ArticleImmunology2013
Modulation of B-cell tolerance by murine gammaherpesvirus 68 infection: requirement for Orf73 viral gene expression and follicular helper T cells.
Article in Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 20 citations in OpenAlex.
- Genetic background modifies host and viral parameters of neonatal gammaherpesvirus infection.Journal of virology · 2026Article
- IL-22 promotes the establishment of chronic gammaherpesvirus infection by supporting the germinal center response.PLoS pathogens · 2026Article
- Article
- B cell-intrinsic interleukin 17 receptor A signaling supports the establishment of chronic murine gammaherpesvirus 68 infection.Journal of virology · 2025Article
- Gammaherpesvirus infection unveils exaggerated germinal center responses in an SR-BI-deficient host.Journal of virology · 2025Article
- Article
- Host Genetic Variation Has a Profound Impact on Immune Responses Mediating Control of Viral Load in Chronic Gammaherpesvirus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- The Antagonism between the Murine Gammaherpesvirus Protein Kinase and Global Interferon Regulatory Factor 1 Expression Shapes the Establishment of Chronic Infection.Journal of virology · 2022Article
- Article
- T Cell-Intrinsic Interleukin 17 Receptor A Signaling Supports the Establishment of Chronic Murine Gammaherpesvirus 68 Infection.Journal of virology · 2022Article
- Mouse Homologue of Human HLA-DO Does Not Preempt Autoimmunity but Controls Murine Gammaherpesvirus MHV68.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Conserved Gammaherpesvirus Protein Kinase Counters the Antiviral Effects of Myeloid Cell-Specific STAT1 Expression To Promote the Establishment of Splenic B Cell Latency.Journal of virology · 2021Article
- Gammaherpesvirus Usurps Host IL-17 Signaling To Support the Establishment of Chronic Infection.mBio · 2021Article
- Review
- B Cell-Intrinsic Expression of Interferon Regulatory Factor 1 Supports Chronic Murine Gammaherpesvirus 68 Infection.Journal of virology · 2020Article
- Gammaherpesviruses and B Cells: A Relationship That Lasts a Lifetime.Viral immunology · 2020Review
- B Cell-Intrinsic SHP1 Expression Promotes the Gammaherpesvirus-Driven Germinal Center Response and the Establishment of Chronic Infection.Journal of virology · 2019Article
- Conserved Gammaherpesvirus Protein Kinase Selectively Promotes Irrelevant B Cell Responses.Journal of virology · 2019Article
- Functional heterogeneity in the CD4+ T cell response to murine γ-herpesvirus 68.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Establishment of murine gammaherpesvirus latency in B cells is not a stochastic event.PLoS pathogens · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viruses such as Epstein-Barr virus (EBV) have been linked to mechanisms that support autoantibody production in diseases such as systemic lupus erythematosus. However, the mechanisms by which viruses contribute to autoantibody production remain poorly defined. This stems in part, from the high level of seropositivity for EBV (> 95%) and the exquisite species specificity of EBV. In this study we overcame these problems by using murine gammaherpesvirus 68 (MHV68), a virus genetically and biologically related to EBV. We first showed that MHV68 drives autoantibody production by promoting a loss of B-cell anergy. We next showed that MHV68 infection resulted in the expansion of follicular helper T (Tfh) cells in vivo, and that these Tfh cells supported autoantibody production and a loss of B-cell anergy. Finally, we showed that the expansion of Tfh cells and autoantibody production was dependent on the establishment of viral latency and expression of a functional viral gene called Orf73. Collectively, our studies highlighted an unexpected role for viral latency in the development of autoantibodies following MHV68 infection and suggest that virus-induced expansion of Tfh cells probably plays a key role in the loss of B-cell anergy.
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.