Feline coronavirus: Insights into viral pathogenesis based on the spike protein structure and function.
Feline coronavirus: Insights into viral pathogenesis based on the spike protein structure and function.
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DOI：
10.1016/j.virol.2017.12.027
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发表时间：
2018-04
期刊：
影响因子：
3.7
通讯作者：
Whittaker GR
中科院分区：
文献类型：
--
作者：
Jaimes JA;Whittaker GR
猫冠状病毒（FCoV）是一种引起良性肠道疾病和致命性全身性疾病猫传染性腹膜炎（FIP）的病原体。FCoV刺突（S）蛋白被认为是结合和进入细胞的病毒调节因子。这种蛋白质还参与FCoV的嗜性和毒力，以及从肠道疾病到FIP的转变。这种调节是通过刺突的主要功能：受体结合和病毒-细胞膜融合来实现的。本文就FCoV的遗传学、复制和致病机制等方面进行综述，重点介绍S.为了更好地理解这一点，基于人冠状病毒NL 63（HCoV-NL 63）S结构构建了FCoV S蛋白模型。我们描述了FCoV S的具体结构特征，与其他冠状病毒刺突相比。我们还修改了FCoVS激活所需的生化事件及其与蛋白质结构特征的关系。
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.
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