ArticleBlood2015
The tumor virus landscape of AIDS-related lymphomas.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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.
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
49 citing papers in PubMed, 86 citations in OpenAlex.
- Immediate Antiretroviral Therapy Reduces Risk of Infection-Related Cancer During Early HIV Infection.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2016Trial
- Epstein-Barr virus (EBV) infection causes human germinal center B cell-derived lymphomas in the absence of EBNA2 expression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Interaction between HIV-1 Tat and EBV Zta favours immune escape of B cells by downregulating HLA-ABC expression.Cellular and molecular life sciences : CMLS · 2026Article
- Incomplete B-cell reconstitution in ART-treated people living with HIV is associated with EBV-linked lymphoma progression.Frontiers in immunology · 2026Article
- The critical role of ferroptosis in virus-associated hematologic malignancies and its potential value in antiviral-antitumor therapy.Virulence · 2025Review
- HIV-associated non-Hodgkin lymphoma tumor-microenvironment axes differ by EBV status across cellular origins.bioRxiv : the preprint server for biology · 2025Article
- EBV Latency Programs: Molecular and Epigenetic Regulation and Its Role in Disease Pathogenesis.Journal of medical virology · 2025Review
- Virus-driven dysregulation of the BCR pathway: a potential mechanism for the high prevalence of HIV related B-cell lymphoma.Annals of hematology · 2024Review
- Double-Hit Diffuse Large B-Cell Lymphoma in AIDS.Cureus · 2024Article
- HIV-associated cancers and lymphoproliferative disorders caused by Kaposi sarcoma herpesvirus and Epstein-Barr virus.Clinical microbiology reviews · 2024Review
- Coexisting of Primary Central Nervous System Lymphoma andInfection and drug resistance · 2024Article
- Targeting latent viral infection in EBV-associated lymphomas.Frontiers in immunology · 2024Review
- Systems-level analyses of protein-protein interaction network dysfunctions via epichaperomics identify cancer-specific mechanisms of stress adaptation.Nature communications · 2023Article
- Diffuse Large B-Cell Lymphoma in the HIV Setting.Cancers · 2023Review
- Diagnosis and monitoring of virus-associated cancer using cell-free DNA.Current opinion in virology · 2023Review
- Review
- Human Immunodeficiency Virus Related Non-Hodgkin's Lymphoma.Blood and lymphatic cancer : targets and therapy · 2023Review
- Review
- Latent membrane proteins from EBV differentially target cellular pathways to accelerate MYC-induced lymphomagenesis.Blood advances · 2022Article
- KSHV/HHV8-mediated hematologic diseases.Blood · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Immunodeficiency dramatically increases susceptibility to cancer as a result of reduced immune surveillance and enhanced opportunities for virus-mediated oncogenesis. Although AIDS-related lymphomas (ARLs) are frequently associated with known oncogenic viruses, many cases contain no known transforming virus. To discover novel transforming viruses, we profiled a set of ARL samples using whole transcriptome sequencing. We determined that Epstein-Barr virus (EBV) was the only virus detected in the tumor samples of this cohort, suggesting that if unidentified pathogens exist in this disease, they are present in <10% of cases or undetectable by our methods. To evaluate the role of EBV in ARL pathogenesis, we analyzed viral gene expression and found highly heterogeneous patterns of viral transcription across samples. We also found significant heterogeneity of viral antigen expression across a large cohort, with many patient samples presenting with restricted type I viral latency, indicating that EBV latency proteins are under increased immunosurveillance in the post-combined antiretroviral therapies era. Furthermore, EBV infection of lymphoma cells in HIV-positive individuals was associated with a distinct host gene expression program. These findings provide insight into the joint host-virus regulatory network of primary ARL tumor samples and expand our understanding of virus-associated oncogenesis. Our findings may also have therapeutic implications, as treatment may be personalized to target specific viral and virus-associated host processes that are only present in a subset of patients.
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What OpenQuestion holds
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.