Vías moleculares patogénicas del linfoma T/NK extranodal de tipo nasal asociadas con virus de Epstein Barr: Revisión narrativa
DOI:
https://doi.org/10.36829/63CTS.v8i2.948Palabras clave:
Síndrome linfoproliferativo, herpesvirus, oncogénesis, evasión inmune, epigenéticaResumen
El virus de Epstein Barr (VEB) se encuentra presente en el 100% de los casos de linfoma T/NK extranodal de tipo nasal (ENKTL) y juega un papel importante en la etiopatogenia de esta enfermedad. El objetivo de esta revisión es actualizar el conocimiento de las vías moleculares genéticas y epigenéticas utilizadas por el VEB en la oncogenesis del ENKTL. Para ello se realizó una revisión de la literatura, en las bases de datos de PubMed y Google Scholar, sobre los mecanismos que utilizan las proteínas virales como la proteína de membrana latente (LMP1) y el antígeno nuclear Epstein Barr 1 (EBNA1) para activar proteínas antiapoptóticas del huésped y proteínas relacionadas a proliferación celular, a través de las vías moleculares JAK/STAT (Janus quinasas/señales de transducción y activación de proteínas de transcripción), NF-κB (el factor nuclear potenciador de las cadenas ligeras kappa de las células B activadas) EZHZ2 (Enhancer of Zeste 2 Polycomb repressive Complex 2) y PI3K/Akt (Fosfoinositido 3 quinasa/proteína quinasa B); también se revisó el papel de las proteínas virales BNLF2a, BILF y BDLF3 en la evasión inmune del virus. También LMP1 aumenta la expresión de PDL-1 (ligando de la muerte celular programada), contribuyendo a la disminución de la respuesta inmunológica. A nivel epigenético se abordan los cambios del perfil de metilación en las áreas promotoras de genes supresores de tumor y se explica la función de los miARN de VEB que participan inhibiendo genes supresores de tumor o activando genes que aumentan la proliferación.
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