Tahara Maino, Takeda Makoto
Department of Virology III, National Institute of Infectious Diseases Gakuen 4-7-1, Musashimurayama, Tokyo 208-0011, Japan.
Uirusu. 2011 Dec;61(2):249-55. doi: 10.2222/jsv.61.249.
Measles is a highly contagious acute viral disease characterized by a maculopapular rash. It causes severe and temporary immune suppression and is often accompanied by secondary bacterial infections. In 2000, signaling lymphocyte activation molecule (SLAM) was identified as a receptor for measles virus (MV). Observations that SLAM is expressed on cells of the immune system provided a good explanation for the lymphotropic and immunosuppressive nature of MV. However, molecular mechanisms of highly contagious nature of MV have remained unclear. Previously we have demonstrated that MV has an intrinsic ability to infect polarized epithelial cells by using a receptor other than SLAM. Recently, nectin4, a cellular adhesion junction molecule, was identified as the epithelial cell receptor for MV. Understanding the molecular mechanisms of MV to infect both epithelial and immune cells provides a deep insight into measles pathogenesis.
麻疹是一种以斑丘疹为特征的高度传染性急性病毒性疾病。它会导致严重且暂时的免疫抑制，并且常伴有继发性细菌感染。2000年，信号淋巴细胞激活分子（SLAM）被确定为麻疹病毒（MV）的受体。SLAM在免疫系统细胞上表达这一观察结果，很好地解释了MV的嗜淋巴细胞性和免疫抑制特性。然而，MV高度传染性的分子机制仍不清楚。此前我们已经证明，MV具有利用除SLAM之外的受体感染极化上皮细胞的内在能力。最近，细胞黏附连接分子nectin4被确定为MV的上皮细胞受体。了解MV感染上皮细胞和免疫细胞的分子机制，能深入洞察麻疹的发病机制。
