ReviewFrontiers in immunology2016
Type-I Interferon Responses: From Friend to Foe in the Battle against Chronic Viral Infection.
Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 3 of them syntheses 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
118 citing papers in PubMed, 3 syntheses or guidelines pooled it, 177 citations in OpenAlex.
- SARS-CoV-2 Causes a Different Cytokine Response Compared to Other Cytokine Storm-Causing Respiratory Viruses in Severely Ill Patients.Frontiers in immunology · 2021Pooled it
- Transcriptional insights into the CD8Journal of translational medicine · 2020Pooled it
- Transcriptomic meta-analysis identifies gene expression characteristics in various samples of HIV-infected patients with nonprogressive disease.Journal of translational medicine · 2017Pooled it
- Interdependent RNA structural motifs at the 3'-terminus of the West Nile virus genome regulate viral growth.Nucleic acids research · 2026Article
- Intrauterine Administration of PBMC Modulated with IFN-τ Before Embryo Transfer Improves Clinical Outcomes of IVF Patients-A Randomized Control Trial.Biomedicines · 2025Article
- Interferon signaling pathways in health and disease.Molecular biomedicine · 2025Review
- Oncolytic virus and immunogenic cell death in cancer therapy.Tumour virus research · 2025Review
- Persistent type I interferon signaling within the brain of people with HIV on ART with cognitive impairment.PLoS pathogens · 2025Article
- Codon-deoptimized single-round infectious virus for therapeutic and vaccine applications.Scientific reports · 2025Article
- Zika virus-induced fetal demise is triggered by strain- and dose-specific RLR-driven activation of the interferon response in the decidua, placenta, and fetus inJournal of virology · 2025Article
- Review
- Comparison of long-term health-related quality of life and symptoms between COVID-19 patients and test-negative controls during the Omicron-predominant period in Japan.Archives of public health = Archives belges de sante publique · 2025Article
- Article
- Central TYK2 inhibition identifies TYK2 as a key neuroimmune modulator.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Multiomics uncovers the epigenomic and transcriptomic response to viral and bacterial stimulation in turbot.GigaScience · 2025Article
- What goes up must come down: dynamics of type 1 interferon signaling across the lifespan.Frontiers in immunology · 2025Review
- Ocular neuroinflammatory response secondary to SARS-CoV-2 infection-a review.Frontiers in immunology · 2025Review
- Preliminary Study on Type I Interferon as a Mucosal Adjuvant for Human Respiratory Syncytial Virus F Protein.Vaccines · 2024Article
- Review
58 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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I interferons (IFN-I) have long been heralded as key contributors to effective antiviral responses. More widely understood in the context of acute viral infection, the role of this pleiotropic cytokine has been characterized as triggering antiviral states in cells and potentiating adaptive immune responses. Upon induction in the innate immune response, IFN-I triggers the expression of interferon-stimulated genes (ISGs), which upregulate the effector function of immune cells (e.g., dendritic cells, B cells, and T cells) toward successful resolution of infections. However, emerging lines of evidence reveal that viral persistence in the course of chronic infections could be driven by deleterious immunomodulatory effects upon sustained IFN-I expression. In this setting, elevation of IFN-I and ISGs is directly correlated to viral persistence and elevated viral loads. It is important to note that the correlation among IFN-I expression, ISGs, and viral persistence may be a cause or effect of chronic infection and this is an important distinction to make toward establishing the dichotomous nature of IFN-I responses. The aim of this mini review is to (i) summarize the interaction between IFN-I and downstream effector responses and therefore (ii) delineate the function of this cytokine on positive and negative immunoregulation in chronic infection. This is a significant consideration given the current therapeutic administration of IFN-I in chronic viral infections whose therapeutic significance is projected to continue despite emergence of increasingly efficacious antiviral regimens. Furthermore, elucidation of the interplay between virus and the antiviral response in the context of IFN-I will elucidate avenues toward more effective therapeutic and prophylactic measures against chronic viral infections.
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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.