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钙离子在轮状病毒及其他病毒感染的复制与发病机制中的作用。

Role of Ca2+in the replication and pathogenesis of rotavirus and other viral infections.

作者信息

Ruiz M C, Cohen J, Michelangeli F

机构信息

Laboratorio de Fisiología Gastrointestinal, Centro de Biofísica y Bioquímica, Instituto Venezolano de Investigaciones Científicas (IVIC) Caracas, Venezuela.

出版信息

Cell Calcium. 2000 Sep;28(3):137-49. doi: 10.1054/ceca.2000.0142.

DOI:10.1054/ceca.2000.0142
PMID:11020376
Abstract

Ca2+ plays a key role in many pathological processes, including viral infections. Rotavirus, the major etiological agent of viral gastroenteritis in children and young animals, provides a useful model to study a number of Ca2+ dependent virus-cell interactions. Rotavirus entry, activation of transcription, morphogenesis, cell lysis, particle release, and the distant action of viral proteins are Ca2+ dependent processes. In the extracellular medium, Ca2+ stabilizes the structure of the viral capsid. During entry into the cell the low cytoplasmic Ca2+ concentration induced the solubilization of the outer protein layer of the capsid and transcriptase activation. Viral protein synthesis modifies Ca2+ homeostasis which, in turn, favours viral morphogenesis and induces cell death. The generation of diarrhea is a multifactorial process involving Ca2+ dependent secretory processes of mediators and water and electrolytes, as well as the induction of cell death in the different cell types that compose the intestinal epithelium. The discovery of the non-structural viral protein NSP4 as a viral enterotoxin and the possible participation of the enteric nervous system in the pathogenesis of diarrhea represent significant advances in its understanding. Ca2+ also plays a role in the replication cycles and pathogenesis of other viral diseases such as poliovirus, Coxsackie virus, cytomegalovirus, vaccinia and measles virus and HIV.

摘要

钙离子在包括病毒感染在内的许多病理过程中起着关键作用。轮状病毒是儿童和幼龄动物病毒性胃肠炎的主要病原体,为研究多种钙离子依赖性病毒 - 细胞相互作用提供了一个有用的模型。轮状病毒的进入、转录激活、形态发生、细胞裂解、颗粒释放以及病毒蛋白的远距离作用都是钙离子依赖性过程。在细胞外介质中,钙离子稳定病毒衣壳的结构。进入细胞时,低细胞质钙离子浓度诱导衣壳外层蛋白层溶解并激活转录酶。病毒蛋白合成改变钙离子稳态,进而有利于病毒形态发生并诱导细胞死亡。腹泻的产生是一个多因素过程,涉及钙离子依赖性的介质、水和电解质分泌过程,以及组成肠上皮的不同细胞类型中的细胞死亡诱导。病毒非结构蛋白NSP4作为病毒肠毒素的发现以及肠道神经系统在腹泻发病机制中的可能参与代表了在理解腹泻方面的重大进展。钙离子在其他病毒性疾病如脊髓灰质炎病毒、柯萨奇病毒、巨细胞病毒、牛痘病毒、麻疹病毒和HIV的复制周期和发病机制中也起作用。

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