ArticleProceedings of the National Academy of Sciences of the United States of America2022
A virus-specific monocyte inflammatory phenotype is induced by SARS-CoV-2 at the immune-epithelial interface.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.
- Early peripheral blood MCEMP1 and HLA-DRA expression predicts COVID-19 prognosis.EBioMedicine · 2023Pooled it
- Single-cell transcriptomics highlights immunological dysregulations of monocytes in the pathobiology of COPD.Respiratory research · 2022Pooled it
- Monitoring Macrophage Polarization in Infectious Disease, Lesson From SARS-CoV-2 Infection.Reviews in medical virology · 2025Review
- The innate immune response in SARS-CoV2 infection: focus on toll-like receptor 4 in severe disease outcomes.Frontiers in immunology · 2025Review
- An interferon-stimulated long non-coding RNA USP30-AS1 as an immune modulator in influenza A virus infection.PLoS pathogens · 2025Article
- PROS1 released by lung basal cells limits inflammation in epithelial and monocytes during SARS-CoV-2 infection.Discovery immunology · 2025Article
- Uncovering cell-type-specific immunomodulatory variants and molecular phenotypes in COVID-19 using structurally resolved protein networks.Cell reports · 2024Article
- Multiple Mechanisms of Action of SulfodyneAntioxidants (Basel, Switzerland) · 2024Article
- Uncovering the Contrasts and Connections in PASC: Viral Load and Cytokine Signatures in Acute COVID-19 versus Post-Acute Sequelae of SARS-CoV-2 (PASC).Biomedicines · 2024Review
- Accelerated tumor progression after COVID-19 infection in patients with glioblastoma: A retrospective case-control study.Neuro-oncology practice · 2024Article
- The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication.bioRxiv : the preprint server for biology · 2024Article
- Heat Inactivation of Nipah Virus for Downstream Single-Cell RNA Sequencing Does Not Interfere with Sample Quality.Pathogens (Basel, Switzerland) · 2024Article
- Airway Basal Stem Cells in COVID-19 Exhibit a Proinflammatory Signature and Impaired Mucocililary Differentiation.American journal of respiratory cell and molecular biology · 2024Article
- Article
- Spatiotemporally organized immunomodulatory response to SARS-CoV-2 virus in primary human broncho-alveolar epithelia.iScience · 2023Article
- T cell responses to SARS-CoV-2 vaccination differ by disease-modifying therapy for multiple sclerosis.JCI insight · 2023Article
- Review
- Establishment of an Inactivation Method for Ebola Virus and SARS-CoV-2 Suitable for Downstream Sequencing of Low Cell Numbers.Pathogens (Basel, Switzerland) · 2023Article
- Bystander effect of SARS-CoV-2 spike protein on human monocytic THP-1 cell activation and initiation of prothrombogenic stimulus representing severe COVID-19.Journal of inflammation (London, England) · 2022Article
- Monocyte distribution width as a pragmatic screen for SARS-CoV-2 or influenza infection.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Infection by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) provokes a potentially fatal pneumonia with multiorgan failure, and high systemic inflammation. To gain mechanistic insight and ferret out the root of this immune dysregulation, we modeled, by in vitro coculture, the interactions between infected epithelial cells and immunocytes. A strong response was induced in monocytes and B cells, with a SARS-CoV-2-specific inflammatory gene cluster distinct from that seen in influenza A or Ebola virus-infected cocultures, and which reproduced deviations reported in blood or lung myeloid cells from COVID-19 patients. A substantial fraction of the effect could be reproduced after individual transfection of several SARS-CoV-2 proteins (Spike and some nonstructural proteins), mediated by soluble factors, but not via transcriptional induction. This response was greatly muted in monocytes from healthy children, perhaps a clue to the age dependency of COVID-19. These results suggest that the inflammatory malfunction in COVID-19 is rooted in the earliest perturbations that SARS-CoV-2 induces in epithelia.
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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.