COVID-19 中的先天免疫学--生动回顾。第一部分:病毒进入、感应和逃避。

Oxford open immunology Pub Date : 2020-12-08 eCollection Date: 2020-01-01 DOI:10.1093/oxfimm/iqaa004
Clarissa Coveney, Michel Tellier, Fangfang Lu, Shayda Maleki-Toyserkani, Ruth Jones, Valentina M T Bart, Ellie Pring, Aljawharah Alrubayyi, Felix C Richter, D Oliver Scourfield, Jan Rehwinkel, Patrícia R S Rodrigues, Luke C Davies, Ester Gea-Mallorquí
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引用次数: 0

摘要

由严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)引起的 2019 年冠状病毒传染病(COVID-19)大流行仍然是世界卫生关注的问题,它可导致易感人群患上严重疾病并造成高死亡率。虽然疫苗提供了治疗疾病的机会,但预防和抗病毒治疗仍然至关重要,特别是考虑到这类病毒的变异能力。因此,必须阐明 SARS-CoV-2 病毒进入、先天感应和免疫逃避的分子机制,这些机制控制着随后过度炎症反应的诱因。病毒逃避策略直接针对抗病毒免疫,抵消宿主限制因子,劫持信号通路以干扰干扰素的产生。在本综述的第一部分,我们研究了 SARS-CoV-2 病毒的进入和所描述的免疫逃避机制,以提供一个视角,说明受感染细胞最初的病毒感应失败如何导致免疫调节失调,引起第二部分讨论的致命的 COVID-19。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Innate immunology in COVID-19-a living review. Part I: viral entry, sensing and evasion.

Innate immunology in COVID-19-a living review. Part I: viral entry, sensing and evasion.

Innate immunology in COVID-19-a living review. Part I: viral entry, sensing and evasion.

The coronavirus infectious disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains a world health concern and can cause severe disease and high mortality in susceptible groups. While vaccines offer a chance to treat disease, prophylactic and anti-viral treatments are still of vital importance, especially in context of the mutative ability of this group of viruses. Therefore, it is essential to elucidate the molecular mechanisms of viral entry, innate sensing and immune evasion of SARS-CoV-2, which control the triggers of the subsequent excessive inflammatory response. Viral evasion strategies directly target anti-viral immunity, counteracting host restriction factors and hijacking signalling pathways to interfere with interferon production. In Part I of this review, we examine SARS-CoV-2 viral entry and the described immune evasion mechanisms to provide a perspective on how the failure in initial viral sensing by infected cells can lead to immune dysregulation causing fatal COVID-19, discussed in Part II.

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