Differential activation of interferon regulatory factors-3 and-7 by non-cytopathogenic and cytopathogenic bovine viral diarrhoea virus
Differential activation of interferon regulatory factors-3 and-7 by non-cytopathogenic and cytopathogenic bovine viral diarrhoea virus
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DOI：
10.1016/j.vetimm.2004.04.003
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发表时间：
2004-08-01
影响因子：
1.8
通讯作者：
McCauley, JW
中科院分区：
文献类型：
--
作者：
Baigent, SJ;Goodbourn, S;McCauley, JW
非致细胞病变性牛病毒性腹泻病毒（ncpBVDV）先前已显示可抑制培养细胞中干扰素调节因子-3的功能[J. Virol. 76（2002）8979]。在本研究中，我们表明，与ncpBVDV一样，当细胞先前暴露于致细胞病变性BVDV（cpBVDV）时，未观察到可由beterobacterium病毒感染诱导的核提取物中出现IRF-3-DNA复合物。用ncpBVDV或cpBVDV感染细胞既不会导致IRF-7从感染细胞的细胞质易位到细胞核，也不会抑制其在Semliki森林病毒超感染细胞中的核易位。我们得出结论，cpBVDV和ncpBVDV均具有抑制IRF-3的全部功能的能力，但既不刺激也不阻断IRF-7的核摄取。(C)2004 Elsevier B. V.保留所有权利。
Non-cytopathogenic bovine viral diarrhoea virus (ncpBVDV) has previously been shown to inhibit the function of interferon regulatory factor-3 in cultured cells [J. Virol. 76 (2002) 8979]. In this study, we show that, like ncpBVDV, when cells were previously exposed to cytopathogenic BVDV (cpBVDV) the appearance of an IRF-3-DNA complex from nuclear extracts that can be induced by beterologous virus infection was not observed. Infection of cells with ncpBVDV or cpBVDV resulted in neither the translocation of IRF-7 from the cytoplasm to the nucleus of infected cells, nor an inhibition of its nuclear trallslocation in cells super-infected by Semliki Forest Virus. We conclude that cpBVDV and ncpBVDV both share the ability to inhibit the full function of IRF-3 but neither stimulate or block the nuclear uptake of IRF-7. (C) 2004 Elsevier B.V. All rights reserved.