Immunophenotyping of COVID-19 and influenza highlights the role of type I interferons in development of severe COVID-19.
Jeong Seok LeeSeongwan ParkHye Won JeongJin Young AhnSeong Jin ChoiHoyoung LeeBaekgyu ChoiSu Kyung NamMoa SaJi-Soo KwonSu Jin JeongHeung Kyu LeeSung Ho ParkSu-Hyung ParkJun Yong ChoiSung Han KimInkyung JungEui-Cheol ShinPublished in: Science immunology (2020)
Although most SARS-CoV-2-infected individuals experience mild coronavirus disease 2019 (COVID-19), some patients suffer from severe COVID-19, which is accompanied by acute respiratory distress syndrome and systemic inflammation. To identify factors driving severe progression of COVID-19, we performed single-cell RNA-seq using peripheral blood mononuclear cells (PBMCs) obtained from healthy donors, patients with mild or severe COVID-19, and patients with severe influenza. Patients with COVID-19 exhibited hyper-inflammatory signatures across all types of cells among PBMCs, particularly up-regulation of the TNF/IL-1β-driven inflammatory response as compared to severe influenza. In classical monocytes from patients with severe COVID-19, type I IFN response co-existed with the TNF/IL-1β-driven inflammation, and this was not seen in patients with milder COVID-19. Interestingly, we documented type I IFN-driven inflammatory features in patients with severe influenza as well. Based on this, we propose that the type I IFN response plays a pivotal role in exacerbating inflammation in severe COVID-19.
Keyphrases
- coronavirus disease
- sars cov
- respiratory syndrome coronavirus
- early onset
- single cell
- rna seq
- inflammatory response
- acute respiratory distress syndrome
- dendritic cells
- immune response
- end stage renal disease
- chronic kidney disease
- gene expression
- high throughput
- cell proliferation
- peritoneal dialysis
- toll like receptor
- endoplasmic reticulum stress