TY - JOUR
T1 - The COVID-19 puzzle
T2 - deciphering pathophysiology and phenotypes of a new disease entity
AU - Osuchowski, Marcin F.
AU - Winkler, Martin S.
AU - Skirecki, Tomasz
AU - Cajander, Sara
AU - Shankar-Hari, Manu
AU - Lachmann, Gunnar
AU - Monneret, Guillaume
AU - Venet, Fabienne
AU - Bauer, Michael
AU - Brunkhorst, Frank M.
AU - Weis, Sebastian
AU - Garcia-Salido, Alberto
AU - Kox, Matthijs
AU - Cavaillon, Jean Marc
AU - Uhle, Florian
AU - Weigand, Markus A.
AU - Flohé, Stefanie B.
AU - Wiersinga, W. Joost
AU - Almansa, Raquel
AU - de la Fuente, Amanda
AU - Martin-Loeches, Ignacio
AU - Meisel, Christian
AU - Spinetti, Thibaud
AU - Schefold, Joerg C.
AU - Cilloniz, Catia
AU - Torres, Antoni
AU - Giamarellos-Bourboulis, Evangelos J.
AU - Ferrer, Ricard
AU - Girardis, Massimo
AU - Cossarizza, Andrea
AU - Netea, Mihai G.
AU - van der Poll, Tom
AU - Bermejo-Martín, Jesús F.
AU - Rubio, Ignacio
N1 - Publisher Copyright:
© 2021 Elsevier Ltd
PY - 2021/6
Y1 - 2021/6
N2 - The zoonotic SARS-CoV-2 virus that causes COVID-19 continues to spread worldwide, with devastating consequences. While the medical community has gained insight into the epidemiology of COVID-19, important questions remain about the clinical complexities and underlying mechanisms of disease phenotypes. Severe COVID-19 most commonly involves respiratory manifestations, although other systems are also affected, and acute disease is often followed by protracted complications. Such complex manifestations suggest that SARS-CoV-2 dysregulates the host response, triggering wide-ranging immuno-inflammatory, thrombotic, and parenchymal derangements. We review the intricacies of COVID-19 pathophysiology, its various phenotypes, and the anti-SARS-CoV-2 host response at the humoral and cellular levels. Some similarities exist between COVID-19 and respiratory failure of other origins, but evidence for many distinctive mechanistic features indicates that COVID-19 constitutes a new disease entity, with emerging data suggesting involvement of an endotheliopathy-centred pathophysiology. Further research, combining basic and clinical studies, is needed to advance understanding of pathophysiological mechanisms and to characterise immuno-inflammatory derangements across the range of phenotypes to enable optimum care for patients with COVID-19.
AB - The zoonotic SARS-CoV-2 virus that causes COVID-19 continues to spread worldwide, with devastating consequences. While the medical community has gained insight into the epidemiology of COVID-19, important questions remain about the clinical complexities and underlying mechanisms of disease phenotypes. Severe COVID-19 most commonly involves respiratory manifestations, although other systems are also affected, and acute disease is often followed by protracted complications. Such complex manifestations suggest that SARS-CoV-2 dysregulates the host response, triggering wide-ranging immuno-inflammatory, thrombotic, and parenchymal derangements. We review the intricacies of COVID-19 pathophysiology, its various phenotypes, and the anti-SARS-CoV-2 host response at the humoral and cellular levels. Some similarities exist between COVID-19 and respiratory failure of other origins, but evidence for many distinctive mechanistic features indicates that COVID-19 constitutes a new disease entity, with emerging data suggesting involvement of an endotheliopathy-centred pathophysiology. Further research, combining basic and clinical studies, is needed to advance understanding of pathophysiological mechanisms and to characterise immuno-inflammatory derangements across the range of phenotypes to enable optimum care for patients with COVID-19.
UR - http://www.scopus.com/inward/record.url?scp=85107130271&partnerID=8YFLogxK
U2 - 10.1016/S2213-2600(21)00218-6
DO - 10.1016/S2213-2600(21)00218-6
M3 - Review article
C2 - 33965003
AN - SCOPUS:85107130271
SN - 2213-2600
VL - 9
SP - 622
EP - 642
JO - The Lancet Respiratory Medicine
JF - The Lancet Respiratory Medicine
IS - 6
ER -