Evidence map›Paper›PMID 27799525›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Expression of HIV-1 matrix protein p17 and association with B-cell lymphoma in HIV-1 transgenic mice.

Virginia A Carroll, Mark K Lafferty, Luigi Marchionni, Joseph L Bryant, Robert C Gallo, Alfredo Garzino-Demo

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Review
  2. HIV reservoirs in lymphomagenesis: hidden driver in the era of viral suppression?Microbiology and molecular biology reviews : MMBR · 2025
    Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. How can we establish animal models of HIV-associated lymphoma?Animal models and experimental medicine · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. GWAS in Mice Maps Susceptibility to HIV-Associated Nephropathy to theJournal of the American Society of Nephrology : JASN · 2022
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors.

Virginia A CarrollInstitute of Human Virology, University of Maryland School of Medicine, Baltimore, MD 21201.
Mark K LaffertyInstitute of Human Virology, University of Maryland School of Medicine, Baltimore, MD 21201.
Luigi MarchionniDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Joseph L BryantInstitute of Human Virology, University of Maryland School of Medicine, Baltimore, MD 21201.
Robert C GalloInstitute of Human Virology, University of Maryland School of Medicine, Baltimore, MD 21201; rgallo@ihv.umaryland.edu agarzinodemo@ihv.umaryland.edu.
Alfredo Garzino-DemoInstitute of Human Virology, University of Maryland School of Medicine, Baltimore, MD 21201; rgallo@ihv.umaryland.edu agarzinodemo@ihv.umaryland.edu.ORCID 0000-0002-4095-6950

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Institute for Clinical and Translational ResearchUL1TR001079 · NCATS · JOHNS HOPKINS UNIVERSITY · PI FORD, DANIEL ERNEST · 2013 to 2017
$60.1M
Training Grant in Cancer BiologyT32CA154274 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI Toni M Antalis, CURT I CIVIN · 2011 to 2026
$6.8M
NCATS NIH HHS UL1 TR001079NCI NIH HHS P30 CA006973NCI NIH HHS T32 CA154274
6 · The paper itself

Abstract

HIV-1 infection is associated with increased risk for B-cell lymphomas. How HIV infection promotes the development of lymphoma is unclear, but it may involve chronic B-cell activation, inflammation, and/or impaired immunity, possibly leading to a loss of control of oncogenic viruses and reduced tumor immunosurveillance. We hypothesized that HIV structural proteins may contribute to lymphomagenesis directly, because they can persist long term in lymph nodes in the absence of viral replication. The HIV-1 transgenic mouse Tg26 carries a noninfectious HIV-1 provirus lacking part of the gag-pol region, thus constituting a model for studying the effects of viral products in pathogenesis. Approximately 15% of Tg26 mice spontaneously develop leukemia/lymphoma. We investigated which viral proteins are associated with the development of leukemia/lymphoma in the Tg26 mouse model, and performed microarray analysis on RNA from spleen and lymph nodes to identify potential mechanisms of lymphomagenesis. Of the viral proteins examined, only expression of HIV-1 matrix protein p17 was associated with leukemia/lymphoma development and was highly expressed in bone marrow before disease. The tumor cells resembled pro-B cells, and were CD19

Indexed as

AnimalsB-LymphocytesBone MarrowDNA-Binding Proteinsgag Gene Products, Human Immunodeficiency VirusGene Expression Regulation, NeoplasticHIV-1HIV AntigensHomeodomain ProteinsHumansLymph NodesLymphoma, B-CellMice, TransgenicDNA-Binding Proteinsgag Gene Products, Human Immunodeficiency VirusHIV AntigensHomeodomain Proteinsp17 protein, Human Immunodeficiency Virus Type 1RAG-1 proteinV(D)J recombination activating protein 2B-cell lymphomaHIV-1matrix protein p17RAGtransgenic mice

Identifiers

PMID27799525
PMCPMC5135339

What OpenQuestion holds

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Registered trials

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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.