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Editorial
. 2020 May 1;52(5):217-221.
doi: 10.1152/physiolgenomics.00033.2020. Epub 2020 Apr 10.

Harnessing innate immunity to eliminate SARS-CoV-2 and ameliorate COVID-19 disease

Affiliations
Editorial

Harnessing innate immunity to eliminate SARS-CoV-2 and ameliorate COVID-19 disease

Rachel M Golonka et al. Physiol Genomics. .
No abstract available

Keywords: deoxyribonuclease I; flagellin; interferon; neutrophil extracellular traps; toll-like receptor 5.

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Conflict of interest statement

No conflicts of interest, financial or otherwise, are declared by the authors.

Figures

Fig. 1.
Fig. 1.
Innate immunity may be the key to defeat severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). In the early stage of infection, coronaviruses are capable of inhibiting host type I interferon (IFN) antiviral immune defenses. We propose to counteract this by utilizing flagellin to activate Toll-like receptor 5 (TLR5). TLR5 can induce the production of cytokines (i.e., IL-22, IL-18) and IFN-β, which may restore the impaired immune responses. In the late stage of infection, there is a proinflammatory cytokine storm initiated by innate immune cells like neutrophils (NEU). Theoretically, this can result in inappropriate levels of neutrophil extracellular traps (NETs) and reactive oxygen species (ROS) that cause unwarranted collateral damage. Deoxyribonuclease I (DNase I)-mediated degradation of NETs could provide a therapeutic avenue to suppress excess injury.

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