paper: Arunachalam, P. S., Wimmers, F., Mok, C. K. P., Perera, R. A., Scott, M., Hagan, T., ... & Pulendran B. (2020). Systems biological assessment of immunity to mild versus severe COVID-19 infection in humans. Science, 369(6508), 1210-1220. Chicago
contributor: Bali Pulendran
contributor_organization: Stanford
contributor_email: bpulend@stanford.edu
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- description: Genes differentially expressed in COVID-19 patients compared to healthy controls
- exact_source: Fig. 4, Table S4 Tab "DEG_healthy_vs_covid-19"
- tissue: PBMC
- immune_exposure: SARS-CoV-2 infection
- cohort: Adults (38 - 90)
- comparison: COVID-19 vs healthy
- repository_id: GSE155673
- platform: CITE-seq
- response_components:
- response_behavior: Up or down
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- description: Interferon-stimulated genes in COVID-19 patients
- exact_source: Fig. 4G and supplementary fig. 15A
- tissue: PBMC
- immune_exposure: SARS-CoV-2 infection
- cohort: Adults (38 - 90)
- comparison: COVID-19 vs healthy
- repository_id: GSE152418
- platform: Bulk RNAseq
- response_components:
- response_behavior: Up
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PMID
32788292
abstract
COVID-19 represents a global crisis, yet major knowledge gaps remain about human immunity to SARS-CoV-2. We analyzed immune responses in 76 COVID-19 patients and 69 healthy individuals from Hong Kong and Atlanta. In PBMCs of COVID-19 patients, there was reduced expression of HLA-DR and pro-inflammatory cytokines by myeloid cells, and impaired mTOR-signaling and IFN-α production by plasmacytoid DCs. In contrast, there were enhanced plasma levels of inflammatory mediators, including EN-RAGE, TNFSF14, and oncostatin-M, which correlated with disease severity and increased bacterial products in human plasma. Single-cell transcriptomics revealed no type-I IFN, reduced HLA-DR in myeloid cells of severe patients, and transient expression of IFN-stimulated genes. This was consistent with bulk PBMC transcriptomics, and transient, low plasma IFN-α levels during infection. These results reveal mechanisms and potential therapeutic targets for COVID-19.
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Science
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2020
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