Entry |
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Name |
COVID-19; Coronavirus disease 2019 |
Description |
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.
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Category |
Infectious disease
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Brite |
Infectious diseases [BR:br08401]
Viral infections
Infections caused by +ssRNA viruses
H02398 COVID-19
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Pathway |
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Network |
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) |
Element |
N01307 | SARS-CoV-2 S to AngII-AT1R-NOX2 signaling pathway |
N01309 | SARS-CoV-2 nsp3 to MDA5-IRF7/3 signaling pathway |
N01310 | SARS-CoV-2 nsp13 to RIG-I-IRF7/3 signaling pathway |
N01312 | SARS-CoV-2 S to lectin pathway of complement activation |
N01314 | SARS-CoV-2 S to classical pathway of complement activation |
N01316 | SARS-CoV-2 S/N to lectin pathway of coagulation activation |
N01318 | SARS-CoV-2 nsp1 to translation initiation |
N01319 | SARS-CoV-2 nsp6 and ORF6 to RIG-I-IRF7/3 signaling pathway |
N01320 | SARS-CoV-2 nsp3 to RIG-I-IRF7/3 signaling pathway |
N01321 | SARS-CoV-2 nsp1/6/13, ORF3a/6/7b and M to IFN signaling pathway |
N01322 | SARS-CoV-2 nsp6/13 and ORF7a/7b to IFN signaling pathway |
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Pathogen |
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Drug |
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Reference |
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Authors |
Wu F, Zhao S, Yu B, Chen YM, Wang W, Song ZG, Hu Y, Tao ZW, Tian JH, Pei YY, Yuan ML, Zhang YL, Dai FH, Liu Y, Wang QM, Zheng JJ, Xu L, Holmes EC, Zhang YZ |
Title |
A new coronavirus associated with human respiratory disease in China. |
Journal |
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Reference |
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Authors |
Hui DS, I Azhar E, Madani TA, Ntoumi F, Kock R, Dar O, Ippolito G, Mchugh TD, Memish ZA, Drosten C, Zumla A, Petersen E |
Title |
The continuing 2019-nCoV epidemic threat of novel coronaviruses to global health - The latest 2019 novel coronavirus outbreak in Wuhan, China. |
Journal |
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Reference |
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Authors |
Kiselevskiy M, Shubina I, Chikileva I, Sitdikova S, Samoylenko I, Anisimova N, Kirgizov K, Suleimanova A, Gorbunova T, Varfolomeeva S |
Title |
Immune Pathogenesis of COVID-19 Intoxication: Storm or Silence? |
Journal |
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Reference |
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Authors |
Hojyo S, Uchida M, Tanaka K, Hasebe R, Tanaka Y, Murakami M, Hirano T |
Title |
How COVID-19 induces cytokine storm with high mortality. |
Journal |
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Reference |
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Authors |
Zhang C, Wu Z, Li JW, Zhao H, Wang GQ |
Title |
Cytokine release syndrome in severe COVID-19: interleukin-6 receptor antagonist tocilizumab may be the key to reduce mortality. |
Journal |
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Reference |
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Authors |
Lo MW, Kemper C, Woodruff TM |
Title |
COVID-19: Complement, Coagulation, and Collateral Damage. |
Journal |
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Reference |
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Authors |
Noris M, Benigni A, Remuzzi G |
Title |
The case of complement activation in COVID-19 multiorgan impact. |
Journal |
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Reference |
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Authors |
Java A, Apicelli AJ, Liszewski MK, Coler-Reilly A, Atkinson JP, Kim AH, Kulkarni HS |
Title |
The complement system in COVID-19: friend and foe? |
Journal |
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