SARS-CoV-2/COVID-19 and its relationship with NOD2 and ubiquitination.
Clin Immunol
; 238: 109027, 2022 05.
Article
in English
| MEDLINE | ID: covidwho-1814259
ABSTRACT
COVID-19 infection activates the immune system to cause autoimmune and autoinflammatory diseases. We provide a comprehensive review of the relationship between SARS-CoV-2, NOD2 and ubiquitination. COVID-19 infection partly results from host inborn errors and genetic factors and can lead to autoinflammatory disease. The interaction between defective NOD2 and viral infection may trigger NOD2-associated disease. SARS-CoV-2 can alter UBA1 and abnormal ubiquitination leading to VEXAS syndrome. Both NOD2 and ubiquitination play important roles in controlling inflammatory process. Receptor interacting protein kinase 2 is a key component of the NOD2 activation pathway and becomes ubiquitinated to recruit downstream effector proteins. NOD2 mutations result in loss of ubiquitin binding and increase ligand-stimulated NOD2 signaling. During viral infection, mutations of either NOD2 or UBA1 genes or in combination can facilitate autoinflammatory disease. COVID-19 infection can cause autoinflammatory disease. There are reciprocal interactions between SARS-CoV-2, NOD2 and ubiquitination.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Hereditary Autoinflammatory Diseases
/
COVID-19
Limits:
Humans
Language:
English
Journal:
Clin Immunol
Journal subject:
Allergy and Immunology
Year:
2022
Document Type:
Article
Affiliation country:
J.clim.2022.109027
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