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SARS-CoV-2 Infection and C1-Esterase Inhibitor: Camouflage Pattern and New Perspective.
Al-Kuraishy, Hayder M; Al-Gareeb, Ali I; Jalal, Naif A; Kabrah, Saeed M; Alexiou, Athanasios; Batiha, Gaber El-Saber.
  • Al-Kuraishy HM; Department of Clinical Pharmacology and Medicine, College of Medicine, Al-Mustansiriyia University, Baghdad, Iraq.
  • Al-Gareeb AI; Department of Clinical Pharmacology and Medicine, College of Medicine, Al-Mustansiriyia University, Baghdad, Iraq.
  • Jalal NA; Department of Microbiology, Faculty of Medicine, Umm Al-Qura University, Makkah, Saudi Arabia.
  • Kabrah SM; Department of Laboratory Medicine, Faculty of Applied Medical Sciences, Umm Al-Qura University, Kingdom of Saudi Arabia.
  • Alexiou A; Department of Science and Engineering, Novel Global Community Educational Foundation, Hebersham, NSW 2770, Australia.
  • Batiha GE; AFNP Med, Austria, 1030 Wien, Austria.
Curr Protein Pept Sci ; 23(7): 465-474, 2022.
Article in English | MEDLINE | ID: covidwho-1993661
ABSTRACT
In Covid-19, the pathological effect of SARS-CoV-2 infection is arbitrated through direct viral toxicity, unusual immune response, endothelial dysfunction, deregulated renin-angiotensin system [RAS], and thrombo-inflammation, leading to acute lung injury (ALI), with a succession of acute respiratory distress syndrome (ARDS) in critical conditions. C1 esterase inhibitor (C1INH) is a protease inhibitor that inhibits the spontaneous activation of complement and contact systems and kinin pathway, clotting, and fibrinolytic systems. Therefore, targeting the complement system through activation of C1INH might be a novel therapeutic modality in the treatment of Covid-19. Therefore, this study aims to illustrate the potential nexus between C1INH and the pathophysiology of SARS-CoV-2 infection. C1INH is highly dysregulated in Covid-19 due to inflammatory and coagulation disorders. C1INH is up-regulated in Covid-19 and sepsis as an acute phase response, but this increase is insufficient to block the activated complement system. In addition, the C1INH serum level predicts the development of ARDS in Covid-19 patients, as its up-regulation is associated with the development of cytokine storm. In Covid-19, C1INH might be inhibited or dysregulated by SARS-CoV-2, leading to propagation of complement system activation with subsequent uncontrolled immunological stimulation due to activation of bradykinin and FXII with sequential activation of coagulation cascades and polymerization of fibrin. Thus, suppression of C1INH by SARS-CoV-2 infection leads to thrombosis and excessive inflammation due to uncontrolled activation of complements and contact systems.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Respiratory Distress Syndrome / Complement C1 Inhibitor Protein / COVID-19 Type of study: Prognostic study Limits: Humans Language: English Journal: Curr Protein Pept Sci Journal subject: Biochemistry Year: 2022 Document Type: Article Affiliation country: 1389203723666220811121803

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Respiratory Distress Syndrome / Complement C1 Inhibitor Protein / COVID-19 Type of study: Prognostic study Limits: Humans Language: English Journal: Curr Protein Pept Sci Journal subject: Biochemistry Year: 2022 Document Type: Article Affiliation country: 1389203723666220811121803