Abstract
Herpes simplex viruses are human pathogens that cause oral and ocular lesions (HSV-1) or genital lesions (HSV-2). These viruses code for enzymes with substrate specificities different from those of the host cell. The pyrimidine metabolism of the cell is augmented by a virus-coded deoxythymidine (dThd) kinase (TK). This enzyme has a relatively broad phosphate acceptor specificity which permits the phosphorylation of several antiviral nucleoside analogs, the first step in their activation. These analogs are selective inhibitors of DNA synthesis in virus-infected cells, in part, because they are phosphorylated to their triphosphate derivatives only in infected cells.
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© 1984 Plenum Press, New York
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Fyfe, J.A. (1984). Selectivity of Antiviral Effectiveness Derived from Differences of Herpes Simplex Virus-Coded Thymidine Kinases. In: De Bruyn, C.H.M.M., Simmonds, H.A., Müller, M.M. (eds) Purine Metabolism in Man-IV. Advances in Experimental Medicine and Biology, vol 165. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4553-4_47
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DOI: https://doi.org/10.1007/978-1-4684-4553-4_47
Publisher Name: Springer, Boston, MA
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