SynthesisFrontiers in immunology2021
SARS-CoV-2 Causes a Different Cytokine Response Compared to Other Cytokine Storm-Causing Respiratory Viruses in Severely Ill Patients.
Synthesis in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
73 citing papers in PubMed, 112 citations in OpenAlex.
- InflawellInflammopharmacology · 2022Trial
- Immune Dysregulation After COVID-19: Longitudinal Analysis up to 9 Months.International journal of molecular sciences · 2026Article
- Coronavirus disease 2019-associated encephalitis and concomitant subdural hematoma: a case report.Journal of medical case reports · 2026Article
- Distinct Cytokine Landscapes Induced by Influenza a Virus, RSV, and SARS-CoV-2 in Older Adults (65+) Using an Ex Vivo Whole Blood Stimulation Model.Pathogens (Basel, Switzerland) · 2026Article
- Differential response of human plasmacytoid pre-dendritic cells to SARS-CoV-2 variants.iScience · 2025Article
- A feedback loop between DNA damage, genomic instability, and cytoplasmic DNA sensing contributes to cytokine production in COVID-19.Archives of virology · 2025Review
- Neurobiology of COVID-19-Associated Psychosis/Schizophrenia: Implication of Epidermal Growth Factor Receptor Signaling.Neuropsychopharmacology reports · 2025Review
- Severity of acute SARS-CoV-2 infection and risk of new-onset autoimmune disease: A RECOVER initiative study in nationwide U.S. cohorts.PloS one · 2025Article
- Influence of Donor-Specific Characteristics on Cytokine Responses in H3N2 Influenza A Virus Infection: New Insights from an Ex Vivo Model.International journal of molecular sciences · 2024Article
- Characterization of Neutrophil Functional Responses to SARS-CoV-2 Infection in a Translational Feline Model for COVID-19.International journal of molecular sciences · 2024Article
- Advanced nanomedicines and immunotherapeutics to treat respiratory diseases especially COVID-19 induced thrombosis.World journal of clinical cases · 2024Review
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- Editorial: Impact of viral co-infection on cellular or human health and its clinical outcome.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
- MicroRNAs Derived from Extracellular Vesicles: Keys to Understanding SARS-CoV-2 Vaccination Response in Cancer Patients?Cancers · 2023Review
- Nanostructures for prevention, diagnosis, and treatment of viral respiratory infections: from influenza virus to SARS-CoV-2 variants.Journal of nanobiotechnology · 2023Review
- Metabolic alterations upon SARS-CoV-2 infection and potential therapeutic targets against coronavirus infection.Signal transduction and targeted therapy · 2023Review
- Risk factors, clinical characteristics and prognostic value of acute kidney injury in COVID-19 compared with influenza virus and respiratory syncytial virus.Journal of nephrology · 2023Article
- Shedding Lights on the Extracellular Vesicles as Functional Mediator and Therapeutic Decoy for COVID-19.Life (Basel, Switzerland) · 2023Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Hyper-induction of pro-inflammatory cytokines, also known as a cytokine storm or cytokine release syndrome (CRS), is one of the key aspects of the currently ongoing SARS-CoV-2 pandemic. This process occurs when a large number of innate and adaptive immune cells activate and start producing pro-inflammatory cytokines, establishing an exacerbated feedback loop of inflammation. It is one of the factors contributing to the mortality observed with coronavirus 2019 (COVID-19) for a subgroup of patients. CRS is not unique to the SARS-CoV-2 infection; it was prevalent in most of the major human coronavirus and influenza A subtype outbreaks of the past two decades (H5N1, SARS-CoV, MERS-CoV, and H7N9). With a comprehensive literature search, we collected changing the cytokine levels from patients upon infection with the viral pathogens mentioned above. We analyzed published patient data to highlight the conserved and unique cytokine responses caused by these viruses. Our curation indicates that the cytokine response induced by SARS-CoV-2 is different compared to other CRS-causing respiratory viruses, as SARS-CoV-2 does not always induce specific cytokines like other coronaviruses or influenza do, such as IL-2, IL-10, IL-4, or IL-5. Comparing the collated cytokine responses caused by the analyzed viruses highlights a SARS-CoV-2-specific dysregulation of the type-I interferon (IFN) response and its downstream cytokine signatures. The map of responses gathered in this study could help specialists identify interventions that alleviate CRS in different diseases and evaluate whether they could be used in the COVID-19 cases.
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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 Socratic graph.