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Med Hypotheses ; 143: 110117, 2020 Oct.
Artículo en Inglés | MEDLINE | ID: covidwho-652869

RESUMEN

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.


Asunto(s)
Betacoronavirus/fisiología , Infecciones por Coronavirus/complicaciones , Modelos Inmunológicos , Síndrome Mucocutáneo Linfonodular/etiología , Pandemias , Neumonía Viral/complicaciones , Enzima Convertidora de Angiotensina 2 , Asia/epidemiología , COVID-19 , Niño , Vasos Coronarios/inmunología , Vasos Coronarios/patología , Infecciones por Coronavirus/epidemiología , Infecciones por Coronavirus/genética , Síndrome de Liberación de Citoquinas/etiología , Progresión de la Enfermedad , Endotelio Vascular/virología , Predisposición Genética a la Enfermedad , Humanos , Inflamación , Activación de Macrófagos , Síndrome Mucocutáneo Linfonodular/epidemiología , Síndrome Mucocutáneo Linfonodular/genética , Síndrome Mucocutáneo Linfonodular/inmunología , Países Bajos/epidemiología , Peptidil-Dipeptidasa A/biosíntesis , Peptidil-Dipeptidasa A/genética , Peptidil-Dipeptidasa A/fisiología , Neumonía Viral/epidemiología , Neumonía Viral/genética , Receptores Virales/biosíntesis , Receptores Virales/genética , Receptores Virales/fisiología , SARS-CoV-2 , Estaciones del Año , Glicoproteína de la Espiga del Coronavirus/fisiología , Factor de Necrosis Tumoral alfa/fisiología , Estados Unidos/epidemiología
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