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Systems biological assessment of immunity to mild versus severe COVID-19 infection in humans
Prabhu S Arunachalam1, Florian Wimmers1, Chris Ka Pun Mok2
1Institute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA 94305, USA.
Insights
Investigating severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) immunity, this study found impaired myeloid cell function and reduced interferon-α (IFN-α) in COVID-19 patients. These immune dysfunctions correlate with disease severity and suggest potential therapeutic targets.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Human immunity to SARS-CoV-2 remains incompletely understood despite the COVID-19 pandemic.
- Knowledge gaps persist regarding the specific immune cell responses and signaling pathways affected by SARS-CoV-2 infection.
Purpose of the Study:
- To analyze and characterize the immune responses in COVID-19 patients compared to healthy individuals.
- To identify specific immune cell dysfunctions and molecular mechanisms contributing to COVID-19 pathogenesis.
Main Methods:
- Immune response analysis in peripheral blood mononuclear cells (PBMCs) from 76 COVID-19 patients and 69 healthy controls.
- Utilized single-cell transcriptomics and bulk PBMC transcriptomics.
- Measured plasma levels of inflammatory mediators and bacterial products.
Main Results:
- COVID-19 patients exhibited reduced human leukocyte antigen class DR (HLA-DR) and impaired interferon-α (IFN-α) production by myeloid and plasmacytoid dendritic cells.
- Elevated plasma inflammatory mediators correlated with disease severity and bacterial presence.
- Single-cell transcriptomics revealed a lack of type I IFNs and transient IFN-stimulated gene expression.
Conclusions:
- SARS-CoV-2 infection leads to significant myeloid cell dysfunction and impaired IFN-α responses.
- These immune alterations are linked to COVID-19 severity and suggest potential therapeutic avenues.
- Understanding these mechanisms is crucial for developing effective COVID-19 treatments.
Abstract:
Coronavirus disease 2019 (COVID-19) represents a global crisis, yet major knowledge gaps remain about human immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We analyzed immune responses in 76 COVID-19 patients and 69 healthy individuals from Hong Kong and Atlanta, Georgia, United States. In the peripheral blood mononuclear cells (PBMCs) of COVID-19 patients, we observed reduced expression of human leukocyte antigen class DR (HLA-DR) and proinflammatory cytokines by myeloid cells as well as impaired mammalian target of rapamycin (mTOR) signaling and interferon-α (IFN-α) production by plasmacytoid dendritic cells. By contrast, we detected enhanced plasma levels of inflammatory mediators-including EN-RAGE, TNFSF14, and oncostatin M-which correlated with disease severity and increased bacterial products in plasma. Single-cell transcriptomics revealed a lack of type I IFNs, reduced HLA-DR in the myeloid cells of patients with severe COVID-19, and transient expression of IFN-stimulated genes. This was consistent with bulk PBMC transcriptomics and transient, low IFN-α levels in plasma during infection. These results reveal mechanisms and potential therapeutic targets for COVID-19.
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