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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 an...

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Detalles Bibliográficos
Autores principales: Coveney, Clarissa, Tellier, Michel, Lu, Fangfang, Maleki-Toyserkani, Shayda, Jones, Ruth, Bart, Valentina M T, Pring, Ellie, Alrubayyi, Aljawharah, Richter, Felix C, Scourfield, D Oliver, Rehwinkel, Jan, Rodrigues, Patrícia R S, Davies, Luke C, Gea-Mallorquí, Ester
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7798570/
https://www.ncbi.nlm.nih.gov/pubmed/34192267
http://dx.doi.org/10.1093/oxfimm/iqaa004
Descripción
Sumario: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.