Human parainfluenza virus type 1 but not Sendai virus replicates in human respiratory cells despite IFN treatment
Human parainfluenza virus type 1 but not Sendai virus replicates in human respiratory cells despite IFN treatment
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DOI：
10.1016/j.virusres.2006.03.012
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发表时间：
2006-10-01
期刊：
影响因子：
5
通讯作者：
Takimoto, Toru
中科院分区：
文献类型：
--
作者：
Bousse, Tatiana;Chambers, Raychel L.;Takimoto, Toru
仙台病毒 (SeV) 和 I 型人类副流感病毒 (hPIV 1) 高度同源，但具有不同的宿主范围（小鼠与人类）。为了确定影响副流感病毒宿主特异性的因素，我们测定了 SeV 和 hPIV1 在人类和小鼠培养细胞中的感染性和抗 IFN 活性。 SeV可有效感染正常人肺MRC-5和鼠肺MM14.Lu或MLg2908细胞。 SeV 感染诱导 MRC-5 细胞将 IFN-β 释放到培养基中，其水平与感染 hPIV1 的细胞相似。 SeV或hPIV1感染以及SeV或hPIV I C蛋白的表达抑制IFN-β诱导的STAT I的核定位，表明SeV和hPIV I C蛋白均阻断MRC-5细胞中的IFN Jak/STAT通路。用 IFN 预处理 MRC-5 细胞可抑制感染早期 SeV 和 hPIV1 的复制。然而，hPIV1 克服了这种抑制，而 SeV 则没有。 SeV 复制在 IFN-β 预处理的小鼠 MM14 中恢复。 Lu 细胞，表明 SeV 抗 IFN 活性具有物种特异性。这些结果表明，SeV 在克服人类细胞的抗病毒活性方面不如 hPIV1，这可能是限制 SeV 宿主范围的因素之一。 (c) 2006 Elsevier B.V. 保留所有权利。
Sendai virus (SeV) and human parainfluenza virus type I (hPIV 1) are highly homologous but have distinct host ranges, murine versus human. To identify the factors that affect the host specificity of parainfluenza viruses, we determined the infectivity and anti-IFN activities of SeV and hPIV1 in human and murine culture cells. SeV infected normal human lung MRC-5 and murine lung MM14.Lu or MLg2908 cells efficiently. Infection with SeV induced the release of IFN-beta into culture medium in MRC-5 cells at similar levels with that of cells infected with hPIV1. SeV or hPIV1 infections, as well as expression of SeV or hPIV I C proteins, inhibited the nuclear localization of STAT I induced by IFN-beta, suggesting that both SeV and hPIV I C proteins block the IFN Jak/STAT pathway in MRC-5 cells. Pretreatment of MRC-5 cells with IFN suppressed replication of SeV and hPIV1 at an early stage of infection. However, hPIV1 overcame this suppression while SeV did not. SeV replication was restored in IFN-beta pretreated murine MM14. Lu cells, suggesting SeV anti-IFN activity is species specific. These results suggest that SeV is less effective than hPIV1 in overcoming antiviral activity in human cells, which could be one of the factors that restrict the host range of SeV. (c) 2006 Elsevier B.V. All rights reserved.