Nishiyama Y, Kurachi R, Daikoku T, Umene K
Laboratory of Virology, Nagoya University School of Medicine, Japan.
Virology. 1993 May;194(1):419-23. doi: 10.1006/viro.1993.1279.
We have studied the pathogenic and latency/reactivation potential of a herpes simplex virus type 1 (HSV-1) variant (N38) which has a deletion of four genes, US9, US10, US11, and US12, in the short unique region of the HSV-1 genome. N38 was as pathogenic as the parental wild-type virus following intracerebral infection of mice and replicated with wild-type kinetics in the brain. After intraperitoneal infection, some restricted replication of N38 was observed in the adrenal gland and the deletion virus was about 20-fold less virulent than the parental virus. There was no significant difference between two viruses in the frequency of reactivation or in reactivation time. The results indicate that US9, US10, US11, and US12 gene products are dispensable for its neurovirulence and latency in mice.
我们研究了1型单纯疱疹病毒（HSV-1）变体（N38）的致病潜力以及潜伏/再激活潜力，该变体在HSV-1基因组的短独特区域缺失了四个基因，即US9、US10、US11和US12。在小鼠脑内感染后，N38与亲本野生型病毒一样具有致病性，并在脑中以野生型动力学进行复制。腹腔感染后，在肾上腺中观察到N38有一些受限的复制，并且缺失病毒的毒力比亲本病毒低约20倍。两种病毒在再激活频率或再激活时间上没有显著差异。结果表明，US9、US10、US11和US12基因产物对于其在小鼠中的神经毒力和潜伏性并非必需。
