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口蹄疫病毒发病机制的分子基础。

Molecular basis of pathogenesis of FMDV.

作者信息

Mason Peter W, Grubman Marvin J, Baxt Barry

机构信息

USDA, ARS Plum Island Animal Disease Center, ARS. PO Box 848, Greenport, NY 11944, USA.

出版信息

Virus Res. 2003 Jan;91(1):9-32. doi: 10.1016/s0168-1702(02)00257-5.

Abstract

Current understanding of the molecular basis of pathogenesis of foot-and-mouth disease (FMD) has been achieved through over 100 years of study into the biology of the etiologic agent, FMDV. Over the last 40 years, classical biochemical and physical analyses of FMDV grown in cell culture have helped to reveal the structure and function of the viral proteins, while knowledge gained by the study of the virus' genetic diversity has helped define structures that are essential for replication and production of disease. More recently, the availability of genetic engineering methodology has permitted the direct testing of hypotheses formulated concerning the role of individual RNA structures, coding regions and polypeptides in viral replication and disease. All of these approaches have been aided by the simultaneous study of other picornavirus pathogens of animals and man, most notably poliovirus. Although many questions of how FMDV causes its devastating disease remain, the following review provides a summary of the current state of knowledge into the molecular basis of the virus' interaction with its host that produces one of the most contagious and frightening diseases of animals or man.

摘要

通过对口蹄疫病毒(FMDV)生物学特性长达100多年的研究,目前已对口蹄疫发病机制的分子基础有了一定了解。在过去40年里,对在细胞培养中生长的FMDV进行的经典生化和物理分析,有助于揭示病毒蛋白的结构和功能,而通过研究病毒的遗传多样性所获得的知识,则有助于确定病毒复制和致病所必需的结构。最近,基因工程方法的应用使得人们能够直接检验关于单个RNA结构、编码区和多肽在病毒复制和致病过程中作用的假设。所有这些方法都得益于对动物和人类的其他小RNA病毒病原体(最显著的是脊髓灰质炎病毒)的同步研究。尽管关于FMDV如何引发其毁灭性疾病仍有许多问题,但以下综述总结了目前关于该病毒与其宿主相互作用的分子基础的知识现状,这种相互作用会引发动物或人类最具传染性和可怕的疾病之一。

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