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沙粒病毒出血热的发病机制。

Pathogenesis of arenavirus hemorrhagic fevers.

机构信息

Institute of Microbiology, University Hospital Center and University of Lausanne, Lausanne, Switzerland.

出版信息

Expert Rev Anti Infect Ther. 2011 Jan;9(1):49-59. doi: 10.1586/eri.10.142.

Abstract

Viral hemorrhagic fevers (VHFs) caused by arenaviruses belong to the most devastating emerging human diseases and represent serious public health problems. Arenavirus VHFs in humans are acute diseases characterized by fever and, in severe cases, different degrees of hemorrhages associated with a shock syndrome in the terminal stage. Over the past years, much has been learned about the pathogenesis of arenaviruses at the cellular level, in particular their ability to subvert the host cell's innate antiviral defenses. Clinical studies and novel animal models have provided important new information about the interaction of hemorrhagic arenaviruses with the host's adaptive immune system, in particular virus-induced immunosuppression, and have provided the first hints towards an understanding of the terminal hemorrhagic shock syndrome. The scope of this article is to review our current knowledge on arenavirus VHF pathogenesis with an emphasis on recent developments.

摘要

病毒性出血热(VHF)由沙粒病毒引起,属于最具破坏性的新发人类疾病,是严重的公共卫生问题。人类沙粒病毒引起的 VHF 是急性疾病,以发热为特征,在严重情况下,不同程度的出血与终末期休克综合征相关。在过去的几年中,人们在细胞水平上对沙粒病毒的发病机制有了更多的了解,特别是它们颠覆宿主细胞固有抗病毒防御的能力。临床研究和新型动物模型为了解出血性沙粒病毒与宿主适应性免疫系统的相互作用提供了重要的新信息,特别是病毒诱导的免疫抑制,并为理解终末期出血性休克综合征提供了第一个线索。本文的目的是综述沙粒病毒 VHF 发病机制的最新进展。

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