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蓝舌病病毒的多种释放途径。

Multiple Routes of Bluetongue Virus Egress.

作者信息

Labadie Thomas, Sullivan Edward, Roy Polly

机构信息

Department of Pathogen Molecular Biology, Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, WC1E 7HT, London WC1E 7HT, UK.

出版信息

Microorganisms. 2020 Jun 27;8(7):965. doi: 10.3390/microorganisms8070965.

Abstract

Bluetongue virus (BTV) is an arthropod-borne virus infecting livestock. Its frequent emergence in Europe and North America had caused significant agricultural and economic loss. BTV is also of scientific interest as a model to understand the mechanisms underlying non-enveloped virus release from mammalian and insect cells. The BTV particle, which is formed of a complex double-layered capsid, was first considered as a lytic virus that needs to lyse the infected cells for cell to cell transmission. In the last decade, however, a more in-depth focus on the role of the non-structural proteins has led to several examples where BTV particles are also released through different budding mechanisms at the plasma membrane. It is now clear that the non-structural protein NS3 is the main driver of BTV release, via different interactions with both viral and cellular proteins of the cell sorting and exocytosis pathway. In this review, we discuss the most recent advances in the molecular biology of BTV egress and compare the mechanisms that lead to lytic or non-lytic BTV release.

摘要

蓝舌病病毒(BTV)是一种感染家畜的节肢动物传播病毒。它在欧洲和北美的频繁出现已造成重大的农业和经济损失。作为理解非包膜病毒从哺乳动物和昆虫细胞释放的潜在机制的模型,BTV也具有科学研究价值。BTV粒子由复杂的双层衣壳构成,最初被认为是一种溶细胞病毒,需要裂解受感染细胞以实现细胞间传播。然而,在过去十年中,对非结构蛋白作用的更深入研究揭示了多个实例,表明BTV粒子也可通过质膜上不同的出芽机制释放。现在已经明确,非结构蛋白NS3是BTV释放的主要驱动因素,它通过与细胞分选和胞吐途径的病毒和细胞蛋白的不同相互作用来实现这一过程。在这篇综述中,我们讨论了BTV释放分子生物学的最新进展,并比较了导致BTV溶细胞性或非溶细胞性释放的机制。

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