ArticleJournal of virology2007
Epstein-Barr virus inhibits Kaposi's sarcoma-associated herpesvirus lytic replication in primary effusion lymphomas.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 49 citations in OpenAlex.
- Determinants of Gammaherpesvirus Shedding in Saliva Among Ugandan Children and Their Mothers.The Journal of infectious diseases · 2018Trial
- CD20-Negative Large B-Cell Lymphomas: The Diagnostic Challenge of Tumors with Downregulation of Mature B-Cell Marker Expression.International journal of molecular sciences · 2025Review
- Epstein-Barr virus (EBV) antibody changes over time in a general population cohort in rural Uganda, 1992-2008.Infectious agents and cancer · 2023Article
- Review
- Review
- Distinct genetic architectures and environmental factors associate with host response to the γ2-herpesvirus infections.Nature communications · 2020Article
- Infection and immune control of human oncogenic γ-herpesviruses in humanized mice.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- A Genome-Wide Epstein-Barr Virus Polyadenylation Map and Its Antisense RNA to EBNA.Journal of virology · 2019Article
- Article
- Tumor Suppressor p53 Stimulates the Expression of Epstein-Barr Virus Latent Membrane Protein 1.Journal of virology · 2017Article
- Kaposi's Sarcoma-Associated Herpesvirus Reduces Cellular Myeloid Differentiation Primary-Response Gene 88 (MyD88) Expression via Modulation of Its RNA.Journal of virology · 2016Article
- Co-infections and Pathogenesis of KSHV-Associated Malignancies.Frontiers in microbiology · 2016Review
- Virus proteins similar to human proteins as possible disturbance on human pathways.Systems and synthetic biology · 2014Article
- Nuclear factor κB represses the expression of latent membrane protein 1 in Epstein-Barr virus transformed cells.World journal of virology · 2014Article
- KSHV LANA and EBV LMP1 induce the expression of UCH-L1 following viral transformation.Virology · 2014Article
- TLR-TRIF pathway enhances the expression of KSHV replication and transcription activator.The Journal of biological chemistry · 2013Article
- Article
- Article
- Toll-like receptor 7 stimulates the expression of Epstein-Barr virus latent membrane protein 1.PloS one · 2012Article
- KSHV Rta Promoter Specification and Viral Reactivation.Frontiers in microbiology · 2012Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The majority of AIDS-associated primary effusion lymphomas (PEL) are latently infected with both Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV). PELs harboring two viruses have higher oncogenic potential, suggesting functional interactions between EBV and KSHV. The KSHV replication and transcription activator (K-RTA) is necessary and sufficient for induction of KSHV lytic replication. EBV latent membrane protein 1 (LMP-1) is essential for EBV transformation and establishment of latency in vitro. We show EBV inhibits chemically induced KSHV lytic replication, in part because of a regulatory loop in which K-RTA induces EBV LMP-1 and LMP-1 in turn inhibits K-RTA expression and furthermore the lytic gene expression of KSHV. Suppression of LMP-1 expression in dually infected PEL cells enhances the expression of K-RTA and lytic replication of KSHV upon chemical induction. Because LMP-1 is known to inhibit EBV lytic replication, KSHV-mediated induction of LMP-1 would potentiate EBV latency. Moreover, KSHV infection of EBV latency cells induces LMP-1, and K-RTA is involved in the induction. Both LMP-1 and K-RTA are expressed during primary infection by EBV of KSHV latency cells. Our findings provide evidence that an interaction between EBV and KSHV at molecular levels promotes the maintenance and possibly establishment of viral latency, which may contribute to pathogenesis of PELs.
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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.