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|Title:||COVID-19 and Hyperinflammatory Syndrome|
|Authors:||Ray, Partho Sarothi|
|Keywords:||Chemokine;Cytokine storm;Lung injury;Lymphohistiocytosis;Neutrophil|
|Abstract:||COVID-19, the multifactorial disease caused by the novel coronavirus SARS-CoV-2 is mediated by specific antiviral and inflammatory responses. It is now recognized that in most severe cases of COVID-19 an excessive and uncontrolled inflammatory response exacerbates lung damage caused by viral infection, and contributes to acute respiratory distress syndrome and respiratory failure. This hyperinflammatory syndrome is characterized by multiple cellular and molecular events, including aberrant neutrophil and lymphocyte function, amplification of the inflammatory response by release of damage associated molecular patterns, cytokine storm, lung damage and edema and a pro-fibrotic condition, ultimately leading to respiratory failure. This review discusses these molecular events in correlation with stages of viral infection and disease progression, underscoring the key points that characterize the clinical manifestations of the hyperinflammatory syndrome in COVID-19. Furthermore, it discusses the available or potential therapeutics that target various important mediators of this hyperinflammatory response that are being considered for treatment of COVID-19.|
|ISSN:||0975-0959 (Online); 0301-1208 (Print)|
|Appears in Collections:||IJBB Vol.57(6) [December 2020]|
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