ArticleAIDS research and human retroviruses2011
Potentiation of EBV-induced B Cell transformation by CXCR4-tropic, but not CCR5-tropic, HIV gp120: implications for HIV-associated lymphomagenesis.
Article in AIDS research and human retroviruses, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
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.
Who cites it
4 citing papers in PubMed.
- Observational
- EBV-dUTPase Modulates Host Immune Responses Potentially Altering the Tumor Microenvironment in EBV-associated Malignancies.Current research on HIV/AIDS · 2016Article
- Epstein-Barr virus-driven lymphomagenesis in the context of human immunodeficiency virus type 1 infection.Frontiers in microbiology · 2013Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Abstract R5 and X4 HIV strains use CCR5 or CXCR4 chemokine receptors (CKRs), respectively, for entry. Preferential growth of X4 vs. R5 HIV in cell lines reflects constitutive expression of CXCR4, but not CCR5 (in contrast to dual expression on primary T cells), and CXCR4 is the predominant CKR found on most tumors. Non-Hodgkin's B cell lymphomas (NHL) are increased among HIV(+) patients, and interactions between HIV envelope and CKRs may contribute to lymphomagenesis. Despite strong evidence for a CXCR4-SDF-1 oncogenic axis, no in vitro evaluation of CXCR4-mediated normal lymphocyte transformation has been published. Exposure of normal B cells to EBV in the presence of X4 gp120 (but not R5 gp120) increased proliferation and BLCL outgrowth, comparable to anti-CD40 mAb costimulation. This suggests a role for X4 tropic viral envelope signaling via CXCR4 and/or CXCR7 in HIV-associated lymphomagenesis.
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Registered trials
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