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J Cell Commun Signal . Coronavirus: a shift in focus away from IFN response and towards other inflammatory targets

tetano

Editor, Senior Moderator
J Cell Commun Signal


. 2020 Sep 7.
doi: 10.1007/s12079-020-00574-3. Online ahead of print.
Coronavirus: a shift in focus away from IFN response and towards other inflammatory targets


Akshaya Thoutam[SUP] 1 [/SUP], Mason Breitzig[SUP] 1 [/SUP], Richard Lockey[SUP] 1 [/SUP], Narasaiah Kolliputi[SUP] 2 3 [/SUP]



Affiliations

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.

Keywords: Interferon regulator factors (IRFs); SARS-CoV-2; Tocilizumab.
 
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