Karupiah G, Chen J H, Nathan C F, Mahalingam S, MacMicking J D
Host Defense Laboratory, Viral Engineering and Cytokines Group, Division of Immunology and Cell Biology, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT 2601, Australia.
J Virol. 1998 Sep;72(9):7703-6. doi: 10.1128/JVI.72.9.7703-7706.1998.
To assess whether nitric oxide synthase 2 (NOS2) fulfills the criteria of an innate resistance locus against an acute viral infection, we inoculated genetically deficient NOS2-/- mice with virulent ectromelia virus (EV), the causative agent of mousepox. NOS2-/- mice proved highly susceptible to EV yet showed no diminution in other well-characterized anti-EV immune responses, i.e. , gamma interferon secretion and NK cell and EV-specific cytotoxic T lymphocyte activities. Thus, the NOS2 locus can be considered a critical monogenic determinant of EV resistance that contributes to host survival.
为了评估一氧化氮合酶2（NOS2）是否符合针对急性病毒感染的固有抗性基因座的标准，我们用致病性痘苗病毒（EV，鼠痘的病原体）接种了基因缺陷型NOS2-/-小鼠。结果表明，NOS2-/-小鼠对EV高度敏感，但在其他特征明确的抗EV免疫反应中，即γ干扰素分泌以及自然杀伤细胞和EV特异性细胞毒性T淋巴细胞活性方面，并未出现降低。因此，NOS2基因座可被视为EV抗性的关键单基因决定因素，对宿主生存有重要作用。
