ArticleScience advances2022
Differential proinflammatory activities of Spike proteins of SARS-CoV-2 variants of concern.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
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
24 citing papers in PubMed, 35 citations in OpenAlex.
- Dual mechanism of human ATG10S in suppressing MEF2A-Driven pro-inflammatory responses.Autophagy · 2026Article
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- Programmed cell death pathways coordinate neutrophil and macrophage clearance in zebrafish and are differentially exploited by Salmonella Typhimurium.Cell death & disease · 2025Article
- The role of 25-hydroxycholesterol in the pathophysiology of brain vessel dysfunction associated with infection and cholesterol dysregulation.Disease models & mechanisms · 2025Article
- Basic implications on three pathways associated with SARS-CoV-2.Biomedical journal · 2025Review
- Age- and disease severity-associated changes in the nasopharyngeal microbiota of COVID-19 patients.iScience · 2025Article
- Dual role of ACE2 in regulating inflammation triggered by Omicron S1 and other SARS-CoV-2 Spike variants.Frontiers in immunology · 2025Article
- ATG10S promotes IFNL1 expression and autophagic degradation of multiple viral proteins mediated by IFNL1.Autophagy · 2024Article
- The role ofHeliyon · 2024Article
- Aggravating mechanisms from COVID-19.Virology journal · 2024Review
- Zebrafish as a model organism for virus disease research: Current status and future directions.Heliyon · 2024Article
- Mechanistic insights into SARS-CoV-2 spike protein induction of the chemokine CXCL10.Scientific reports · 2024Article
- Article
- Salivary biomarkers as pioneering indicators for diagnosis and severity stratification of pediatric long COVID.Frontiers in cellular and infection microbiology · 2024Article
- Immunologic and inflammatory consequences of SARS-CoV-2 infection and its implications in renal disease.Frontiers in immunology · 2024Review
- The nasopharyngeal microbiome in COVID-19.Emerging microbes & infections · 2023Article
- Identification of side effects of COVID-19 drug candidates on embryogenesis using an integrated zebrafish screening platform.Scientific reports · 2023Article
- Animal models of silicosis: fishing for new therapeutic targets and treatments.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- Review
- Photobiomodulation Reduces the Cytokine Storm Syndrome Associated with COVID-19 in the Zebrafish Model.International journal of molecular sciences · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The coronavirus disease 2019 (COVID-19) pandemic turned the whole world upside down in a short time. One of the main challenges faced has been to understand COVID-19-associated life-threatening hyperinflammation, the so-called cytokine storm syndrome (CSS). We report here the proinflammatory role of Spike (S) proteins from different severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern in zebrafish. We found that wild-type/Wuhan variant S1 (S1WT) promoted neutrophil and macrophage recruitment, local and systemic hyperinflammation, emergency myelopoiesis, and hemorrhages. In addition, S1γ was more proinflammatory S1δ was less proinflammatory than S1WT, and, notably, S1β promoted delayed and long-lasting inflammation. Pharmacological inhibition of the canonical inflammasome alleviated S1-induced inflammation and emergency myelopoiesis. In contrast, genetic inhibition of angiotensin-converting enzyme 2 strengthened the proinflammatory activity of S1, and angiotensin (1-7) fully rescued S1-induced hyperinflammation and hemorrhages. These results shed light into the mechanisms orchestrating the COVID-19-associated CSS and the host immune response to different SARS-CoV-2 S protein variants.
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What OpenQuestion holds
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.