Article ; Online: Kawasaki-like disease in children with COVID-19: A hypothesis.
2020 Volume 143, Page(s) 110117
Abstract: With rapid spread of severe acute respiratory syndrome- corona virus-2 (SARS-COV-2) globally, some new aspects of the disease have been reported. Recently, it has been reported the incidence of Kawasaki-like disease among children with COVID-19. Since, ... ...
Abstract | With rapid spread of severe acute respiratory syndrome- corona virus-2 (SARS-COV-2) globally, some new aspects of the disease have been reported. Recently, it has been reported the incidence of Kawasaki-like disease among children with COVID-19. Since, children had been known to be less severely affected by the virus in part due to the higher concentration of Angiotensin converting enzyme (ACE)-2 receptor, this presentation has emerged concerns regarding the infection of children with SARS-COV2. ACE2 has anti-inflammatory, anti-fibrotic and anti-proliferative characteristics through converting angiotensin (Ag)-II to Ang (1-7). ACE2 receptor is downregulated by the SARS-COV through the spike protein of SARS-CoV (SARS-S) via a process that is tightly coupled with Tumor necrosis factor (TNF)-α production. TNF-α plays a key role in aneurysmal formation of coronary arteries in Kawasaki disease (KD). Affected children by COVID-19 with genetically-susceptible to KD might have genetically under-expression of ACE2 receptor that might further decrease the expression of ACE2 due to the downregulation of the receptor by the virus in these patients. It appears that TNF- α might be the cause and the consequence of the ACE2 receptor downregulation which results in arterial walls aneurysm. Conclusion: Genetically under-expression of ACE2 receptor in children with genetically-susceptible to KD who are infected with SARS-CoV-2 possibly further downregulates the ACE2 expression by TNF-α and leads to surge of inflammation including TNF-α and progression to Kawasaki-like disease. |
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MeSH term(s) | Angiotensin-Converting Enzyme 2 ; Asia/epidemiology ; Betacoronavirus/physiology ; COVID-19 ; Child ; Coronary Vessels/immunology ; Coronary Vessels/pathology ; Coronavirus Infections/complications ; Coronavirus Infections/epidemiology ; Coronavirus Infections/genetics ; Cytokine Release Syndrome/etiology ; Disease Progression ; Endothelium, Vascular/virology ; Genetic Predisposition to Disease ; Humans ; Inflammation ; Macrophage Activation ; Models, Immunological ; Mucocutaneous Lymph Node Syndrome/epidemiology ; Mucocutaneous Lymph Node Syndrome/etiology ; Mucocutaneous Lymph Node Syndrome/genetics ; Mucocutaneous Lymph Node Syndrome/immunology ; Netherlands/epidemiology ; Pandemics ; Peptidyl-Dipeptidase A/biosynthesis ; Peptidyl-Dipeptidase A/genetics ; Peptidyl-Dipeptidase A/physiology ; Pneumonia, Viral/complications ; Pneumonia, Viral/epidemiology ; Pneumonia, Viral/genetics ; Receptors, Virus/biosynthesis ; Receptors, Virus/genetics ; Receptors, Virus/physiology ; SARS-CoV-2 ; Seasons ; Spike Glycoprotein, Coronavirus/physiology ; Tumor Necrosis Factor-alpha/physiology ; United States/epidemiology |
Chemical Substances | Receptors, Virus ; Spike Glycoprotein, Coronavirus ; Tumor Necrosis Factor-alpha ; spike protein, SARS-CoV-2 ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) |
Keywords | covid19 |
Language | English |
Publishing date | 2020-07-18 |
Publishing country | United States |
Document type | Letter |
ZDB-ID | 193145-3 |
ISSN | 1532-2777 ; 0306-9877 |
ISSN (online) | 1532-2777 |
ISSN | 0306-9877 |
DOI | 10.1016/j.mehy.2020.110117 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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