ReviewFrontiers in microbiology2016
Interplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the Host.
Review in Frontiers in microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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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.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- B cell-intrinsic interleukin 17 receptor A signaling supports the establishment of chronic murine gammaherpesvirus 68 infection.Journal of virology · 2025Article
- Gammaherpesvirus infection triggers the formation of tRNA fragments from premature tRNAs.mBio · 2025Article
- Article
- B cells present a double-sided effect in digestive system tumors: a review for tumor microenvironment.Translational gastroenterology and hepatology · 2024Review
- B cell-intrinsic STAT3-mediated support of latency and interferon suppression during murine gammaherpesvirus 68 infection revealed through anbioRxiv : the preprint server for biology · 2023Article
- Conquering the Host: Determinants of Pathogenesis Learned from Murine Gammaherpesvirus 68.Annual review of virology · 2021Article
- RNA-guided gene editing of the murine gammaherpesvirus 68 genome reduces infectious virus production.PloS one · 2021Article
- Review
- Gammaherpesvirus-infected germinal center cells express a distinct immunoglobulin repertoire.Life science alliance · 2020Article
- Endosomal Toll-Like Receptors 7 and 9 Cooperate in Detection of Murine Gammaherpesvirus 68 Infection.Journal of virology · 2019Article
- SOCS and Herpesviruses, With Emphasis on Cytomegalovirus Retinitis.Frontiers in immunology · 2019Review
- Inhibition of murine herpesvirus-68 replication by IFN-gamma in macrophages is counteracted by the induction of SOCS1 expression.PLoS pathogens · 2018Article
- Viral FGARAT ORF75A promotes early events in lytic infection and gammaherpesvirus pathogenesis in mice.PLoS pathogens · 2018Article
- RTA Occupancy of the Origin of Lytic Replication during Murine Gammaherpesvirus 68 Reactivation from B Cell Latency.Pathogens (Basel, Switzerland) · 2017Article
- Tick-Borne Transmission of Murine Gammaherpesvirus 68.Frontiers in cellular and infection microbiology · 2017Article
- Effects of tanshinol on markers of bone turnover in ovariectomized rats and osteoblast cultures.PloS one · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Herpesviruses establish a chronic infection in the host characterized by intervals of lytic replication, quiescent latency, and reactivation from latency. Murine gammaherpesvirus 68 (MHV68) naturally infects small rodents and has genetic and biologic parallels with the human gammaherpesviruses (gHVs), Kaposi's sarcoma-associated herpesvirus and Epstein-Barr virus. The murine gammaherpesvirus model pathogen system provides a platform to apply cutting-edge approaches to dissect the interplay of gammaherpesvirus and host determinants that enable colonization of the host, and that shape the latent or lytic fate of an infected cell. This knowledge is critical for the development of novel therapeutic interventions against the oncogenic gHVs. The nuclear factor kappa B (NF-κB) signaling pathway is well-known for its role in the promotion of inflammation and many aspects of B cell biology. Here, we review key aspects of the virus lifecycle in the host, with an emphasis on the route that the virus takes to gain access to the B cell latency reservoir. We highlight how the murine gammaherpesvirus requires components of the NF-κB signaling pathway to promote replication, latency establishment, and maintenance of latency. These studies emphasize the complexity of gammaherpesvirus interactions with NF-κB signaling components that direct innate and adaptive immune responses of the host. Importantly, multiple facets of NF-κB signaling have been identified that might be targeted to reduce the burden of gammaherpesvirus-associated diseases.
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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.