Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506, USA.
Virology. 2011 Feb 5;410(1):1-6. doi: 10.1016/j.virol.2010.10.027. Epub 2010 Nov 11.
PB2 627K is a determinant of influenza host range and contributes to the pathogenicity of human-, avian-, and mouse-adapted influenza viruses in the mouse model. Here we used mouse and pig models to analyze the contribution of a swine-origin and avian-origin PB2 carrying either 627K or 627E in the background of the classical swine H1N1 (A/Swine/Iowa/15/30; 1930) virus. The results showed PB2 627K is crucial for virulence in the mouse model, independent of whether PB2 is derived from an avian or swine influenza virus (SIV). In the pig model, PB2 627E decreases pathogenicity of the classical 1930 SIV when it contains the swine-origin PB2, but not when it possesses the avian-origin PB2. Our study suggests the pathogenicity of SIVs with different PB2 genes and mutation of codon 627 in mice does not correlate with the pathogenicity of the same SIVs in the natural host, the pig.
PB2 627K 是决定流感宿主范围的因素之一，有助于人类、禽类和鼠源流感病毒在小鼠模型中的致病性。在这里，我们使用小鼠和猪模型来分析在经典猪源 H1N1（A/Swine/Iowa/15/30；1930）病毒的背景下，携带 627K 或 627E 的猪源和禽源 PB2 对病毒的贡献。结果表明，PB2 627K 是在小鼠模型中产生毒力的关键因素，而与 PB2 是源自禽源还是猪源流感病毒无关。在猪模型中，当经典的 1930 年 SIV 含有猪源 PB2 时，PB2 627E 降低了其致病性，但当含有禽源 PB2 时则不会。我们的研究表明，具有不同 PB2 基因的 SIV 在小鼠中的致病性与其在天然宿主猪中的致病性并不相关，而 PB2 627 密码子的突变也是如此。
