SARS-CoV-2 pathogenesis

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...

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Vydáno v:Nature reviews. Microbiology Ročník 20; číslo 5; s. 270 - 284
Hlavní autoři: Lamers, Mart M, Haagmans, Bart L
Médium: Journal Article
Jazyk:angličtina
Vydáno: England Nature Publishing Group 01.05.2022
Témata:
Alveoli
Cell culture
Coagulation
Coronaviruses
COVID-19
CRISPR
Endothelium
Epithelium
Humans
Immune response
Immune system
Inflammation
Inflammation - pathology
Organoids
Pandemics
Pathogenesis
Pathophysiology
Respiratory diseases
Respiratory distress syndrome
Respiratory tract
Respiratory tract diseases
SARS-CoV-2
Severe acute respiratory syndrome coronavirus 2
Therapeutic applications
Viral diseases
Virus Replication
ISSN:1740-1526, 1740-1534, 1740-1534
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Shrnutí: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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ISSN:1740-1526
1740-1534
1740-1534
DOI:10.1038/s41579-022-00713-0