Efstathiou S, Kemp S, Darby G, Minson A C
Department of Pathology, University of Cambridge, U.K.
J Gen Virol. 1989 Apr;70 ( Pt 4):869-79. doi: 10.1099/0022-1317-70-4-869.
A genetically engineered herpes simplex virus type 1 (HSV-1)thymidine kinase (TK) deletion mutant has been constructed and used to investigate the role of this gene in pathogenesis. Inoculation of mice with the HSV TK deletion mutant resulted in the establishment of latent ganglionic infection as demonstrated by superinfection of explanted ganglia with wild-type (wt) virus but not by routine explant culture suggesting that the virus-encoded TK is not essential for the establishment of latent infection but may be necessary for either reactivation or virus replication following reactivation. In addition, Southern blot hybridization has been used to demonstrate in vivo complementation of this mutant by wt virus in both peripheral and central nervous system tissues of mice during acute infection and to show that such complementation can result in the establishment and reactivation of latent TK- infection.
已构建出一种基因工程改造的单纯疱疹病毒1型（HSV-1）胸苷激酶（TK）缺失突变体，并用于研究该基因在发病机制中的作用。用HSV TK缺失突变体接种小鼠后，如通过野生型（wt）病毒对取出的神经节进行超感染所证明的那样，导致了潜伏性神经节感染的建立，但常规取出培养未证明这一点，这表明病毒编码的TK对于潜伏感染的建立不是必需的，但对于再激活或再激活后的病毒复制可能是必需的。此外，Southern印迹杂交已用于证明在急性感染期间，wt病毒在小鼠的外周和中枢神经系统组织中对该突变体进行体内互补，并表明这种互补可导致潜伏性TK感染的建立和再激活。
