ArticleeLife2015
Phenotypic complementation of genetic immunodeficiency by chronic herpesvirus infection.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 75 citations in OpenAlex.
- Pyoderma gangrenosum caused by the molecular uncoupling of OTULIN catalytic activity and LUBAC binding.Nature immunology · 2026Article
- The Lung Microbiome and Its Impact on Obstructive Sleep Apnea: A Diagnostic Frontier.Diagnostics (Basel, Switzerland) · 2025Review
- Relationship between pediatric asthma and respiratory microbiota, intestinal microbiota: a narrative review.Frontiers in microbiology · 2025Review
- The role of IFN-γ-mediated host immune responses in monitoring and the elimination of Toxoplasma gondii infection.International immunology · 2024Review
- Lung microbiome: new insights into the pathogenesis of respiratory diseases.Signal transduction and targeted therapy · 2024Review
- HOIL1 Regulates Group 3 Innate Lymphoid Cells in the Colon and Protects against Systemic Dissemination, Colonic Ulceration, and Lethality from Citrobacter rodentium Infection.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Article
- Glycogen synthase downregulation rescues the amylopectinosis of murine RBCK1 deficiency.Brain : a journal of neurology · 2022Article
- HOIL-1 ubiquitin ligase activity targets unbranched glucosaccharides and is required to prevent polyglucosan accumulation.The EMBO journal · 2022Article
- Bacterial and Viral Co-Infection in the Intestine: Competition Scenario and Their Effect on Host Immunity.International journal of molecular sciences · 2022Review
- Lessons from Toxoplasma: Host responses that mediate parasite control and the microbial effectors that subvert them.The Journal of experimental medicine · 2021Review
- LUBAC: a new player in polyglucosan body disease.Biochemical Society transactions · 2021Review
- Conquering the Host: Determinants of Pathogenesis Learned from Murine Gammaherpesvirus 68.Annual review of virology · 2021Article
- NF-κB: At the Borders of Autoimmunity and Inflammation.Frontiers in immunology · 2021Review
- The HOIL-1L ligase modulates immune signalling and cell death via monoubiquitination of LUBAC.Nature cell biology · 2020Article
- Broad Virus Detection and Variant Discovery in Fecal Samples of Hematopoietic Transplant Recipients Using Targeted Sequence Capture Metagenomics.Frontiers in microbiology · 2020Article
- Cross-Domain and Viral Interactions in the Microbiome.Microbiology and molecular biology reviews : MMBR · 2019Review
- Immune Relevant and Immune Deficient Mice: Options and Opportunities in Translational Research.ILAR journal · 2018Review
- HOIL1 Is Essential for the Induction of Type I and III Interferons by MDA5 and Regulates Persistent Murine Norovirus Infection.Journal of virology · 2018Article
- Kaposi's Sarcoma-Associated Herpesvirus Latency Locus Renders B Cells Hyperresponsive to Secondary Infections.Journal of virology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 5 institutions in 3 countries.
Funding
Abstract
Variation in the presentation of hereditary immunodeficiencies may be explained by genetic or environmental factors. Patients with mutations in HOIL1 (RBCK1) present with amylopectinosis-associated myopathy with or without hyper-inflammation and immunodeficiency. We report that barrier-raised HOIL-1-deficient mice exhibit amylopectin-like deposits in the myocardium but show minimal signs of hyper-inflammation. However, they show immunodeficiency upon acute infection with Listeria monocytogenes, Toxoplasma gondii or Citrobacter rodentium. Increased susceptibility to Listeria was due to HOIL-1 function in hematopoietic cells and macrophages in production of protective cytokines. In contrast, HOIL-1-deficient mice showed enhanced control of chronic Mycobacterium tuberculosis or murine γ-herpesvirus 68 (MHV68), and these infections conferred a hyper-inflammatory phenotype. Surprisingly, chronic infection with MHV68 complemented the immunodeficiency of HOIL-1, IL-6, Caspase-1 and Caspase-1;Caspase-11-deficient mice following Listeria infection. Thus chronic herpesvirus infection generates signs of auto-inflammation and complements genetic immunodeficiency in mutant mice, highlighting the importance of accounting for the virome in genotype-phenotype studies.
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.