Jaimes Javier A, Whittaker Gary R
Department of Microbiology, College of Agricultural and Life Sciences, Cornell University, 930 Campus Rd. VMC C4-133, Ithaca, NY 14853, USA.
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, VMC C4-127, Ithaca, NY 14853, USA.
Virology. 2018 Apr;517:108-121. doi: 10.1016/j.virol.2017.12.027. Epub 2018 Jan 10.
Feline coronavirus (FCoV) is an etiological agent that causes a benign enteric illness and the fatal systemic disease feline infectious peritonitis (FIP). The FCoV spike (S) protein is considered the viral regulator for binding and entry to the cell. This protein is also involved in FCoV tropism and virulence, as well as in the switch from enteric disease to FIP. This regulation is carried out by spike's major functions: receptor binding and virus-cell membrane fusion. In this review, we address important aspects in FCoV genetics, replication and pathogenesis, focusing on the role of S. To better understand this, FCoV S protein models were constructed, based on the human coronavirus NL63 (HCoV-NL63) S structure. We describe the specific structural characteristics of the FCoV S, in comparison with other coronavirus spikes. We also revise the biochemical events needed for FCoV S activation and its relation to the structural features of the protein.
猫冠状病毒（FCoV）是一种病原体，可引起良性肠道疾病和致命的全身性疾病——猫传染性腹膜炎（FIP）。FCoV刺突（S）蛋白被认为是病毒结合并进入细胞的调节因子。该蛋白还与FCoV的嗜性和毒力有关，以及与从肠道疾病向FIP的转变有关。这种调节是通过刺突的主要功能实现的：受体结合和病毒-细胞膜融合。在本综述中，我们阐述了FCoV遗传学、复制和发病机制中的重要方面，重点关注S蛋白的作用。为了更好地理解这一点，基于人冠状病毒NL63（HCoV-NL63）的S结构构建了FCoV S蛋白模型。我们描述了FCoV S蛋白与其他冠状病毒刺突相比的特定结构特征。我们还探讨了FCoV S蛋白激活所需的生化事件及其与该蛋白结构特征的关系。
