Kemper C, Atkinson J P
Division of Rheumatology, St. Louis, MO 63110, USA.
Curr Top Microbiol Immunol. 2009;329:31-57. doi: 10.1007/978-3-540-70523-9_3.
Measles virus (MV) was isolated in 1954 (Enders and Peeble 1954). It is among the most contagious of viruses and a leading cause of mortality in children in developing countries (Murray and Lopez 1997; Griffin 2001; Bryce et al. 2005). Despite intense research over decades on the biology and pathogenesis of the virus and the successful development in 1963 of an effective MV vaccine (Cutts and Markowitz 1994), cell entry receptor(s) for MV remained unidentified until 1993. Two independent studies showed that transfection of nonsusceptible rodent cells with human CD46 renders these cells permissive to infection with the Edmonston and Halle vaccine strains of measles virus (Dorig et al. 1993; Naniche et al. 1993). A key finding in these investigations was that MV binding and infection was inhibited by monoclonal and polyclonal antibodies to CD46. These reports established CD46 as a MV cell entry receptor. This chapter summarizes the role of CD46 in measles virus infection.
麻疹病毒(MV)于1954年被分离出来(恩德斯和皮布尔,1954年)。它是传染性最强的病毒之一,也是发展中国家儿童死亡的主要原因(默里和洛佩兹,1997年;格里芬,2001年;布莱斯等人,2005年)。尽管数十年来对该病毒的生物学和发病机制进行了深入研究,并且在1963年成功研发出了有效的麻疹疫苗(卡茨和马科维茨,1994年),但直到1993年,麻疹病毒的细胞进入受体仍未被确定。两项独立研究表明,用人CD46转染不易感的啮齿动物细胞会使这些细胞对麻疹病毒的埃德蒙斯顿和哈雷疫苗株感染敏感(多里格等人,1993年;纳米什等人,1993年)。这些研究中的一个关键发现是,针对CD46的单克隆抗体和多克隆抗体可抑制麻疹病毒的结合和感染。这些报告确立了CD46作为麻疹病毒细胞进入受体的地位。本章总结了CD46在麻疹病毒感染中的作用。