COVID-19;
Coronavirus disease 2019

Coronavirus disease of 2019 (COVID-19) is a highly contagious respiratory infection that is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 infects alveolar epithelial cells [mainly alveolar epithelial type 2 (AEC2) cells] through the angiotensin-converting enzyme 2 (ACE2) receptor. Upon the occupancy of ACE2 by SARS-CoV-2, the increased serum level of free Angiotensin II (Ang II) due to a reduction of ACE2-mediated degradation promotes activation of the NF-kappa B pathway via Ang II type 1 receptor (AT1R), followed by  interleukin-6 (IL-6) production. SARS-CoV-2 also activates the innate immune system; macrophage stimulation triggers the overproduction of pro-inflammatory cytokines, including IL-6, and the "cytokine storm", which results in systemic inflammatory response syndrome and multiple organ failure. The combined effects of complement activation, dysregulated neutrophilia, endothelial injury, and hypercoagulability appear to be intertwined to drive the severe features of COVID-19.

Infectious disease

nt06122  IFN signaling (viruses)
nt06133  RLR signaling (viruses)
nt06136  Complement activation (viruses)
nt06141  Translation (viruses)
nt06171  Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)

SARS-CoV-2 [GN:T40361]

Remdesivir [DR:D11472]

PMID:32015508

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Nature 10.1038/s41586-020-2008-3 (2020)
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PMID:31953166

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PMID:32722596

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Pharmaceuticals (Basel) 13:E166 (2020)
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PMID:33014208

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Inflamm Regen 40:37 (2020)
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PMID:32234467

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Int J Antimicrob Agents 55:105954 (2020)
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PMID:32699160

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J Immunol 205:1488-1495 (2020)
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PMID:32461141

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Kidney Int 98:314-322 (2020)
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PMID:32554923

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The complement system in COVID-19: friend and foe?

JCI Insight 5:140711 (2020)
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