EBNA1
- PMID: 40399573
- DOI: 10.1007/82_2025_299
EBNA1
Abstract
EBNA1 plays multiple important roles in EBV latent infection and has also been shown to impact EBV lytic infection. EBNA1 is required for the stable persistence of the EBV genomes in latent infection and activates the expression of other EBV latency genes through interactions with specific DNA sequences in the viral episomes. EBNA1 also interacts with several cellular proteins and cellular DNA sites to modulate multiple cellular pathways important for viral persistence and cell survival. These cellular effects are also implicated in oncogenesis, suggesting a direct role of EBNA1 in the development of EBV-associated tumours.
Keywords: DNA binding; DNA replication; Immune evasion; Mitotic segregation; PML bodies; Transcriptional activation; USP7.
© 2025. The Author(s), under exclusive license to Springer Nature Switzerland AG.
References
-
- Altmann M, Pich D, Ruiss R, Wang J, Sugden B, Hammerschmidt W (2006) Transcriptional activation by EBV nuclear antigen 1 is essential for the expression of EBV’s transforming genes. Proc Natl Acad Sci USA 103(38):14188–14193
-
- Ambinder RF, Shah WA, Rawlins DR, Hayward GS, Hayward SD (1990) Definition of the sequence requirements for binding of the EBNA-1 protein to its palindromic target sites in Epstein-Barr virus DNA. J Virol 64:2369–2379
-
- Ambinder RF, Mullen M, Chang Y, Hayward GS, Hayward SD (1991) Functional domains of Epstein-Barr nuclear antigen EBNA-1. J Virol 65:1466–1478
-
- Apcher S, Komarova A, Daskalogianni C, Yin Y, Malbert-Colas L, Fahraeus R (2009) mRNA translation regulation by the Gly-Ala repeat of Epstein-Barr virus nuclear antigen 1. J Virol 83(3):1289–1298
-
- Apcher S, Daskalogianni C, Manoury B, Fahraeus R (2010) Epstein Barr virus-encoded EBNA1 interference with MHC class I antigen presentation reveals a close correlation between mRNA translation initiation and antigen presentation. PLoS Pathog 6(10):e1001151. https://doi.org/10.1371/journal.ppat.1001151 - DOI
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