Palabras clave
Virus de Epstein Barr
oncogenes
proteínas virales
latencia
expresión génica
herpesvirus
oncogenes
proteínas virales
latencia
expresión génica
herpesvirus
Cómo citar
Plata, L., Oviedo, J., & Rincón Orozco, B. (2018). Revisión sistemática: estrategias virales para la inducción de cáncer “virus de Epstein-Barr: latencia y mecanismos asociados a la oncogénesis viral”. Salud UIS, 50(3), 257–268. https://doi.org/10.18273/revsal.v50n3-2018010
Resumen
La infección crónica con virus oncogénicos es responsable de aproximadamente el 20% de todos los cánceres reportados en humanos, este proceso de oncogénesis viral presenta una naturaleza compleja, multietapa y multifactorial. Un ejemplo de ello es el Virus de Epstein- Barr (EBV), un herpesvirus que infecta de manera latente a más del 90% de la población. Aunque la infección a menudo cursa de manera asintomática, el EBV es capaz de modificar su expresión genómica estableciendo diferentes fases de latencia, alterando así el metabolismo de sus células blanco, como son los linfocitos B y las células epiteliales, proceso que resulta determinante en la aparición y desarrollo de diferentes patologías que van desde la mononucleosis infecciosa hasta procesos oncológicos como el linfoma de Burkitt, el cáncer gástrico o el cáncer nasofaríngeo.
Referencias
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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.
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