >99% with dAdo and EHNA, the level of dATP increases 50-fold or more, and synthesis of HSV DNA is inhibited. However, there is no depletion of any other DNA precursor, and HSV multiplication is not restored by simultaneous provision of dGuo, deoxythymidine, deoxycytidine, or a combination of all three of these nucleosides. Thus, the inhibition of HSV replication by dAdo cannot be explained as a block of precursor provision through inhibition of ribonucleotide reductase. In contrast, dGuo treatment of HSV-infected cells leads to depletion of dCTP, and virus multiplication is partially restored by provision of deoxycytidine. HSV-infected cells may serve as a useful system for study of the toxic effects of dAdo that are unrelated to inhibition of ribonucleotide reductase by dATP.

Original languageEnglish (US)
Pages (from-to)1415-1419
Number of pages5
JournalCancer Research
Volume44
Issue number4
StatePublished - 1984
Externally publishedYes

Fingerprint

Deoxyribonucleosides
Simplexvirus
Virus Replication
Deoxyguanosine
Ribonucleotide Reductases
Deoxycytidine
Adenosine Deaminase Inhibitors
Human Herpesvirus 2
Poisons
DNA
HeLa Cells
Nucleosides
Thymidine
purine
2'-deoxyadenosine
Viruses
9-(2-hydroxy-3-nonyl)adenine
Growth

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Inhibition of herpes simplex virus replication by purine deoxyribonucleosides. / North, T. W.

In: Cancer Research, Vol. 44, No. 4, 1984, p. 1415-1419.

Research output: Contribution to journalArticle

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