ReviewCurrent opinion in immunology2022
Type I interferons and SARS-CoV-2: from cells to organisms.
Review in Current opinion in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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
53 citing papers in PubMed, 82 citations in OpenAlex.
- Genetic research on childhood obesity and asthma: exploring genetic risk factors and biological mechanisms.Pediatric research · 2026Review
- SARS-CoV-2 virus infection ofbioRxiv : the preprint server for biology · 2026Article
- Previous COVID-19 Vaccination Modulates Type I Interferon and Natural Killer Cell Responses During SARS-CoV-2 Infection.Journal of cellular and molecular medicine · 2026Article
- Entry, replication and innate immunity evasion of BANAL-236, a SARS-CoV-2-related bat virus, in Rhinolophus and human cells.PLoS pathogens · 2026Article
- Host-pathogen interaction in community-acquired pneumonia: a focus on the immune response.Frontiers in cellular and infection microbiology · 2026Review
- Evolutionary divergence of induced versus constitutive antiviral gene expression levels between primates and rodents.PLoS computational biology · 2025Article
- Nerve- and airway-associated interstitial macrophages mitigate SARS-CoV-2 pathogenesis via type I interferon signaling.Immunity · 2025Article
- A common form of dominant human IFNAR1 deficiency impairs IFN-α and -ω but not IFN-β-dependent immunity.The Journal of experimental medicine · 2025Article
- Enhancing the immunogenicity of lipid-nanoparticle mRNA vaccines by adjuvanting the ionizable lipid and the mRNA.Nature biomedical engineering · 2025Article
- Antibodies to the RBD of SARS-CoV-2 spike mediate productive infection of primary human macrophages.Nature communications · 2024Article
- The Microbe, the Infection Enigma, and the Host.Annual review of microbiology · 2024Review
- Aberrant innate immune profile associated with COVID-19 mortality in Pretoria, South Africa.Clinical immunology (Orlando, Fla.) · 2024Article
- A genome-wide arrayed CRISPR screen identifies PLSCR1 as an intrinsic barrier to SARS-CoV-2 entry that recent virus variants have evolved to resist.PLoS biology · 2024Article
- Exploring the potency of polyphenol-rich blend fromHeliyon · 2024Article
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- LINC01002 functions as a ceRNA to regulate FRMD8 by sponging miR-4324 for the development of COVID-19.Virology journal · 2024Article
- The ouroboros of autoimmunity.Nature immunology · 2024Review
- The antiviral state of the cell: lessons from SARS-CoV-2.Current opinion in immunology · 2024Review
- Primary nasal viral infection rewires the tissue-scale memory response.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Type I interferons (IFNs) have broad and potent antiviral activity. We review the interplay between type I IFNs and SARS-CoV-2. Human cells infected with SARS-CoV-2 in vitro produce low levels of type I IFNs, and SARS-CoV-2 proteins can inhibit various steps in type I IFN production and response. Exogenous type I IFNs inhibit viral growth in vitro. In various animal species infected in vivo, type I IFN deficiencies underlie higher viral loads and more severe disease than in control animals. The early administration of exogenous type I IFNs improves infection control. In humans, inborn errors of, and auto-antibodies against type I IFNs underlie life-threatening COVID-19 pneumonia. Overall, type I IFNs are essential for host defense against SARS-CoV-2 in individual cells and whole organisms.
Indexed as
Identifiers
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.