Innate immunity to SARS-CoV-2 infection: a review

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, first notified in China, has spread around the world causing high morbidity and mortality, which is due to factors such as the subversion of the immune response. The aims of the study are to summarise and present the immunopathological relationship of COVID-19 with innate immunity. This is a systematic review conducted by the National Library of Medicine -National Institutes of Health, USA (PUBMED), Latin American and Caribbean Literature on Health Sciences (LILACS), Medical Literature Analysis and Retrieval System Online (MEDLINE) and Scientific Electronic Library Online (SCIELO) databases with clinical trials, in vitro assays, case-controls, cohort studies, systematic reviews and meta-analyses between February 2020 and July 2021. The version 2 of the Cochrane risk-of-bias tool for RCTs (RoB 2), Joana Briggs Institute (JBI) Critical Appraisal (for the review articles) and the Risk of Bias in Non-randomised Studies of Interventions (ROBINS-I) tools were used to evaluate the quality and the risk of bias of the studies included in this review. The innate immune response through the generation of interferons, alternative pathways and complement system lectins and the joint action of innate immune cells and cytokines and chemokines lead to different clinical outcomes, taking into account the exacerbated inflammatory response and pathogenesis. Then, in addition to interacting as a bridge for adaptive immunity, the innate immune response plays an essential role in primary defense and is one of the starting points for immune evasion by SARS-CoV-2.

Adaptive immunity to SARS-CoV-2 infection: A systematic review

“…CD123, the α chain of receptors of the interleukin 3, is a surface cell marker present in APCs, such as plasmacytoid dendritic cells (pDCs) and monocytes, critical for activation of adaptive CD4+ and CD8+ T cell responses. Increased binding of T-monocyte cells in males may explain the reported higher plasma concentrations of IL-8 and IL-18 in COVID-19 patients, as IL-3 leads to monocyte mobilization and since high serum levels of unconventional monocytes have been recorded in men, such as CD14+/CD16+, which activate inflammation through the release of these cytokines ( 94 ). By encouraging the recruitment of circulating pDCs into the airways and inducing the release of CXCL12 from pulmonary CD123+ epithelial cells, IL-3 boosts innate antiviral immunity ( 49 , 95 ).…”

A Genome-Wide Arrayed CRISPR Screen Reveals PLSCR1 as an Intrinsic Barrier to SARS-CoV-2 Entry

“…Approximately 1-5% of critical COVID-19 patients have mutations that compromise the production of or response to type I IFNs, while an additional 15% possess autoantibodies that neutralize type I IFNs [1][2][3][4][5][6][7]. This highlights the essential role of type I IFN in the defense against the SARS-CoV-2 virus that caused the COVID-19 pandemic [8,9]. Consequently, investigating IFN-stimulated genes (ISGs) is crucial to our understanding of the remarkable antiviral systems that evolved in nature.…”

Hyperinflammatory Response in COVID-19: A Systematic Review

“…Moreover, in their arsenal of defense mechanisms, neutrophils can produce antimicrobial granules, neutrophil elastase (NE), and create NETs. NETs can cause tissue damage by killing the epithelial and endothelial cells of pulmonary tissue in infection and sterile illness since they are known contributors to the pathological inflammation of pneumonia [ 36 ].…”