Takeuchi Kaoru, Miyajima Naoko, Nagata Noriyo, Takeda Makoto, Tashiro Masato
Department of Infection Biology, Institute of Basic Medical Sciences, University of Tsukuba, 1-1-1 Tennodai, Ibaragi 305-8575, Tsukuba, Japan.
Virus Res. 2003 Jul;94(1):11-6. doi: 10.1016/s0168-1702(03)00117-5.
In the natural course of measles virus (MV) infection, epithelial cells are primary targets of MV. However, it has been shown that wild-type MV utilizes signaling lymphocyte activation molecule (SLAM or CD150) as a cellular receptor, which is expressed only in some T and B cells, thymocytes, and dendritic cells. To understand how wild-type MV infects non-lymphoid cells, several non-lymphoid cells were examined for their susceptibility to wild-type MV. Here, we show that wild-type MV can infect primary human small airway epithelial cells (SAEC) and induce formation of large syncytia in vitro. mRNA specific for SLAM was not detected in SAEC, indicating that wild-type MV infects SAEC and induces syncytia formation via a SLAM-independent mechanism.
在麻疹病毒(MV)感染的自然过程中,上皮细胞是MV的主要靶细胞。然而,已经表明野生型MV利用信号淋巴细胞激活分子(SLAM或CD150)作为细胞受体,该受体仅在某些T细胞和B细胞、胸腺细胞及树突状细胞中表达。为了解野生型MV如何感染非淋巴细胞,研究人员检测了几种非淋巴细胞对野生型MV的易感性。在此,我们表明野生型MV可感染原代人小气道上皮细胞(SAEC)并在体外诱导形成大的多核巨细胞。在SAEC中未检测到SLAM特异性mRNA,这表明野生型MV通过不依赖SLAM的机制感染SAEC并诱导多核巨细胞形成。