Coronavirus: a shift in focus away from IFN response and towards other inflammatory targets.
J Cell Commun Signal
; 14(4): 469-470, 2020 Dec.
Article
em En
| MEDLINE
| ID: mdl-32895779
ABSTRACT
In the past two decades, two beta-coronaviruses, severe acute respiratory syndrome-related coronavirus (SARS-CoV-1) and the Middle East respiratory syndrome-related coronavirus (MERS-CoV), have infected approximately 8000 and 2500 across the globe, respectively (de Wit et al. 2016; Amanat and Krammer 2020). The current viral pandemic, caused by SARS-CoV-2, has already affected 4.23 M in less than a year. Of greater concern, the disease caused by SARS-CoV-2, COVID-19, still has a rapidly increasing global burden (Wu et al. 2020; Zhu et al. 2020). To better understand the biology of COVID-19, an initial barrage of studies compared SARS-CoV-2 to other respiratory viruses MERS-CoV, SARS-CoV-1, human parainfluenza virus 3 (HPIV3), respiratory syncytial virus (RSV), and Influenza A Virus (IAV). These studies indicate that SARS-CoV-2 infected individuals have a consistent chemokine signature comprising cytokines and monocyte-associated chemokines (CCL2 and CCL8). Therefore, it appears that monocyte cytokine production, particularly in those with a diminished innate immunity, is a driving feature of COVID-19 infection.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
J Cell Commun Signal
Ano de publicação:
2020
Tipo de documento:
Article
País de afiliação:
Estados Unidos