ReviewJournal of molecular biology2022
Mechanisms of Antiviral Immune Evasion of SARS-CoV-2.
Review in Journal of molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
66 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy of interferon alpha for the treatment of hospitalized patients with COVID-19: A meta-analysis.Frontiers in immunology · 2023Pooled it
- Effect of inhaled interferon-β1a on SARS-CoV-2 diversity and evolution.Microbiology spectrum · 2026Trial
- Dysregulation of RIG-I activation by picornavirus 3A protein.Journal of virology · 2026Article
- Unraveling the layers of epigenetic control in respiratory antiviral defense.Journal of virology · 2026Review
- Redundant and distinct mechanisms suppress innate immune activation during SARS-CoV-2 infection.PLoS biology · 2026Article
- IFITM3 deficiency drives SARS-CoV-2 adaptation while preserving variant-specific traits.Nature communications · 2026Article
- From Viral Infection to Malignancy: The Dual Threat of EBV and COVID-19 in Cancer Development.Viruses · 2025Review
- Review
- SARS-CoV-2 infection of human cortical cells is influenced by the interaction between aneuploidy and biological sex: insights from a Down syndrome in vitro model.Acta neuropathologica · 2025Article
- A Genomic Surveillance Circuit for Emerging Viral Pathogens.Microorganisms · 2025Article
- Positive Selection on Mammalian Immune Genes-Effects of Gene Function and Selective Constraint.Molecular biology and evolution · 2025Article
- Screening of RNA methyltransferase NSP16 inhibitors against SARS-CoV-2 coronavirus and study of related mechanisms.American journal of translational research · 2025Article
- Review
- Article
- Metabolic Dependency Shapes Bivalent Antiviral Response in Host Cells in Response to Poly:IC: The Role of Glutamine.Viruses · 2024Article
- Preclinical Evaluation and Pilot Clinical Study ofACS pharmacology & translational science · 2024Article
- IFN-λ uniquely promotes CD8 T cell immunity against SARS-CoV-2 relative to type I IFN.JCI insight · 2024Article
- Omicron Spike confers enhanced infectivity and interferon resistance to SARS-CoV-2 in human nasal tissue.Nature communications · 2024Article
- Transcriptomic analysis of sorted lung cells revealed a proviral activity of the NF-κB pathway toward SARS-CoV-2.iScience · 2023Article
- An Overview of SARS-CoV-2 Etiopathogenesis and Recent Developments in COVID-19 Vaccines.Biomolecules · 2023Review
6 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronavirus disease (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is characterized by a delayed interferon (IFN) response and high levels of proinflammatory cytokine expression. Type I and III IFNs serve as a first line of defense during acute viral infections and are readily antagonized by viruses to establish productive infection. A rapidly growing body of work has interrogated the mechanisms by which SARS-CoV-2 antagonizes both IFN induction and IFN signaling to establish productive infection. Here, we summarize these findings and discuss the molecular interactions that prevent viral RNA recognition, inhibit the induction of IFN gene expression, and block the response to IFN treatment. We also describe the mechanisms by which SARS-CoV-2 viral proteins promote host shutoff. A detailed understanding of the host-pathogen interactions that unbalance the IFN response is critical for the design and deployment of host-targeted therapeutics to manage COVID-19.
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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.