Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients
Open accessPublished version of a preprint
Abstract
Interferons interfere with lung repair: Interferons (IFNs) are central to antiviral immunity. Viral recognition elicits IFN production, which in turn triggers the transcription of IFN-stimulated genes (ISGs), which engage in various antiviral functions. Type I IFNs (IFN-α and IFN-β) are widely expressed and can result in immunopathology during viral infections. By contrast, type III IFN (IFN-λ) responses are primarily restricted to mucosal surfaces and are thought to confer antiviral protection without driving damaging proinflammatory responses. Accordingly, IFN-λ has been proposed as a therapeutic in coronavirus disease 2019 (COVID-19) and other such viral respiratory diseases (see the Perspective by Grajales-Reyes and Colonna). Broggi et al. report that COVID-19 patient morbidity correlates with the high expression of type I and III IFNs in the lung. Furthermore, IFN-λ secreted by dendritic cells in the lungs of mice exposed to synthetic viral RNA causes damage to the lung epithelium, which increases susceptibility to lethal bacterial superinfections. Similarly, using a mouse model of influenza infection, Major et al. found that IFN signaling (especially IFN-λ) hampers lung repair by inducing p53 and inhibiting epithelial proliferation and differentiation. Complicating this picture, Hadjadj et al. observed that peripheral blood immune cells from severe and critical COVID-19 patients have diminished type I IFN and enhanced proinflammatory interleukin-6– and tumor necrosis factor-α–fueled responses. This suggests that in contrast to local production, systemic production of IFNs may be beneficial. The results of this trio of studies suggest that the location, timing, and duration of IFN exposure are critical parameters underlying the success or failure of therapeutics for viral respiratory infections. Science , this issue p. 706 , p. 712 , p. 718 ; see also p. 626
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People who cannot produce or respond to type I interferon face a higher risk of severe COVID-19.
“Furthermore, humans deficient in producing or responding to type I interferon have an increased risk of severe COVID-19 (refs66–68).”
From Immunological mechanisms of vaccine-induced protection against COVID-19 in humans (2021) · cites this paper as [68]
An early study in patients reported that type I IFNs were either not detected (particularly IFNβ) irrespective of disease severity or at lower levels (IFNα) in plasma mainly derived from patients with severe disease.
“An early study in patients reported that type I IFNs were either not detected (particularly IFNβ) irrespective of disease severity or at lower levels (IFNα) in plasma mainly derived from patients with severe disease (Hadjadj et al., 2020).”
From COVID-19 and the human innate immune system (2021) · cites this paper as Hadjadj et al., 2020
Proinflammatory genes upregulated in innate immune cells of severe or critical COVID-19 patients mainly belong to the NF-κB pathway.
“Proinflammatory genes upregulated in innate immune cells in severe or critical patients mainly belonged to the NF-κB pathway”
From COVID-19 and the human innate immune system (2021) · cites this paper as Hadjadj et al., 2020
IL-6 and TNF bioactivity in COVID-19 is supported by transcriptomic signatures in circulating immune cells.
“Bioactivity of some of these mediators of inflammation, particularly IL-6 and TNF, has been validated by transcriptomics in blood-derived cells”
From COVID-19 and the human innate immune system (2021) · cites this paper as Hadjadj et al., 2020
NF-κB-dependent proinflammatory mediators can drive accumulation of pathogenic neutrophils and macrophages in the lung, perpetuating cytokine and chemokine elevation in BALF and circulation.
“Accumulation of NF-κB-dependent proinflammatory mediators can provoke an accumulation of pathogenic inflammatory neutrophils and macrophages in the lung”
From COVID-19 and the human innate immune system (2021) · cites this paper as Hadjadj et al., 2020
Severe COVID-19 is characterized by increased circulating neutrophils and decreased lymphocytes.
“An increase in circulating neutrophils versus a decrease in lymphocytes has been appreciated as a hallmark of severe COVID-19”
From COVID-19 and the human innate immune system (2021) · cites this paper as Hadjadj et al., 2020
Impaired and delayed type I and type III IFN responses are associated with risk of severe COVID-19.
“Impaired and delayed type I and type III IFN responses are associated with risk of severe COVID-19 (Galani et al., 2021; Hadjadj et al., 2020).”
From Adaptive immunity to SARS-CoV-2 and COVID-19 (2021) · cites this paper as Hadjadj et al., 2020
Reduced type I interferon levels have been observed in the serum of patients with life-threatening COVID-19.
“Reduced type I IFN levels have been observed in the serum of patients with life-threatening COVID-19102.”
From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [102]
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- Authors
- Hadjadj, J., Yatim, N., Barnabei, L., Corneau, A., Boussier, J., Smith, N., Péré, H., Charbit, B., Bondet, V., Chenevier-Gobeaux, C., Breillat, P., Carlier, N., Gauzit, R., Morbieu, C., Pène, F., Marin, N., Roche, N., Szwebel, T.-A., Merkling, S. H., Treluyer, J.-M., Veyer, D., Mouthon, L., Blanc, C., Tharaux, P.-L., Rozenberg, F., Fischer, A., Duffy, D., Rieux-Laucat, F., Kernéis, S., & Terrier, B.
- Affiliations
- Inserm (FR)
- Sorbonne Université (FR)
- Institut Pasteur, Laboratory of Dendritic Cell Immunobiology, INSERM U1223, Department of Immunology, F-75015 Paris, France.
- Institut Pasteur (FR)
- Department of Automated Diagnostic Biology, Hôpital Cochin, APHP, APHP-CUP, F-75014 Paris, France.
- Université Paris Cité (FR)
- Centre National de la Recherche Scientifique (FR)
- Hôpital Cochin (FR)
- Université de Paris, Pharmacologie et Evaluation des Thérapeutiques Chez l’Enfant et la Femme Enceinte EA7323, F-75006 Paris, France.
- Hôpital Necker-Enfants Malades (FR)
- Université de Paris, Imagine Institute Laboratory of Immunogenetics of Pediatric Autoimmune Diseases, INSERM UMR 1163, F-75015 Paris, France.
- Corresponding author
- Terrier, Benjamin
- ORCID
- Hadjadj, Jérôme
- Yatim, Nader
- Barnabei, Laura
- Corneau, Aurélien
- Boussier, Jeremy
- Smith, Nikaïa
- Péré, Hélène
- Charbit, Bruno
- Bondet, Vincent
- Breillat, Paul
- Carlier, Nicolas
- Gauzit, Rémy
- Morbieu, Caroline
- Pène, Frédéric
- Roche, Nicolas
- Szwebel, Tali-Anne
- Merkling, Sarah H.
- Veyer, David
- Mouthon, Luc
- Blanc, Catherine
- Tharaux, Pierre-Louis
- Rozenberg, Flore
- Fischer, Alain
- Duffy, Darragh
- Rieux-Laucat, Frédéric
- Kernéis, Solen
- Terrier, Benjamin
- Venue
- Science
- Published
- 2020-08-07
- Volume
- 369
- Issue
- 6504
- Pages
- 718-724
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC7402632
- OpenAlex
- W3041960835
- Cited by
- 2,984
- References
- 33
- Citations by year
- 2026: 108 · 2025: 174 · 2024: 289 · 2023: 413 · 2022: 640 · 2021: 949 · 2020: 404 · 2019: 2 · 2015: 1 · 2014: 1 · 2013: 1 · 2012: 1
- FWCI
- 210.87
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Science (publishedVersion, cc-by)
- medRxiv (acceptedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- Funders
- Agence Nationale de la Recherche (ANR-10-IAHU-01, ANR-10-LABX-69-01)
- Fonds Immunov
- Institut Imagine
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Keywords
- COVID-19 pandemic, type I interferon, interferon lambda, interferon-alpha, interferon-beta, lung repair, lung epithelium, dendritic cells, secondary bacterial infection, p53, epithelial cell proliferation, interleukin-6, TNF-α, inflammation, antiviral immunity, influenza, respiratory viral infections
- MeSH terms
- Betacoronavirus, Interferon alpha-2, COVID-19, SARS-CoV-2, Adult, Aged, Cross-Sectional Studies, Female, Humans, Immunity, Innate, Inflammation, Male, Middle Aged, Pneumonia, Viral, Tumor Necrosis Factor-alpha, Signal Transduction, Interleukin-6, T-Lymphocyte Subsets, NF-kappa B, Critical Illness, Interferon-alpha, Interferon-beta, Coronavirus Infections, Viral Load, Gene Expression Profiling, Pandemics
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