Borca Manuel V, Gudmundsdottir Ingigerdur, Fernández-Sainz Ignacio J, Holinka Lauren G, Risatti Guillermo R
Plum Island Animal Disease Center, Agricultural Research Service, United States Department of Agriculture, Greenport, NY 11944, United States.
Virus Res. 2008 Dec;138(1-2):89-96. doi: 10.1016/j.virusres.2008.08.009. Epub 2008 Oct 10.
Experimental exposure of swine to highly virulent classical swine fever virus (CSFV) strain Brescia causes an invariably fatal disease of all infected animals by 8-14 days post-infection. Host mechanisms involved in this severe outcome of infection have not been clearly established. To understand these mechanisms, we analyzed the response of primary cultured swine macrophages, a CSFV primary target cell, to infection with Brescia strain. Steady state levels of mRNA accumulation were assessed for 58 genes involved in modulation of the host immune response, at 24 and 48 h post-infection (hpi), by means of quantitative reverse transcription real-time PCR analysis (qrt-PCR). Eighteen genes showed altered expression upon infection with CSFV strain Brescia including: cytokines (IL-1alpha, IL-1beta, IL-6, and IL-12p35); cytokine receptors (IL-2Ralpha, IL-12Rbeta, and TGF-betaIIIR); chemokines (IL-8, AMCF-1, AMCF-2, MCP-2, and RANTES); interferons (INFalpha and INFbeta); and toll-like receptors (TLR3, TLR5, TLR9, and TLR10). Although these genes are associated with mechanisms of innate immune response and antiviral activity, their altered expression does not curtail CSFV Brescia growth kinetics and virus yield in swine macrophages. Data gathered here suggests that the observed gene expression profile might explain immunological and pathological changes associated with virulent CSFV infections.
将猪实验性暴露于高致病性经典猪瘟病毒(CSFV)布雷西亚株,会使所有受感染动物在感染后8 - 14天内患上必死无疑的疾病。感染这种严重后果所涉及的宿主机制尚未明确。为了解这些机制,我们分析了原代培养的猪巨噬细胞(CSFV的主要靶细胞)对布雷西亚株感染的反应。在感染后24小时和48小时(hpi),通过定量逆转录实时PCR分析(qrt - PCR)评估了58个参与宿主免疫反应调节的基因的mRNA积累稳态水平。18个基因在感染CSFV布雷西亚株后表达发生改变,包括:细胞因子(IL - 1α、IL - 1β、IL - 6和IL - 12p35);细胞因子受体(IL - 2Rα、IL - 12Rβ和TGF - βIIIR);趋化因子(IL - 8、AMCF - 1、AMCF - 2、MCP - (此处原文有误,推测应为MCP - 1)2和RANTES);干扰素(INFα和INFβ);以及Toll样受体(TLR3、TLR5、TLR9和TLR10)。尽管这些基因与先天免疫反应和抗病毒活性机制相关,但其表达改变并未抑制CSFV布雷西亚株在猪巨噬细胞中的生长动力学和病毒产量。此处收集的数据表明,观察到的基因表达谱可能解释了与强毒CSFV感染相关的免疫和病理变化。 (注:原文中“MCP - 2”推测有误,应为“MCP - 1”,翻译时按推测修正后翻译)