胸苷激酶活性改变或缺乏的单纯疱疹病毒对西多福韦敏感性增加的生化基础。
Biochemical basis for increased susceptibility to Cidofovir of herpes simplex viruses with altered or deficient thymidine kinase activity.
作者信息
Mendel D B, Barkhimer D B, Chen M S
机构信息
Department of Biochemistry and Virology, Gilead Sciences, Foster City, California 94404, USA.
出版信息
Antimicrob Agents Chemother. 1995 Sep;39(9):2120-2. doi: 10.1128/AAC.39.9.2120.
Abstract
It has been observed that herpes simplex virus mutants with deficient or altered thymidine kinase activity are more susceptible to Cidofovir (CDV; 1-[(S)-3-hydroxy-2-(phosphonomethoxy)propyl]cytosine dihydrate) in tissue culture than are the parental strains. During infection of cells, the elevation of the dCTP pool by thymidine kinase mutant viruses is less than that induced by the wild-type virus. The competition between CDV diphosphate and dCTP at the viral polymerase is therefore changed in favor of CDV diphosphate, enhancing its activity.
摘要
据观察，在组织培养中，胸苷激酶活性缺陷或改变的单纯疱疹病毒突变体比亲代菌株对西多福韦（CDV；1-[(S)-3-羟基-2-(膦酰甲氧基)丙基]胞嘧啶二水合物）更敏感。在细胞感染过程中，胸苷激酶突变病毒引起的dCTP池升高低于野生型病毒诱导的升高。因此，病毒聚合酶处CDV二磷酸和dCTP之间的竞争发生改变，有利于CDV二磷酸，从而增强其活性。
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