Mendenhall Michelle, Wong Min-Hui, Skirpstunas Ramona, Morrey John D, Gowen Brian B
Institute for Antiviral Research, Utah State University, Logan, UT 84322-5600, USA.
Virology. 2009 Dec 5;395(1):143-51. doi: 10.1016/j.virol.2009.09.003. Epub 2009 Sep 26.
The Adames strain of Punta Toro virus (PTV-A, Bunyaviridae, Phlebovirus) causes an acute lethal disease in hamsters and mice. The Balliet strain of the virus (PTV-B) is generally considered to be avirulent. The difference in hamster susceptibility is likely due to the ability of PTV-A to suppress interferon (IFN)-beta similarly to that described for Rift Valley fever virus. Here we investigated strain differences in PTV pathogenesis and the IFN response in mice. Although PTV-B infection in mice did not induce systemic IFN-beta release, primary macrophages produced dramatically higher levels when exposed to the virus in culture. The importance of IFN in resistance to PTV infection was borne out in studies employing STAT-1 knock-out mice. Also, a number of genes specific to IFN response pathways were upregulated in PTV-B-infected macrophages. Our findings provide new insights into the type I IFN response during PTV infection in the mouse model of phleboviral disease.
蓬塔托罗病毒（PTV，布尼亚病毒科，白蛉病毒属）的阿达姆斯毒株（PTV-A）可在仓鼠和小鼠中引发急性致死性疾病。该病毒的巴利埃毒株（PTV-B）通常被认为无致病性。仓鼠易感性的差异可能是由于PTV-A抑制干扰素（IFN）-β的能力，这与裂谷热病毒的情况类似。在此，我们研究了PTV在小鼠发病机制和IFN反应方面的毒株差异。虽然PTV-B感染小鼠不会诱导全身性IFN-β释放，但原代巨噬细胞在培养中接触该病毒时会产生显著更高水平的IFN-β。在使用STAT-1基因敲除小鼠的研究中证实了IFN在抵抗PTV感染中的重要性。此外，在PTV-B感染的巨噬细胞中，一些IFN反应途径特有的基因上调。我们的研究结果为白蛉病毒疾病小鼠模型中PTV感染期间的I型IFN反应提供了新的见解。
