The COVID-19 outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global major concern. In this review, we addressed a theoretical model on immunopathogenesis associated with severe COVID-19, based on the current literature of SARS-CoV-2 and other epidemic pathogenic coronaviruses, such as SARS and MERS. Several studies have suggested that immune dysregulation and hyperinflammatory response induced by SARS-CoV-2 are more involved in disease severity than the virus itself. Immune dysregulation due to COVID-19 is characterized by delayed and impaired interferon response, lymphocyte exhaustion and cytokine storm that ultimately lead to diffuse lung tissue damage and posterior thrombotic phenomena. Considering there is a lack of clinical evidence provided by randomized clinical trials, the knowledge about SARS-CoV-2 disease pathogenesis and immune response is a cornerstone to develop rationale-based clinical therapeutic strategies. In this narrative review, the authors aimed to describe the immunopathogenesis of severe forms of COVID-19.
【저자키워드】 COVID-19, immunology, SARS-CoV-2, Inflammation, Cytokine storm, thrombosis, cytokine, macrophage activation syndrome, 【초록키워드】 coronavirus, immune response, Pathogenesis, severe COVID-19, knowledge, disease severity, MERS, virus, lymphocyte, Epidemic, COVID-19 outbreak, Immunopathogenesis, Therapeutic strategies, randomized clinical trials, interferon response, immune dysregulation, dysregulation, SARS-CoV-2 disease, acute respiratory syndrome, thrombotic, lung tissue, clinical evidence, pathogenic coronaviruses, Hyperinflammatory, lack, develop, caused, involved, form, provided, characterized, suggested, addressed,