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埃博拉病毒致病的分子机制。

Molecular mechanisms of Ebola pathogenesis.

作者信息

Rivera Andrea, Messaoudi Ilhem

机构信息

Division of Biomedical Sciences, University of California, Riverside, Riverside, California, USA.

Division of Biomedical Sciences, University of California, Riverside, Riverside, California, USA

出版信息

J Leukoc Biol. 2016 Nov;100(5):889-904. doi: 10.1189/jlb.4RI0316-099RR. Epub 2016 Sep 1.

DOI:10.1189/jlb.4RI0316-099RR
PMID:27587404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6608070/
Abstract

Ebola viruses (EBOVs) and Marburg viruses (MARVs) are among the deadliest human viruses, as highlighted by the recent and widespread Ebola virus outbreak in West Africa, which was the largest and longest epidemic of Ebola virus disease (EVD) in history, resulting in significant loss of life and disruptions across multiple continents. Although the number of cases has nearly reached its nadir, a recent cluster of 5 cases in Guinea on March 17, 2016, has extended the enhanced surveillance period to June 15, 2016. New, enhanced 90-d surveillance windows replaced the 42-d surveillance window to ensure the rapid detection of new cases that may arise from a missed transmission chain, reintroduction from an animal reservoir, or more important, reemergence of the virus that has persisted in an EVD survivor. In this review, we summarize our current understanding of EBOV pathogenesis, describe vaccine and therapeutic candidates in clinical trials, and discuss mechanisms of viral persistence and long-term health sequelae for EVD survivors.

摘要

埃博拉病毒(EBOV)和马尔堡病毒(MARV)是最致命的人类病毒之一,近期在西非爆发的大规模埃博拉病毒疫情便凸显了这一点。此次疫情是历史上规模最大、持续时间最长的埃博拉病毒病(EVD)疫情,导致了大量人员死亡,并在多个大洲造成了混乱。尽管病例数量已接近最低点,但2016年3月17日几内亚出现的5例聚集性病例将强化监测期延长至2016年6月15日。新的、强化的90天监测窗口取代了42天监测窗口,以确保能迅速检测出可能因遗漏传播链、从动物宿主重新引入病毒,或者更重要的是,在埃博拉病毒病幸存者体内持续存在的病毒再次出现而产生的新病例。在这篇综述中,我们总结了目前对埃博拉病毒发病机制的认识,描述了临床试验中的疫苗和治疗候选药物,并讨论了病毒持续存在的机制以及埃博拉病毒病幸存者的长期健康后遗症。

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