Tetrahydrouridine specifically facilitates deoxycytidine incorporation into herpes simplex virus DNA

T. W. North, C. K. Mathews

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

As reported by Jamieson and Subak-Sharpe (J. Gen. Virol. 31:303-313, 1976), exogenous deoxycytidine is very poorly incorporated into herpes simplex virus DNA. Here it is shown that this incorporation was dramatically increased in the presence of tetrahydrouridine (THU), a specific inhibitor of cytidine-deoxycytidine deaminase. Thus, the exclusion of deoxycytidine from herpes simplex virus DNA probably results from massive degradation by the deaminase, which is consistent with the observation that in the absence of THU, most of the nucleotides formed from exogenous deoxycytidine are dUMP. The effect of THU upon deoxycytidine incorporation was specific for herpes simplex virus-infected cells; THU did not increase deoxycytidine incorporation into DNA of uninfected cells. Therefore, one might expect THU to enhance the antiviral activity of 1-β-D-arabinofuranasylcytosine since this analog is also readily deaminated. However, THU increased both the antiviral activity and the cell toxicity only slightly and to about the same extent. Therefore, the metabolism of 1-β-D-arabinofuranosylcytosine is different from that of deoxycytidine in herpes simplex virus-infected cells.

Original languageEnglish (US)
Pages (from-to)987-993
Number of pages7
JournalJournal of Virology
Volume37
Issue number3
StatePublished - 1981
Externally publishedYes

ASJC Scopus subject areas

  • Immunology

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