4.6 Review

Hyperinflammatory Response in COVID-19: A Systematic Review

Journal

VIRUSES-BASEL
Volume 15, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/v15020553

Keywords

SARS-CoV-2; COVID-19; ARDS; cytokine storm; immunity

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This research aimed to review the immunopathological elements that contribute to the progression of COVID-19. A systematic review was conducted using various databases and search terms. The study identified several key factors, such as SARS-CoV-2 spike proteins, cellular proteases, leukocytes, cytokines, and proteolytic cascades, that play a role in the hyperinflammatory response and subsequent complications. It is important to control the dysregulation of the immune response and systemic inflammation for patients' recovery.
COVID-19 is a multisystemic disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The immunopathogenic conditions of the hyperinflammatory response that cause systemic inflammation are extremely linked to its severity. This research sought to review the immunopathological elements that contribute to its progression. This is a systematic review using the PUBMED, LILACS, MEDLINE, and SCIELO databases using articles between May 2020 and July 2022 with the following search terms in conjunction with AND: SARS-CoV-2; COVID-19; ARDS and Cytokine Storm. The quality appraisal and risk of bias were assessed by the JBI checklists and the Cochrane Collaboration's RoB 2.0 and ROBINS-I tools, respectively, and the risk of bias for in vitro studies by a pre-defined standard in the literature. The search resulted in 39 articles. The main actors in this response denote SARS-CoV-2 Spike proteins, cellular proteases, leukocytes, cytokines, and proteolytic cascades. The cytokine storm itself brings several complications to the host through cytokines such as IL-6 and chemokines (such as CCL2), which influence tissue inflammation through apoptosis and pyroptosis. The hyperinflammatory response causes several unfavorable outcomes in patients, and systemic inflammation caused largely by the dysregulation of the immune response should be controlled for their recovery.

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