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SARS-CoV-2 pathogenesis. ​

文献信息 ​

DOI10.1038/s41579-022-00713-0
PMID35354968
期刊Nature reviews. Microbiology
影响因子103.3
JCR 分区Q1
发表年份2022
被引次数446
关键词SARS-CoV-2, 病理生理学, 急性呼吸窘迫综合症, 免疫反应, 炎症
文献类型Journal Article, Review
ISSN1740-1526
页码270-284
期号20(5)
作者Mart M Lamers, Bart L Haagmans

一句话小结 ​

本综述探讨了SARS-CoV-2引发的严重肺炎及急性呼吸窘迫综合症的病理生理机制，强调单细胞组学和CRISPR筛选等新技术带来的重要发现，揭示了病毒如何通过感染下呼吸道引发免疫失调和肺泡损伤。这些研究为开发针对COVID-19的新治疗方法提供了关键的理论基础和实践指导。

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SARS-CoV-2 · 病理生理学 · 急性呼吸窘迫综合症 · 免疫反应 · 炎症

摘要 ​

严重急性呼吸综合症冠状病毒2（SARS-CoV-2）的出现引发了一场毁灭性的全球大流行。尽管大多数感染SARS-CoV-2的人表现出轻度到中度的疾病，且病毒主要在上呼吸道进行复制，但有些人会发展为危及生命的肺炎。在本综述中，我们探讨了关于SARS-CoV-2病理生理的最新临床和实验进展，并讨论了与SARS-CoV-2相关的急性呼吸窘迫综合症（ARDS）背后的潜在机制，特别关注通过单细胞组学、有机体感染模型和CRISPR筛选等新技术获得的新见解。我们描述了SARS-CoV-2如何感染下呼吸道并导致肺泡损伤，这是由于免疫反应功能失调所致。我们讨论了这可能如何导致上皮和内皮的“漏状态”诱导，促进炎症和凝血，而免疫细胞的涌入则导致过度的炎症反应和免疫病理。最后，我们强调这些发现如何有助于开发针对COVID-19的新治疗干预措施。

英文摘要 ​

The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a devastating pandemic. Although most people infected with SARS-CoV-2 develop a mild to moderate disease with virus replication restricted mainly to the upper airways, some progress to having a life-threatening pneumonia. In this Review, we explore recent clinical and experimental advances regarding SARS-CoV-2 pathophysiology and discuss potential mechanisms behind SARS-CoV-2-associated acute respiratory distress syndrome (ARDS), specifically focusing on new insights obtained using novel technologies such as single-cell omics, organoid infection models and CRISPR screens. We describe how SARS-CoV-2 may infect the lower respiratory tract and cause alveolar damage as a result of dysfunctional immune responses. We discuss how this may lead to the induction of a 'leaky state' of both the epithelium and the endothelium, promoting inflammation and coagulation, while an influx of immune cells leads to overexuberant inflammatory responses and immunopathology. Finally, we highlight how these findings may aid the development of new therapeutic interventions against COVID-19.

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主要研究问题 ​

  1. SARS-CoV-2如何通过不同的机制导致急性呼吸窘迫综合征（ARDS）？
  2. 在SARS-CoV-2感染中，单细胞组学技术如何帮助我们理解病毒的致病机制？
  3. SARS-CoV-2感染对上呼吸道和下呼吸道的影响有何不同，如何影响疾病的严重程度？
  4. CRISPR筛选技术在研究SARS-CoV-2的致病性方面可以提供哪些新见解？
  5. 针对SARS-CoV-2引起的免疫失调，有哪些潜在的治疗干预措施正在开发？

核心洞察 ​

1. 研究背景和目的 ​

新型冠状病毒（SARS-CoV-2）的出现导致了全球范围内的严重疫情。尽管大多数感染者表现出轻度至中度的症状，病毒复制主要局限于上呼吸道，但部分患者却发展为危及生命的肺炎。本文旨在探讨SARS-CoV-2的致病机制，特别是其引发急性呼吸窘迫综合征（ARDS）的潜在机制，通过分析当前的临床和实验研究进展，以期为COVID-19的治疗干预提供新的思路。

2. 主要方法和发现 ​

研究者采用了包括单细胞组学、器官类感染模型和CRISPR筛选等新技术，深入探讨了SARS-CoV-2的病理生理特征。通过这些方法，研究揭示了病毒如何感染下呼吸道并导致肺泡损伤，主要由于免疫反应的功能失调。研究发现，感染后可能诱导上皮和内皮的“渗漏状态”，这会加重炎症反应和凝血过程。同时，免疫细胞的涌入会导致过度的炎症反应和免疫病理学的发生。

3. 核心结论 ​

SARS-CoV-2通过复杂的机制影响呼吸系统，尤其是在严重病例中，病毒感染导致的免疫反应失调是引发ARDS的关键因素。研究强调了“渗漏状态”的形成如何促进炎症和凝血，从而加重病情。这些发现为理解SARS-CoV-2的致病机制提供了新的视角，并为未来的干预措施奠定了基础。

4. 研究意义和影响 ​

该研究对COVID-19的病理生理学有重要的理论意义，揭示了病毒感染与免疫反应之间的复杂相互作用，强调了需要针对免疫调节的治疗策略。这一发现不仅有助于深入理解SARS-CoV-2引发的严重肺炎机制，也为新疗法的开发提供了切实的依据，有望改善COVID-19的临床管理和患者预后。通过应用现代生物技术，研究为新冠病毒的诊断和治疗提供了新的研究方向和可能的临床应用。

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引用本文的文献 ​

  1. Clinical and Imaging Features of COVID-19-Associated Pulmonary Aspergillosis. - Tim Fischer;Yassir El Baz;Nicole Graf;Simon Wildermuth;Sebastian Leschka;Gian-Reto Kleger;Urs Pietsch;Manuel Frischknecht;Giulia Scanferla;Carol Strahm;Stephan Wälti;Tobias Johannes Dietrich;Werner C Albrich - Diagnostics (Basel, Switzerland) (2022)
  2. Neurotrophin Signaling Impairment by Viral Infections in the Central Nervous System. - Karen Bohmwald;Catalina A Andrade;Valentina P Mora;José T Muñoz;Robinson Ramírez;María F Rojas;Alexis M Kalergis - International journal of molecular sciences (2022)
  3. Significantly Reduced Retinol Binding Protein 4 (RBP4) Levels in Critically Ill COVID-19 Patients. - Richard Vollenberg;Phil-Robin Tepasse;Manfred Fobker;Anna Hüsing-Kabar - Nutrients (2022)
  4. What Can an Organ-on-a-Chip Teach Us About Human Lung Pathophysiology? - Haiqing Bai;Donald E Ingber - Physiology (Bethesda, Md.) (2022)
  5. COVID-19 coagulopathy - what should we treat? - Pratima Chowdary - Experimental physiology (2022)
  6. The Omicron variant BA.1.1 presents a lower pathogenicity than B.1 D614G and Delta variants in a feline model of SARS-CoV-2 infection. - Mathias Martins;Gabriela M do Nascimento;Mohammed Nooruzzaman;Fangfeng Yuan;Chi Chen;Leonardo C Caserta;Andrew D Miller;Gary R Whittaker;Ying Fang;Diego G Diel - bioRxiv : the preprint server for biology (2022)
  7. Prevalence and risk factors for postinfectious cough in discharged patients with coronavirus disease 2019 (COVID-19). - Yuehan Chen;Xu Zhang;Xiansheng Zeng;Tingting Xu;Wei Xiao;Xuejiao Yang;Wenzhi Zhan;Chen Zhan;Kefang Lai - Journal of thoracic disease (2022)
  8. Blood Hyperviscosity: A Novel Link Between Hyperinflammation and Hypercoagulability in COVID-19. - Aldo Bonaventura;Nicola Potere - Journal of the American College of Cardiology (2022)
  9. Advances in understanding interferon-mediated immune responses to enteric viruses in intestinal organoids. - Lila S Nolan;Megan T Baldridge - Frontiers in immunology (2022)
  10. Two Years into the COVID-19 Pandemic: Lessons Learned. - Severino Jefferson Ribeiro da Silva;Jessica Catarine Frutuoso do Nascimento;Renata Pessôa Germano Mendes;Klarissa Miranda Guarines;Caroline Targino Alves da Silva;Poliana Gomes da Silva;Jurandy Júnior Ferraz de Magalhães;Justin R J Vigar;Abelardo Silva-Júnior;Alain Kohl;Keith Pardee;Lindomar Pena - ACS infectious diseases (2022)

... (436 更多 篇文献)

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