Schneider-Schaulies J, ter Meulen V, Schneider-Schaulies S
Institute for Virology and Immunobiology, University of Würzburg, Würzburg, Germany.
J Neurovirol. 2001 Oct;7(5):391-9. doi: 10.1080/135502801753170246.
Although CNS complications occurring early and late after acute measles are a serious problem and often fatal, the transient immunosuppression lasting for several weeks after the rash is the major cause of measles-related morbidity and mortality worldwide. This review is focused on the interactions of measles virus (MV) with cellular receptors on neural and lymphoid cells which are important elements in viral pathogenesis. First, the cognate MV receptors, CD46 and CD150, are important components of viral tropism by mediating binding and entry. Second, however, additional unknown cellular surface molecules may (independently of viral uptake) after interaction with the MV glycoprotein complex act as signaling molecules and thereby modulate cellular survival, proliferation, and specific functions.
尽管急性麻疹发病早期和晚期出现的中枢神经系统并发症是一个严重问题,且往往致命,但皮疹出现后持续数周的短暂免疫抑制是全球范围内麻疹相关发病和死亡的主要原因。本综述聚焦于麻疹病毒(MV)与神经细胞和淋巴细胞上的细胞受体之间的相互作用,这些受体是病毒发病机制中的重要因素。首先,同源MV受体CD46和CD150通过介导结合和进入,是病毒嗜性的重要组成部分。其次,然而,其他未知的细胞表面分子可能(独立于病毒摄取)在与MV糖蛋白复合物相互作用后充当信号分子,从而调节细胞存活、增殖和特定功能。