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Editorial
. 2020 Jun;8(6):1798-1801.
doi: 10.1016/j.jaip.2020.04.014. Epub 2020 Apr 18.

Weathering the Cytokine Storm in Susceptible Patients with Severe SARS-CoV-2 Infection

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Editorial

Weathering the Cytokine Storm in Susceptible Patients with Severe SARS-CoV-2 Infection

Brian Lipworth et al. J Allergy Clin Immunol Pract. 2020 Jun.
No abstract available

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Figures

Figure 1
Figure 1
The cytokine cascade resulting from acute severe SARS-CoV-2 infection, with downstream IL-6 activation considered to be a hallmark feature in terms of progression of COVID-19 pneumonia to hyperinflammation and ARDS. Also shown are the putative mechanisms of action for bromhexine and hydroxychloroquine in attenuating upstream SARS-CoV-2 tissue binding, the effect of antivirals on replication, azithromycin as an antiviral and immunomudulator, nonspecific cytokine suppression by corticosteroids, together with the selective downstream effect of IL-6 blockade with tocilizumab or sarilumab and effects of anti-TNF and interferon beta-1-a. ACE2, Angiotensin converting enzyme 2; ACEI, angiotensin converting enzyme inhibitor; ARB, angiotensin II receptor blocker; ARDS, acute respiratory distress syndrome; CRP, C reactive protein; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; TNF, tumour necrosis factor; TMPRSS2, transmembrane protease, serine 2.

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