ArticleJournal of virology2019
Conserved Gammaherpesvirus Protein Kinase Selectively Promotes Irrelevant B Cell Responses.
Article in Journal of virology, 2019. 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
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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
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Who cites it
21 citing papers in PubMed, 21 citations in OpenAlex.
- Genetic background modifies host and viral parameters of neonatal gammaherpesvirus infection.Journal of virology · 2026Article
- Conserved gammaherpesvirus protein kinase counters myeloid cell-specific type I IFN receptor but not IRF-3 expression to promote the establishment of chronic latent infection in the spleen.Journal of virology · 2026Article
- IL-22 promotes the establishment of chronic gammaherpesvirus infection by supporting the germinal center response.PLoS pathogens · 2026Article
- B cell-intrinsic interleukin 17 receptor A signaling supports the establishment of chronic murine gammaherpesvirus 68 infection.Journal of virology · 2025Article
- B cell-intrinsic IRF-1 and conserved gammaherpesvirus protein kinase cooperate to promote murine gammaherpesvirus-driven germinal center response and splenic latent reservoir.Journal of virology · 2025Article
- Gammaherpesvirus infection unveils exaggerated germinal center responses in an SR-BI-deficient host.Journal of virology · 2025Article
- Article
- Nontypeable Haemophilus influenzae challenge during gammaherpesvirus infection enhances viral reactivation and latency.Virology · 2024Article
- T cell-extrinsic IL-1 signaling controls long-term gammaherpesvirus infection by suppressing viral reactivation.Virology · 2022Article
- 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
- 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
- Conquering the Host: Determinants of Pathogenesis Learned from Murine Gammaherpesvirus 68.Annual review of virology · 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
- Interferon Regulatory Factor 3 Supports the Establishment of Chronic Gammaherpesvirus Infection in a Route- and Dose-Dependent Manner.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
- Gammaherpesvirus-infected germinal center cells express a distinct immunoglobulin repertoire.Life science alliance · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Gammaherpesviruses are ubiquitous pathogens that are associated with B cell lymphomas. In the early stages of chronic infection, these viruses infect naive B cells and subsequently usurp the B cell differentiation process through the germinal center response to ensure latent infection of long-lived memory B cells. A unique feature of early gammaherpesvirus chronic infection is a robust differentiation of irrelevant, virus-nonspecific B cells with reactivities against self-antigens and antigens of other species. In contrast, protective, virus-specific humoral responses do not reach peak levels until a much later time. While several host factors are known to either promote or selectively restrict gammaherpesvirus-driven germinal center response, viral mechanisms that contribute to the irrelevant B cell response have not been defined. In this report we show that the expression and the enzymatic activity of the gammaherpesvirus-encoded conserved protein kinase selectively facilitates the irrelevant, but not virus-specific, B cell responses. Further, we show that lack of interleukin-1 (IL-1) receptor attenuates gammaherpesvirus-driven B cell differentiation and viral reactivation. Because germinal center B cells are thought to be the target of malignant transformation during gammaherpesvirus-driven lymphomagenesis, identification of host and viral factors that promote germinal center responses during gammaherpesvirus infection may offer an insight into the mechanism of gammaherpesvirus pathogenesis.
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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.