MacLean A, Wei X Q, Huang F P, Al-Alem U A, Chan W L, Liew F Y
Division of Virology, University of Glasgow, UK.
J Gen Virol. 1998 Apr;79 ( Pt 4):825-30. doi: 10.1099/0022-1317-79-4-825.
Mice deficient in the inducible nitric-oxide synthase (iNOS), constructed by gene-targeting, were significantly more susceptible to herpes simplex virus (HSV)-1 infection, displayed a delayed clearance of virus from the dorsal root ganglia (DRG) and exhibited an increase in the frequency of virus reactivation in DRG compared with similarly infected heterozygous mice. The infected iNOS-deficient mice developed enhanced Th1-type immune responses and their spleen cells produced higher concentrations of IL-12 than similarly infected heterozygous mice. This finding suggests that iNOS plays an important role in resistance against HSV-1 infection. Furthermore, nitric oxide (NO) may block the development of Th1 cells via inhibition of IL-12 synthesis and thereby play a role in immune regulation.
通过基因靶向构建的诱导型一氧化氮合酶（iNOS）缺陷小鼠，与同样感染的杂合小鼠相比，对单纯疱疹病毒1型（HSV-1）感染的易感性显著更高，从背根神经节（DRG）清除病毒的速度延迟，并且DRG中病毒再激活的频率增加。感染的iNOS缺陷小鼠产生增强的Th1型免疫反应，其脾细胞产生的白细胞介素-12浓度高于同样感染的杂合小鼠。这一发现表明，iNOS在抵抗HSV-1感染中起重要作用。此外，一氧化氮（NO）可能通过抑制白细胞介素-12的合成来阻断Th1细胞的发育，从而在免疫调节中发挥作用。
