Piroozmand Ahmad, Koyama A Hajime, Shimada Yoshiko, Fujita Mikako, Arakawa Tsutomu, Adachi Akio
Department of Virology, The University of Tokushima Graduate School of Medicine, Tokushima 770-8503, Japan.
Int J Mol Med. 2004 Oct;14(4):641-5.
The sensitivity of a Us3-deletion mutant virus of herpes simplex virus type 1 (HSV-1) to consensus interferon (IFN) was compared with that of parental wild-type (wt) and the repaired viruses. Although one-step growth of the Us3-deficient virus in the IFN-treated HEp-2 cells was not markedly affected at a high multiplicity of infection (MOI), both the progeny virus yield and cytopathic effect were suppressed in a significantly higher degree in the mutant virus-infected cells than those in wt or the repaired virus-infected cells. This enhanced IFN-sensitivity of the mutant virus was more clearly demonstrated by the infection at a low MOI. In addition, both the size and number of plaques of the Us3-deficient virus in Vero cells were remarkably reduced with increasing concentrations of IFN, compared to those of wt or the repaired virus. These results indicate that the deletion of Us3 gene makes HSV-1 more sensitive to IFN.
将1型单纯疱疹病毒（HSV-1）的Us3缺失突变病毒与亲本野生型（wt）病毒及修复病毒对通用干扰素（IFN）的敏感性进行了比较。尽管在高感染复数（MOI）下，IFN处理的HEp-2细胞中Us3缺陷病毒的一步生长未受到明显影响，但与野生型或修复病毒感染的细胞相比，突变病毒感染的细胞中后代病毒产量和细胞病变效应均受到更显著程度的抑制。在低MOI感染时，突变病毒这种增强的IFN敏感性表现得更为明显。此外，与野生型或修复病毒相比，随着IFN浓度的增加，Vero细胞中Us3缺陷病毒的噬斑大小和数量均显著减少。这些结果表明，Us3基因的缺失使HSV-1对IFN更敏感。
