ArticlePLoS pathogens2018
EBV persistence without its EBNA3A and 3C oncogenes in vivo.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 35 citations in OpenAlex.
- CD20 bispecific T-cell engager depletes B-cell progenitors preventing EBV-associated lymphomagenesis in humanized mice.Blood advances · 2026Article
- Humanized Mouse Models of Epstein Barr Virus Infection.Current protocols · 2025Article
- Review
- How Epstein Barr Virus Causes Lymphomas.Viruses · 2024Review
- Targeted adenovirus-mediated transduction of human T cellsMolecular therapy. Methods & clinical development · 2023Article
- Review
- Virus-Mediated Inhibition of Apoptosis in the Context of EBV-Associated Diseases: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2022Review
- EBV-associated diseases: Current therapeutics and emerging technologies.Frontiers in immunology · 2022Review
- Article
- Review
- KSHV infection drives poorly cytotoxic CD56-negative natural killer cell differentiation in vivo upon KSHV/EBV dual infection.Cell reports · 2021Article
- Immune Escape by Non-coding RNAs of the Epstein Barr Virus.Frontiers in microbiology · 2021Review
- Modification of EBV-Associated Pathologies and Immune Control by Coinfections.Frontiers in oncology · 2021Review
- Modification of EBV Associated Lymphomagenesis and Its Immune Control by Co-Infections and Genetics in Humanized Mice.Frontiers in immunology · 2021Review
- Modeling oncogenic herpesvirus infections in humanized mice.Current opinion in virology · 2020Review
- Review
- An EBNA3A-Mutated Epstein-Barr Virus Retains the Capacity for Lymphomagenesis in a Cord Blood-Humanized Mouse Model.Journal of virology · 2020Article
- In vivo analysis of γH2AX+ cells in skeletal muscle from aged and obese humans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Immunosuppressive FK506 treatment leads to more frequent EBV-associated lymphoproliferative disease in humanized mice.PLoS pathogens · 2020Article
- Probing Reconstituted Human Immune Systems in Mice With Oncogenic γ-Herpesvirus Infections.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oncogenic Epstein Barr virus (EBV) infects the majority of the human population and usually persists within its host for life without symptoms. The EBV oncoproteins nuclear antigen 3A (EBNA3A) and 3C (EBNA3C) are required for B cell transformation in vitro and are expressed in EBV associated immunoblastic lymphomas in vivo. In order to address the necessity of EBNA3A and EBNA3C for persistent EBV infection in vivo, we infected NOD-scid γcnull mice with reconstituted human immune system components (huNSG mice) with recombinant EBV mutants devoid of EBNA3A or EBNA3C expression. These EBV mutants established latent infection in secondary lymphoid organs of infected huNSG mice for at least 3 months, but did not cause tumor formation. Low level viral persistence in the absence of EBNA3A or EBNA3C seemed to be supported primarily by proliferation with the expression of early latent EBV gene products transitioning into absent viral protein expression without elevated lytic replication. In vitro, EBNA3A and EBNA3C deficient EBV infected B cells could be rescued from apoptosis through CD40 stimulation, mimicking T cell help in secondary lymphoid tissues. Thus, even in the absence of the oncogenes EBNA3A and 3C, EBV can access a latent gene expression pattern that is reminiscent of EBV persistence in healthy virus carriers without prior expression of its whole growth transforming program.
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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.