COVID-19: A New Virus, but a Familiar Receptor and Cytokine Release Syndrome
By T. Hirano, M. Murakami. Immunity, 2020
688 citations recorded by the source corpus.
Summary Zhou et al. (Nature) and Hoffmann et al. (Cell) identify ACE2 as a SARS-CoV-2 receptor, and the latter show its entry mechanism depends on cellular serine protease TMPRSS2. These results may explain proinflammatory cytokine release via the associated angiotestin II pathway and a possible therapeutic target via the IL-6-STAT3 axis.
Subfields: Infectious Diseases, Neurology
View Paper: https://www.semanticscholar.org/paper/92d94dd352c9ebd593a8e2a6abcbc58310508628
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In Infectious Diseases
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Citations in the corpus
- NF-κB in biology and targeted therapy: new insights and translational implications (2024, background): “473 The activation of NF-κ B by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) leads to the production of pro-in fl ammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α ).”
- IL-6 in inflammation, autoimmunity and cancer (2020, background): “ARDS in COVID-19 is considered the result of cytokine storm (12–17), re-sembling the disease caused by SARS-CoV-1 and Middle East respiratory syndrome coronavirus (MERS-CoV) (335).”
- Immunology of COVID-19: Current State of the Science (2020, positive): “Successful antibody-mediated neutralization of SARS-CoV-2 seemed to be dependent on the inhibition of ACE2/RBD binding.”
- The cytokine storm and COVID‐19 (2020, background): “Hirano et al.(37) proposed a potential mechanism of the cytokine storm caused by the angiotensin 2 (AngII) pathway.”