ArticleJournal of virology1999
Genetic evidence that EBNA-1 is needed for efficient, stable latent infection by Epstein-Barr virus.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 131 citations in OpenAlex.
- Epstein-Barr virus antibodies and risk of non-Hodgkin lymphoma: a pooled analysis of four prospective cohorts.Blood cancer journal · 2026Article
- Design and Optimization of Benzoic Acid Inhibitors Targeting the EBNA1 DNA-Binding Interface.ACS medicinal chemistry letters · 2026Article
- Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025Review
- Review
- Subcellular Distribution of BALF2 and the Role of Rab1 in the Formation of Epstein-Barr Virus Cytoplasmic Assembly Compartment and Virion Release.Microbiology spectrum · 2023Article
- The Epstein-Barr Virus Enhancer Interaction Landscapes in Virus-Associated Cancer Cell Lines.Journal of virology · 2022Article
- EBV-associated diseases: Current therapeutics and emerging technologies.Frontiers in immunology · 2022Review
- Herpesviral Latency-Common Themes.Pathogens (Basel, Switzerland) · 2020Review
- Article
- Molecular pathogenic pathways in extranodal NK/T cell lymphoma.Journal of hematology & oncology · 2019Review
- The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency.Pathogens (Basel, Switzerland) · 2018Review
- Cytomegalovirus latency and reactivation: recent insights into an age old problem.Reviews in medical virology · 2016Review
- Interplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the Host.Frontiers in microbiology · 2016Review
- The role of Epstein-Barr virus infection in the pathogenesis of nasopharyngeal carcinoma.Virologica Sinica · 2015Review
- Epstein-Barr virus infection and persistence in nasopharyngeal epithelial cells.Chinese journal of cancer · 2014Review
- The placental specific gene, PLAC1, is induced by the Epstein-Barr virus and is expressed in human tumor cells.Virology journal · 2014Article
- Live-cell imaging reveals multiple interactions between Epstein-Barr virus nuclear antigen 1 and cellular chromatin during interphase and mitosis.Journal of virology · 2012Article
- The Epstein-Barr Virus EBNA1 Protein.Scientifica · 2012Review
- Review
- C-terminal region of EBNA-2 determines the superior transforming ability of type 1 Epstein-Barr virus by enhanced gene regulation of LMP-1 and CXCR7.PLoS pathogens · 2011Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Replication and maintenance of the 170-kb circular chromosome of Epstein-Barr virus (EBV) during latent infection are generally believed to depend upon a single viral gene product, the nuclear protein EBNA-1. EBNA-1 binds to two clusters of sites at oriP, an 1, 800-bp sequence on the EBV genome which can support replication and maintenance of artificial plasmids introduced into cell lines that contain EBNA-1. To investigate the importance of EBNA-1 to latent infection by EBV, we introduced a frameshift mutation into the EBNA-1 gene of EBV by recombination along with a flanking selectable marker. EBV genomes carrying the frameshift mutation could be isolated readily after superinfecting EBV-positive cell lines, but not if recombinant virus was used to infect EBV-negative B-cell lines or to immortalize peripheral blood B cells. EBV mutants lacking almost all of internal repeat 3, which encode a repetitive glycine and alanine domain of EBNA-1, were generated in the same way and found to immortalize B cells normally. An EBNA-1-deficient mutant of EBV was isolated and found to be incapable of establishing a latent infection of the cell line BL30 at a detectable frequency, indicating that the mutant was less than 1% as efficient as an isogenic, EBNA-1-positive strain in this assay. The data indicate that EBNA-1 is required for efficient and stable latent infection by EBV under the conditions tested. Evidence from other studies now indicates that autonomous maintenance of the EBV chromosome during latent infection does not depend on the replication initiation function of oriP. It is therefore likely that the viral chromosome maintenance (segregation) function of oriP and EBNA-1 is what is required.
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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.