ArticleNature communications2022
Defective activation and regulation of type I interferon immunity is associated with increasing COVID-19 severity.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 62 citations in OpenAlex.
- Patterns of autoantibody expression in multiple sclerosis identified through development of an autoantigen discovery technology.The Journal of clinical investigation · 2025Trial
- Autoantibodies neutralizing type I interferons in COVID-19 patients from southern Brazil.Journal of human immunity · 2026Article
- Functional diversity of natural humanScience advances · 2026Article
- Integration of the circulating miRNome and clinical information to predict 90-day mortality in elderly COVID-19 subphenotypes.iScience · 2026Article
- SARS-CoV-2 Infection-Induced Alterations in ADAR Editing Patterns Differ Between Patients Who Developed Critical Compared to Non-Critical COVID-19.International journal of molecular sciences · 2026Article
- Selected Cannabinoids, Cannabimimetic Agents andPharmaceuticals (Basel, Switzerland) · 2026Review
- Systemic multi-omics analysis reveals interferon response heterogeneity and links lipid metabolism to immune alterations in severe COVID-19.Genome medicine · 2026Article
- Single-cell transcriptomic analysis deciphers heterogeneity and transcriptional regulatory programs of sepsis with different prognosis.Biology direct · 2026Article
- Review
- Multiorgan Molecular Landscape of Severe COVID-19 Revealed by Consensus Gene Signatures and RAB8B Targeting.Journal of medical virology · 2026Article
- Modeling neonatal immune response to B. pertussis identifies early B cell activation and differentiation.PLoS pathogens · 2026Article
- Overexpression ofJournal of clinical medicine · 2026Article
- The emerging role of TLR7-mediated signaling in respiratory viral infections and autoimmune diseases.Cellular and molecular life sciences : CMLS · 2026Review
- Innate immune regulation of adaptive immunity: mechanisms, implications, and bias.Frontiers in immunology · 2026Review
- Direct pharmacological AMPK activation inhibits mucosal SARS-CoV-2 infection by reducing lipid metabolism, restoring autophagy flux and the type I IFN response.Journal of virology · 2025Article
- Enhanced TLR7-dependent production of type I interferon by pDCs underlies pandemic chilblains.The Journal of experimental medicine · 2025Article
- Cytokine profiles dynamics in COVID-19 patients: a longitudinal analysis of disease severity and outcomes.Scientific reports · 2025Article
- Neutrophils Display Novel Partners of Cytosolic Proliferating Cell Nuclear Antigen Involved in Interferon Response in COVID-19 Patients.Journal of innate immunity · 2025Article
- Innate immune signatures in the nasopharynx after SARS-CoV-2 infection and links with the clinical outcome of COVID-19 in Omicron-dominant period.Cellular and molecular life sciences : CMLS · 2024Article
- Interfer-on time: lessons from genetically diverse mouse models of SARS-CoV-2 infection.Genes and immunity · 2024Article
Corrections and comments
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Authors and funding
23 authors at 5 institutions in 3 countries.
Funding
Abstract
Host immunity to infection with SARS-CoV-2 is highly variable, dictating diverse clinical outcomes ranging from asymptomatic to severe disease and death. We previously reported reduced type I interferon in severe COVID-19 patients preceded clinical worsening. Further studies identified genetic mutations in loci of the TLR3- or TLR7-dependent interferon-I pathways, or neutralizing interferon-I autoantibodies as risk factors for development of COVID-19 pneumonia. Here we show in patient cohorts with different severities of COVID-19, that baseline plasma interferon α measures differ according to the immunoassay used, timing of sampling, the interferon α subtype measured, and the presence of autoantibodies. We also show a consistently reduced induction of interferon-I proteins in hospitalized COVID-19 patients upon immune stimulation, that is not associated with detectable neutralizing autoantibodies against interferon α or interferon ω. Intracellular proteomic analysis shows increased monocyte numbers in hospitalized COVID-19 patients but impaired interferon-I response after stimulation. We confirm this by ex vivo whole blood stimulation with interferon-I which induces transcriptomic responses associated with inflammation in hospitalized COVID-19 patients, that is not seen in controls or non-hospitalized moderate cases. These results may explain the dichotomy of the poor clinical response to interferon-I based treatments in late stage COVID-19, despite the importance of interferon-I in early acute infection and may guide alternative therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.