MOLECULAR MECHANISMS OF ANTIVIRAL RESISTANCE
MOLECULAR MECHANISMS OF ANTIVIRAL RESISTANCE
复制标题
DOI：
10.1016/0166-3542(95)00027-j
复制
发表时间：
1995-04-01
影响因子：
7.6
通讯作者：
WHITLEY, RJ
中科院分区：
文献类型：
--
作者：
KIMBERLIN, DW;COEN, DM;WHITLEY, RJ
在HSV感染开始后，病毒基因的表达以高度调节的方式发生。已经鉴定了三类HSV基因，并根据其表达的时间和要求进行分类。这些类是alpha、beta和gamma。α或立即早期基因负责病毒基因组的调节表达。它们在不存在病毒蛋白合成的情况下在感染的宿主细胞中转录。β或早期基因类需要功能性α基因产物来有效表达。β基因产物包括直接参与病毒DNA合成的蛋白质，以及参与核苷酸代谢的酶。因此，它们为抗病毒剂提供了极好的靶标。这种早期基因产物的实例包括病毒DNA聚合酶和胸苷激酶（TK）。虽然病毒DNA聚合酶对于HSV基因组的复制是必需的，但病毒TK对于细胞培养物中的病毒复制不是必需的。然而，体内分析表明，HSV TK在以下方面起关键作用：
Upon initiation of infection by HSV, expression of viral genes occurs in a highly regulated fashion. Three classes of HSV genes have been identified and are classified by both the timing of and the requirements for their expression. These classes are alpha, beta, and gamma. Alpha, or immediate-early, genes are responsible for the regulated expression of the viral genome. They are transcribed in infected host cells in the absence of viral protein synthesis. The beta, or early, gene class requires functional alpha gene products for efficient expression. Beta gene products include proteins which are directly involved in viral DNA synthesis, as well as enzymes involved in nucleotide metabolism. As such, they provide excellent targets for antiviral agents. Examples of such early gene products include viral DNA polymerase and thymidine kinase (TK). While viral DNA polymerase is essential for replication of the HSV genome, viral TK is not essential for viral replication in cell culture. However, in vivo analyses demonstrate that HSV TK plays a pivotal role in