Moriyama K, Mohri S, Watanabe T, Mori R
Department of Virology, School of Medicine, Kyushu University, Fukuoka, Japan.
Microbiol Immunol. 1992;36(8):841-53. doi: 10.1111/j.1348-0421.1992.tb02086.x.
Some SCID mice survived primary infection with herpes simplex virus 1 without the development of peripheral lesions but established coculture-positive ganglionic latency when a low dose of a wild-type strain was inoculated intracutaneously. The latency was also evidenced by the development of the fatal zosteriform skin lesions and the isolation of the virus during pregnancy. We consider that the viral entry into neurons without successive replication, rather than the arrest of the lytic infection within the cells, is an important mechanism in the establishment of latency.
一些重症联合免疫缺陷（SCID）小鼠在初次感染单纯疱疹病毒1后存活下来，未出现外周病变，但在皮内接种低剂量野生型毒株时，建立了共培养阳性的神经节潜伏感染。潜伏感染还通过致命的带状疱疹样皮肤病变的出现以及孕期病毒的分离得到证实。我们认为，病毒进入神经元后不进行连续复制，而非细胞内溶细胞性感染的停滞，是建立潜伏感染的重要机制。
