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猫肠道冠状病毒的流行病学及猫传染性腹膜炎的发病机制研究进展

Perspectives on the epizootiology of feline enteric coronavirus and the pathogenesis of feline infectious peritonitis.

作者信息

Evermann J F, McKeirnan A J, Ott R L

机构信息

Department of Veterinary Clinical Medicine and Surgery, College of Veterinary Medicine, Washington State University, Pullman 99164-6610.

出版信息

Vet Microbiol. 1991 Aug 15;28(3):243-55. doi: 10.1016/0378-1135(91)90079-u.

DOI:10.1016/0378-1135(91)90079-u
PMID:1654668
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7117328/
Abstract

This review presents some current thoughts regarding the epizootiology of the feline coronaviruses; feline infectious peritonitis virus (FIPV) and feline coronavirus (FECV) with primary emphasis on the pathogenesis of these viruses in nature. Although the mechanism(s) whereby FIPV causes disease are still incompletely understood, there have been significant contributions to the literature over the past decade which provide a framework upon which plausible explanations can be postulated. Two concepts are presented which attempt to clarify the pathogenesis of FIPV and at the same time may serve as an impetus for further research. The first involves the hypothesis, originally promulgated by Pedersen in 1981, that FIPV is derived from FECV during virus replication in the gastrointestinal tract. The second involves a unique mechanism of the mucosal immune system referred to as oral tolerance, which under normal conditions promotes the production of secretory immunity and suppresses the production of systemic immunity. In the case of FIPV infection, we propose that oral tolerance is important in the control of the virus at the gastrointestinal tract level. Once oral tolerance is disrupted, FIPV is capable of systemic spread resulting in immune-mediated vasculitis and death. Thus, it may be that clinical forms of FIP are due to a combination of two events, the first being the generation of FIPV from FECV, and the second being the capacity of FIPV to circumvent oral tolerance.

摘要

本综述介绍了一些关于猫冠状病毒(猫传染性腹膜炎病毒,FIPV;猫冠状病毒,FECV)流行病学的当前观点,主要侧重于这些病毒在自然环境中的发病机制。尽管FIPV致病的机制仍未完全明了,但在过去十年中,已有大量文献对此做出了重要贡献,为提出合理的解释提供了框架。本文提出了两个概念,旨在阐明FIPV的发病机制,同时也可能为进一步研究提供动力。第一个概念涉及1981年由佩德森最初提出的假说,即FIPV是在胃肠道病毒复制过程中由FECV衍生而来。第二个概念涉及黏膜免疫系统的一种独特机制,称为口服耐受,在正常情况下,它促进分泌性免疫的产生并抑制全身性免疫的产生。在FIPV感染的情况下,我们认为口服耐受在胃肠道水平控制病毒方面很重要。一旦口服耐受被破坏,FIPV就能够全身扩散,导致免疫介导的血管炎和死亡。因此,FIP的临床形式可能是由于两个事件的结合,第一个事件是FIPV从FECV产生,第二个事件是FIPV规避口服耐受的能力。

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An enteric coronavirus infection of cats and its relationship to feline infectious peritonitis.猫的一种肠道冠状病毒感染及其与猫传染性腹膜炎的关系。
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