ArticlePLoS pathogens2016
Type I Interferon Receptor Deficiency in Dendritic Cells Facilitates Systemic Murine Norovirus Persistence Despite Enhanced Adaptive Immunity.
Article in PLoS pathogens, 2016. 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 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, 65 citations in OpenAlex.
- Plscr1 inhibits murine norovirus entry.bioRxiv : the preprint server for biology · 2026Article
- Type I and III interferons synergize with TNF to promote virally-triggered damage to the intestinal epithelium.bioRxiv : the preprint server for biology · 2026Article
- Trim7 does not have a role in the restriction of murine norovirus infectionJournal of virology · 2025Article
- Development of a replication competent murine norovirus reporter system.PLoS pathogens · 2025Article
- Norovirus co-opts NINJ1 for selective protein secretion.Science advances · 2025Article
- The systemic lupus erythematosus-associated NCF1Nature communications · 2025Article
- Regulation of host/pathogen interactions in the gastrointestinal tract by type I and III interferons.Current opinion in immunology · 2024Review
- Crosstalk Between Microbiota, Microbial Metabolites, and Interferons in the Inflammatory Bowel Disease Gut.Journal of the Canadian Association of Gastroenterology · 2024Review
- Age-associated features of norovirus infection analysed in mice.Nature microbiology · 2023Article
- Recent insights into reverse genetics of norovirus.Virus research · 2023Review
- Reprogramming viral immune evasion for a rational design of next-generation vaccines for RNA viruses.Frontiers in immunology · 2023Review
- Tuft-cell-intrinsic and -extrinsic mediators of norovirus tropism regulate viral immunity.Cell reports · 2022Article
- Article
- Restriction of Viral Replication, Rather than T Cell Immunopathology, Drives Lethality in Murine Norovirus CR6-Infected STAT1-Deficient Mice.Journal of virology · 2022Article
- Article
- Advances in understanding interferon-mediated immune responses to enteric viruses in intestinal organoids.Frontiers in immunology · 2022Review
- Advances in understanding of the innate immune response to human norovirus infection using organoid models.The Journal of general virology · 2022Review
- Article
- Differential roles of interferons in innate responses to mucosal viral infections.Trends in immunology · 2021Review
- Interferon responses to norovirus infections: current and future perspectives.The Journal of general virology · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
In order for a virus to persist, there must be a balance between viral replication and immune clearance. It is commonly believed that adaptive immunity drives clearance of viral infections and, thus, dysfunction or viral evasion of adaptive immunity is required for a virus to persist. Type I interferons (IFNs) play pleiotropic roles in the antiviral response, including through innate control of viral replication. Murine norovirus (MNoV) replicates in dendritic cells (DCs) and type I IFN signaling in DCs is important for early control of MNoV replication. We show here that the non-persistent MNoV strain CW3 persists systemically when CD11c positive DCs are unable to respond to type I IFN. Persistence in this setting is associated with increased early viral titers, maintenance of DC numbers, increased expression of DC activation markers and an increase in CD8 T cell and antibody responses. Furthermore, CD8 T cell function is maintained during the persistent phase of infection and adaptive immune cells from persistently infected mice are functional when transferred to Rag1-/- recipients. Finally, increased early replication and persistence are also observed in mixed bone marrow chimeras where only half of the CD11c positive DCs are unable to respond to type I IFN. These findings demonstrate that increased early viral replication due to a cell-intrinsic innate immune deficiency is sufficient for persistence and a functional adaptive immune response is not sufficient for viral clearance.
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.