Keywords
Epstein-Barr virus
oncogenes
viral proteins
latency
gene expression
herpesvirus
oncogenes
viral proteins
latency
gene expression
herpesvirus
How to Cite
Plata, L., Oviedo, J., & Rincón Orozco, B. (2018). Viral strategies for cancer induction “Epstein-Barr virus: latency and mechanisms associated with viral oncogenesis”. Salud UIS, 50(3), 257–268. https://doi.org/10.18273/revsal.v50n3-2018010
Abstract
Chronic infection with oncogenic viruses is responsible for approximately 20% of all cancers worldwide in humans, this viral transformation represents a complex, multistage and multifactorial process. An example is the Epstein-Barr virus (EBV), a herpesvirus that latently infects over 90% of the population. Although the infection often courses asymptomatically, EBV is able to modify its genomic expression by establishing different latency phases, thus altering the B lymphocytes and epithelial cells metabolism, a determinant process in the appearance and development of different pathologies ranging from infectious mononucleosis to oncological processes such as Burkitt’s lymphoma, gastric cancer and nasopharyngeal cancer.
References
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3. Damania B, Pipas JM. DNA tumor viruses.DNA Tumor Viruses; Springer. 2009.doi: https://doi.org/10.1007/978-0-387-68945-6.
4. Shannon-Lowe C, Rowe M. Epstein Barr virus entry; Kissing and conjugation. Curr Opin Virol. 2014; 4: 78-84. doi: http://dx.doi.org/10.1016/j.coviro.2013.12.001.
5. Rivailler P, Cho Y-G, Wang F. Complete genomic sequence of an Epstein-Barr virus-related herpesvirus naturally infecting a new world primate: a defining point in the evolution of oncogenic lymphocryptoviruses. J Virol. 2002; 76(23): 12055-12068.
6. Competition L, Affects D, In I. NIH Public Access. 2008; 86(12): 3279-3288.
7. Sathiyamoorthy K, Jiang J, Hu YX, Rowe CL, Möhl BS, Chen J, et al. Assembly and Architecture of the EBV B Cell Entry Triggering Complex. PLoS Pathog. 2014; 10(8): e1004309. doi: 10.1371/journal.ppat.1004309.
8. Ali AS, Al-Shraim M, Al-Hakami AM, Jones IM. Epstein- Barr Virus: clinical and epidemiological revisits and genetic basis of oncogenesis. Open Virol J. 2015; 9: 7-28. doi:
10.2174/1874357901509010007.
9. Szabo FK, Hoffman GE. NIH Public Access. 2012; 37(1): 62-70.
10. Warner WA, Sanchez R, Dawoodian A, Li E, Momand J. NIH Public Access. 2013; 80(4): 631-637.
11. Kalla M, Schmeinck A, Bergbauer M, Pich D, Hammerschmidt W. AP-1 homolog BZLF1 of Epstein-Barr virus has two essential functions dependent on the epigenetic state of the viral
genome. Proc Natl Acad Sci USA. 2010; 107(2): 850-855. doi: 10.1073/pnas.0911948107.
12. Dreyfus DH, Liu Y, Ghoda LY, Chang JT. Analysis of an ankyrin-like region in Epstein Barr Virus encoded (EBV) BZLF-1 (ZEBRA) protein: implications for interactions with NF-κB and p53. Virol J 2011; 8(1): 422. doi: 10.1186/1743-422X-8-422.
13. Flower K, Thomas D, Heather J, Ramasubramanyan S, Jones S, Sinclair AJ. Epigenetic control of viral Life-Cycle by a DNA-Methylation dependent transcription factor. PLoS One. 2011; 6(10): e25922. doi: 10.1371/journal.pone.0025922.
14. Yang YC, Chang LK. Role of TAF4 in Transcriptional Activation by Rta of Epstein-Barr Virus. PLoS One. 2013; 8(1). e54075. doi: 10.1371/journal.pone.0054075.
15. LaJeunesse DR, Brooks K, Adamson AL. Epstein-Barr virus immediate-early proteins BZLF1 and BRLF1 alter mitochondrial morphology during lytic replication. Biochem Biophys Res Commun. 2005;333(2): 438-442. doi: 10.1016/j.bbrc.2005.05.120.
16. Milián E, Prats E, Cairó JJ, Gòdia F, Vives J. BHRF1 exerts an antiapoptotic effect and cell cycle arrest via Bcl-2 in murine hybridomas. J Biotechnol. 2015; 209: 58-67. doi: http://dx.doi.org/10.1016/j.jbiotec.2015.06.379.
17. Kvansakul M, Wei AH, Fletcher JI, Willis SN, Chen L, Roberts AW, et al. Structural basis for apoptosis inhibition by Epstein-Barr virus bhrf1. PLoS Pathog. 2010; 6(12): e1001236. doi: 10.1371/journal.ppat.1001236.
18. Aubry V, Mure F, Mariame B, Deschamps T, Wyrwicz LS, Manet E, et al. Epstein-Barr Virus late gene transcription depends on the assembly of a Virus-Specific preinitiation complex. J Virol. 2014; 88(21): 12825-12838. doi: http://jvi.asm.org/cgi/doi/10.1128/JVI.02139-14.
19. Gruffat H, Kadjouf F, Mariame B, Manet E. The Epstein-Barr Virus BcRF1 Gene Product Is a TBPLike protein with an essential role in late gene expression. J Virol. 2012; 86(11): 6023-6032. doi: 10.1128/JVI.00159-12.
20. Jochum S, Moosmann A, Lang S, Hammerschmidt W, Zeidler R. The EBV immunoevasins vIL-10 and BNLF2a protect newly infected B cellsfrom immune recognition and elimination. PLoS Pathog. 2012; 8(5): e1002704. doi: 10.1371/journal.
ppat.1002704.
21. Gruffat H, Marchione R, Manet E. Herpesvirus late gene expression: a viral-specific pre-initiation complex is key. Front Microbiol. 2016; 7: 869. doi: 10.3389/fmicb.2016.00869.
22. Roy SG, Robertson ES, Saha A. Epigenetic impact on EBV associated B-cell lymphomagenesis. Biomolecules. 2016; 6(4): 46. doi: 10.3390/biom6040046.
23. Hazra A, Fuchs CS, Chan AT, Giovannucci EL, Hunter J. NIH Public Access. Cancer. 2009;19(9): 975-980.
24. Tempera I, Lieberman PM. Epigenetic regulation of EBV persistence and oncogenesis. Semin Cancer Biol. 2014; 26: 22-29. doi: http://dx.doi.org/10.1016/j.semcancer.2014.01.003.
25. Frappier LD. EBNA1 and epstein-barr virus associated tumours. EBNA1 and Epstein-Barr Virus associated tumours. Springer; 2013. doi: 10.1007/978-1-4614-6886-8.
26. Jha HC, Pei Y, Robertson ES. Epstein-barr virus: Diseases linked to infection and transformation. Front Microbiol. 2016; 7: 1602. doi: 10.3389/fmicb.2016.01602.
27. Gruhne B, Sompallae R, Masucci MG. Three Epstein-Barr virus latency proteins independently promote genomic instability by inducing DNA damage, inhibiting DNA repair and inactivating cell cycle checkpoints. Oncogene. 2009; 28(45): 3997-4008. doi: 10.1038/onc.2009.258.
28. Gruhne B, Sompallae R, Marescotti D, Kamranvar S, Gastaldello S, Masucci M. The Epstein-Barr virus nuclear antigen-1 promotes genomic instability via induction of reactive oxygen species. Proc Natl Acad Sci USA. 2009; 106(7): 2313-2318. doi: 10.1073/pnas.0810619106.
29. Fuchs KP, Bommer G, Dumont E, Christoph B, Vidal M, Kremmer E, et al. Mutational analysis of the J recombination signal sequence binding protein (RBP-J)/ Epstein ± Barr virus nuclear antigen 2 (EBNA2) and RBP-J / Notch interaction. Eur J Biochem. 2001; 268(17): 4639-4646.
30. Parker GA, Touitou R, Allday MJ. Epstein-Barr virus EBNA3C can disrupt multiple cell cycle checkpoints and induce nuclear division divorced from cytokinesis. Oncogene. 2000; 19(5): 700-709. doi: 10.1038/sj.onc.1203327.
31. Calderwood MA, Sungwook L, Holthaus AM, Blacklow SC, Kieff E, Johannsen E. Epstein-Barr Virus Nuclear Protein 3C binds to the N-terminal (NTD) and beta trefoil domains (BTD) of RBP/CSL; only the NTD interaction is essential for
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