PMC:7200337 / 15436-18766 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7200337","sourcedb":"PMC","sourceid":"7200337","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7200337","text":"Prior Knowledge from SARS-CoV-1, MERS-CoV, and Murine Coronaviruses\nWhile data on COVID-19 patients continues to rapidly emerge, studies of myeloid cell dysfunction in SARS-CoV-1 and MERS-CoV can provide an important roadmap to understanding COVID-19 pathogenesis (Figure 2 ). SARS-CoV-1 infection in mouse models results in an aberrant AM phenotype that limits DC trafficking and T cell activation (Zhao et al., 2009). Additionally, YM1+ FIZZ1+ alternative macrophages can increase airway hypersensitivity, thus exacerbating SARS-associated fibrosis (Page et al., 2012). Further, as described above, murine SARS-CoV-1 studies have demonstrated that delayed IFN-I signaling and inflammatory monocytes-macrophages promote lung cytokine and chemokine levels, vascular leakage, and impaired antigen-specific T cell responses, culminating in lethal disease (Channappanavar et al., 2016). The role played by prominent IFN-producing pDCs in SARS-CoV-2 control or pathogenesis warrants investigation, as they have been shown to be critical in murine CoV (MHV) control (Cervantes-Barragan et al., 2007). Longitudinal studies in SARS-CoV-2 models are awaited, but initial phenotypic studies in humanized hACE2 mice have shown the characteristic alveolar interstitial pneumonia, with infiltration of lymphocytes and monocytes and accumulation of macrophages in the alveolar lumen (Bao et al., 2020a), which recapitulates patient findings (Xu et al., 2020c). Lastly, non-human primate (NHP) studies and patient data on SARS-CoV-1 have also shown that virus spike-specific immunoglobulin G (IgG) responses can exacerbate acute lung injury due to repolarization of alveolar macrophages into proinflammatory phenotypes and enhanced recruitment of inflammatory monocyte via CCL2 and IL-8 (Clay et al., 2012, Liu et al., 2019). However, the extent to which the antibody response contributes to disease pathophysiology remains to be confirmed.\nFigure 2 SARS-CoV-2 Infection Results in Myeloid Cell Activation and Changes NK Cell Function\nBased on data from preliminary COVID-19 studies and earlier studies in related coronaviruses.\nIL-6, IL-1β, and IFN-I/III from infected pulmonary epithelia can induce inflammatory programs in resident (alternate) macrophages while recruiting inflammatory monocytes, as well as granulocytes and lymphocytes from circulation. Sustained IL-6 and TNF-ɑ by incoming monocytes can drive several hyperinflammation cascades. Inflammatory monocyte-derived macrophages can amplify dysfunctional responses in various ways (listed in top-left corner). The systemic CRS- and sHLH-like inflammatory response can induce neutrophilic NETosis and microthrombosis, aggravating COVID-19 severity. Other myeloid cells, such as pDCs, are purported to have an IFN-dependent role in viral control. Monocyte-derived CXCL9/10/11 might recruit NK cells from blood. Preliminary data suggest that the antiviral function of these NK cells might be regulated through crosstalk with SARS-infected cells and inflammatory monocytes.\nDashed lines indicate pathways to be confirmed. Arg1, arginase 1; iNOS, inducible-nitric oxide synthase; Inflamm., inflammatory; Mono., monocytes; Macs, macrophages; Eosino, eosinophils; Neutro, neutrophils; NETosis, neutrophil extracellular trap cell death; SHLH, secondary hemophagocytic 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