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XMRV se estimula por inflamación y Epstein Bar

Publicado: 18 Mar 2011, 15:44
por EndSFC
Parece que el XMRV empieza a demostrar cómo se comporta:

En este estudio, se demuestra que el XMRV en humanos es estimulado por la proteína inflamatoria NFkB, y por el Epstein Bar:

http://jvi.asm.org/cgi/content/abstract/85/7/3179" onclick="window.open(this.href);return false;

En otras palabras, el XMRV sería cuanto menos parte de un círculo vicioso, en el que una vez asentado un estado de inflamación crónica y de un sistema inmune deprimido, que permite la entrada y cronificación de infecciones, como el Eptein Bar, ésto hace que el XMRV prolifere, lo que como demostraba el estudio anterior que he colgado, crea más inflamación y afecta a la funcionalidad de las células que infecta (NKS, linf B, T, macrófagos...). No hace falta que recuerde que esto está en la base del SFC...

Sergio



Journal of Virology, April 2011, p. 3179-3186, Vol. 85, No. 7
0022-538X/11/$012.00+0 doi:10.1128/JVI.02333-10
American Society for Microbiology. All Rights Reserved.
NF-{kappa}B Activation Stimulates Transcription and Replication of Retrovirus XMRV in Human B-Lineage and Prostate Carcinoma Cells{triangledown}
Shuhei Sakakibara,1* Kaori Sakakibara,2 and Giovanna Tosato1

Laboratory of Cellular Oncology,1 Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 208922

Received 8 November 2010/ Accepted 20 January 2011

Xenotropic murine leukemia virus-related virus (XMRV) is a gammaretrovirus linked to prostate carcinoma and chronic fatigue syndrome. Here we report that NF-{kappa}B activation can markedly increase XMRV production. The inflammatory cytokine tumor necrosis factor alpha (TNF-{alpha}), which activates NF-{kappa}B, significantly augmented viral Gag protein production in XMRV-infected cells. Reporter assays showed that TNF-{alpha} and Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1), an intrinsic NF-{kappa}B activator, increased long terminal repeat (LTR)-dependent XMRV transcription. We identified two NF-{kappa}B binding sites (designated {kappa}B-1 and {kappa}B-2) in the LTR U3 region of XMRV and demonstrated that both sites bind to the NF-{kappa}B component p65/RelA. Mutation of the {kappa}B-1 site, but not the {kappa}B-2 site, impaired responsiveness to TNF-{alpha} and LMP1 in reporter assays. A mutant XMRV with a mutation at the {kappa}B-1 site replicated significantly less efficiently than the wild-type XMRV in the prostate carcinoma LNCaP, DU145, and PC-3 cell lines, HEK293 cells, the EBV-immortalized cell line IB4, and the Burkitt's lymphoma cell line BJAB. These results demonstrate that TNF-{alpha} and EBV LMP1 enhance XMRV replication in prostate carcinoma and B-lineage cells through the {kappa}B-1 site in the XMRV LTR, suggesting that inflammation, EBV infection, and other conditions leading to NF-{kappa}B activation may promote XMRV spread in humans.

* Corresponding author. Mailing address: Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 4134, Bethesda, MD 20892-1907. Phone: (301) 594-9597. Fax: (301) 594-9585. E-mail: [email protected]