ArticleJournal of virology2010
Blimp-1-dependent plasma cell differentiation is required for efficient maintenance of murine gammaherpesvirus latency and antiviral antibody responses.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 32 citations in OpenAlex.
- A role for host activation-induced cytidine deaminase in innate immune defense against KSHV.PLoS pathogens · 2013Trial
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment.Nature communications · 2025Article
- The unappreciated role of developing B cells in chronic gammaherpesvirus infections.PLoS pathogens · 2024Review
- Article
- 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
- Age-associated B cells are long-lasting effectors that impede latent γHV68 reactivation.Scientific reports · 2022Article
- Article
- Lytic Replication and Reactivation from B Cells Is Not Required for Establishing or Maintaining Gammaherpesvirus LatencyJournal of virology · 2022Article
- Conquering the Host: Determinants of Pathogenesis Learned from Murine Gammaherpesvirus 68.Annual review of virology · 2021Article
- Review
- Gammaherpesvirus Colonization of the Spleen Requires Lytic Replication in B Cells.Journal of virology · 2018Article
- 1, 25(OH)2 D3 Induces Reactivation and Death of Kaposi's Sarcoma-Associated Herpesvirus of Primary Effusion Lymphoma cells.Scientific reports · 2017Article
- MicroRNA miR-155 Is Necessary for Efficient Gammaherpesvirus Reactivation from Latency, but Not for Establishment of Latency.Journal of virology · 2016Article
- Article
- Interplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the Host.Frontiers in microbiology · 2016Review
- Blimp-1, an intrinsic factor that represses HIV-1 proviral transcription in memory CD4+ T cells.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Murine gammaherpesvirus 68 reactivation from B cells requires IRF4 but not XBP-1.Journal of virology · 2014Article
- What lies within: coinfections and immunity.Cell host & microbe · 2014Article
- Article
- Tyrosine 129 of the murine gammaherpesvirus M2 protein is critical for M2 function in vivo.PloS one · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Recent evidence from the study of Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus supports a model in which terminal differentiation of B cells to plasma cells leads to virus reactivation. Here we address the role of Blimp-1, the master transcriptional regulator of plasma cell differentiation, in murine gammaherpesvirus 68 (MHV68) latency and reactivation. Blimp-1 expression in infected cells was dispensable for acute virus replication in the lung following intranasal inoculation and in the spleen following intraperitoneal inoculation with MHV68. However, we observed a role for Blimp-1 in both the establishment of latency and reactivation from latency in vivo. Additionally, plasma cell-deficient mice also exhibited a significant defect in the establishment of latency in the spleen, as well as reactivation from latency, similar to mice that lacked Blimp-1 only in MHV68-infected cells. In the absence of plasma cells, MHV68 infection failed to elicit a strong germinal center response and fewer B cells in the germinal center were MHV68 infected. Notably, the absence of a functional Blimp-1 gene only in MHV68-infected cells led to a decrease in both B-cell and CD4(+) T-cell responses during the establishment of latency. Finally, Blimp-1 expression in infected cells played a critical role in the maintenance of both MHV68 latency in the spleen and antibody responses to MHV68. Together, these studies support a model wherein episodic Blimp-1-mediated plasma cell differentiation leads to MHV68 reactivation, which serves to both renew the latency reservoirs and stimulate long-lived plasma cells to secrete virus-specific antibody.
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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.