Bousse Tatiana, Chambers Raychel L, Scroggs Ruth Ann, Portner Allen, Takimoto Toru
Department of Microbiology and Immunology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 672, NY 14642, USA.
Virus Res. 2006 Oct;121(1):23-32. doi: 10.1016/j.virusres.2006.03.012. Epub 2006 May 3.
Sendai virus (SeV) and human parainfluenza virus type I (hPIV1) 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 hPIV1 C proteins, inhibited the nuclear localization of STAT1 induced by IFN-beta, suggesting that both SeV and hPIV1 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.
仙台病毒（SeV）和人I型副流感病毒（hPIV1）高度同源，但具有不同的宿主范围，分别为鼠类和人类。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在人和鼠类培养细胞中的感染性及抗干扰素活性。SeV能有效感染正常人肺MRC-5细胞以及鼠肺MM14.Lu或MLg2908细胞。SeV感染诱导MRC-5细胞向培养基中释放IFN-β，其水平与hPIV1感染的细胞相似。SeV或hPIV1感染以及SeV或hPIV1 C蛋白的表达均抑制了IFN-β诱导的STAT1核定位，这表明SeV和hPIV1的C蛋白均在MRC-5细胞中阻断了IFN Jak/STAT途径。用IFN预处理MRC-5细胞可在感染早期抑制SeV和hPIV1的复制。然而，hPIV1能克服这种抑制作用而SeV不能。在经IFN-β预处理的鼠类MM14.Lu细胞中SeV复制得以恢复，这表明SeV的抗干扰素活性具有物种特异性。这些结果表明，在克服人类细胞中的抗病毒活性方面，SeV不如hPIV1有效，这可能是限制SeV宿主范围的因素之一。
