Understanding the immunopathogenesis of COVID-19: Its implication for therapeutic strategy.

paythelady.612 shared this article with you from Inoreader Understanding the immunopathogenesis of COVID-19: Its implication for therapeutic strategy. Μέσω pubmed: "world j clin cases"... Related Articles Understanding the immunopathogenesis of COVID-19: Its implication for therapeutic strategy. World J Clin Cases. 2020 Dec 06;8(23):5835-5843 Authors: Shimizu Y Abstract Although 80% of individuals infected with the severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) recover without antiviral treatments, the other 20% progress to severe forms of pulmonary disease, suggesting that the host's immune response to the virus could influence the outcome of coronavirus disease 2019 (COVID-19). SARS-CoV-2 infects alveolar epithelial type 2 cells expressing angiotensin-converting enzyme 2, and these infected epithelial cells recruit dendritic cells, neutrophils and monocytes /macrophages, leading to the activation of CD4+ and CD8+ T cells. These cells launch an antiviral immune response, but are able to completely suppress viral replication or completely eradicate virus in a limited proportion of infected patients. In other patients, viral suppression is incomplete and the numbers of circulating B and T cells are subsequently reduced by as yet unknown mechanisms. Some patients with sustained viral replication progress to a severe condition cal led cytokine storm. Although antiviral drug(s) should be considered early in infection to prevent progression, there have been no antiviral therapies proven to be effective for significantly inhibiting the viral replication in vivo and suppressing the progression to cytokine storm. Blocking the action of cytokines with dexamethasone or anti-interleukin-6 could have a pivotal role in treatment of those patients. Therapeutic strategy should therefore be based on viral kinetics and the immunopathology of COVID-19. PMID: 33344582 [PubMed] View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.