Evidence map›Paper›PMID 23365457›Full record

ArticleBlood2013

Viral latency locus augments B-cell response in vivo to induce chronic marginal zone enlargement, plasma cell hyperplasia, and lymphoma.

Sang-Hoon Sin, Dirk P Dittmer

Abstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. The Role of Lytic Infection for Lymphomagenesis of Human γ-Herpesviruses.Frontiers in cellular and infection microbiology · 2021
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Journal of virology · 2019
    Review
  14. Review
  15. Kaposi sarcoma.Nature reviews. Disease primers · 2019
    Review
  16. Article
  17. Article
  18. Human herpesvirus-encoded kinase induces B cell lymphomas in vivo.The Journal of clinical investigation · 2018
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Sang-Hoon SinDepartment of Microbiology and Immunology and Lineberger Comprehensive Cancer Center, Center for AIDS Research, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Dirk P Dittmer
University of North Carolina at Chapel Hill · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Vironomics and Biostatistics CoreP01CA019014 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOSSOM A DAMANIA, NANCY JOAN RAAB-TRAUB · 1985 to 2026
$43.8M
Regulation of the KSHV Latent PromoterR01CA109232 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DITTMER, DIRK P · 2004 to 2014
$2.5M
NCI NIH HHS CA019014NCI NIH HHS CA109232NCI NIH HHS P01 CA019014NCI NIH HHS P30CA06086NCI NIH HHS R01 CA109232
6 · The paper itself

Abstract

Kaposi sarcoma (KS) is associated with KS-associated herpesvirus (KSHV). This virus also causes B-cell lymphoma and B-cell hyperplasia. There exists no in vivo model for KSHV-associated B-cell malignancies or premalignant persistence in B cells. We generated a transgenic mouse that expresses multiple viral latent genes, including LANA, vFLIP, vCYC, all viral micro RNAs, and kaposin under the transcriptional control of their natural regulatory region. This promoter is B-cell specific, though it is a weak promoter. Mature B cells were chronically activated, leading to hyperglobulinemia triggered by increased plasma cell frequency and marginal zone (MZ) B-cell hyperplasia. The mice had an augmented response to T-dependent antigen as well as the TLR4 ligand LPS, leading to exacerbated MZ and germinal center responses and increased CD138(+) plasma cells. It is the first model to assess the viral micro RNA function in vivo. These data support a potentially novel mechanism of viral persistence in which virally infected B cells become hyper-responsive to coincident, but unrelated, pathogen exposure, leading to preferential expansion and ultimately lymphoma in a small subset of cases.

Indexed as

AnimalsB-LymphocytesCells, CulturedFlow CytometryGerminal CenterHerpesvirus 8, HumanHyperplasiaLipopolysaccharidesLymphomaMiceMice, Inbred C57BLMice, SCIDMice, TransgenicModels, ImmunologicalPlasma CellsReverse Transcriptase Polymerase Chain ReactionLipopolysaccharidesRNA, Viral

Identifiers

PMID23365457
PMCPMC3624941
OpenAlexW2092079898

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.