Taguchi Fumihiro, Matsuyama Shutoku
Laboratory of Virology and Viral Diseases, Faculty of Veterinary Medicine, Nippon Veterinary and Life Science University.
Uirusu. 2009 Dec;59(2):215-22. doi: 10.2222/jsv.59.215.
Enveloped viruses enter into cells via fusion of their envelope and cellular membrane. Spike (S) protein of coronavirus (CoV) is responsible for entry events. We studied the cell entry mechanisms of two different CoVs, murine coronavirus mouse hepatitis virus (MHV) and severe acute respiratory syndrome coronavirus (SARS-CoV). MHV-JHM that induces syncytia in infected cells entered directly from cell surface, i.e., fusion of envelope and plasma membrane, whereas SARS-CoV and MHV-2 that fail to induce syncytia entered via endosome in a protease-dependent fashion, i.e., fusion of envelope and endosomal membrane. The latter viruses entered directly from cell surface, when receptor-bound viruses were treated with proteases that activate fusion activity of their S proteins. The entry pathway of SARS-CoV could influence the severity of the disease. It was also reveled that a highly neurovirulent JHM spread in a receptor-independent fashion, which could result in a high neuropathogenicity of the virus.
包膜病毒通过其包膜与细胞膜融合进入细胞。冠状病毒(CoV)的刺突(S)蛋白负责进入细胞的过程。我们研究了两种不同冠状病毒,即鼠冠状病毒小鼠肝炎病毒(MHV)和严重急性呼吸综合征冠状病毒(SARS-CoV)的细胞进入机制。在感染细胞中诱导形成多核巨细胞的MHV-JHM直接从细胞表面进入,即包膜与质膜融合,而不能诱导形成多核巨细胞的SARS-CoV和MHV-2则通过内体以蛋白酶依赖的方式进入,即包膜与内体膜融合。当用激活其S蛋白融合活性的蛋白酶处理与受体结合的病毒时,后一种病毒直接从细胞表面进入。SARS-CoV的进入途径可能会影响疾病的严重程度。还发现一种高神经毒性的JHM以不依赖受体的方式传播,这可能导致该病毒的高神经致病性。