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10.1007/s12079-020-00574-3

http://scihub22266oqcxt.onion/10.1007/s12079-020-00574-3
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32895779!7476676!32895779
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suck abstract from ncbi


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pmid32895779      J+Cell+Commun+Signal 2020 ; 14 (4): 469-470
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  • Coronavirus: a shift in focus away from IFN response and towards other inflammatory targets #MMPMID32895779
  • Thoutam A; Breitzig M; Lockey R; Kolliputi N
  • J Cell Commun Signal 2020[Dec]; 14 (4): 469-470 PMID32895779show ga
  • 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.
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