TAILIEUCHUNG - Báo cáo y học: " Cell line-dependent variability in HIV activation employing DNMT inhibitors"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Cell line-dependent variability in HIV activation employing DNMT inhibitors | Fernandez and Zeichner Virology Journal 2010 7 266 http content 7 1 266 VIROLOGY JOURNAL SHORT REPORT Open Access Cell line-dependent variability in HIV activation employing DNMT inhibitors Guerau Fernandez1 Steven L Zeichner1 2 Abstract Long-lived reservoirs of Human Immunodeficiency Virus HIV latently infected cells present the main barrier to a cure for HIV infection. Much interest has focused on identifying strategies to activate HIV which would be used together with antiretrovirals to attack reservoirs. Several HIV activating agents including Tumor Necrosis Factor alpha TNFa and other agents that activate via NF-kB are not fully effective in all latent infection models due to epigenetic restrictions such as DNA methylation and the state of histone acetylation. DNA methyltransferases DNMT inhibitors like 5-aza-2 deoxycytidine Aza-CdR and histone deacetylase HDAC inhibitors like Trichostatin A TSA have been proposed as agents to enhance reactivation and have shown activity in model systems. However it is not clear how the activities of DNMT and HDAC inhibitors range across different latently infected cell lines potential models for the many different latently infected cells within an HIV patient. We determined HIV activation following treatment with TNFa TSA and Aza-CdR across a range of well known latently infected cell lines. We assessed the activity of these compounds in four different Jurkat T cell-derived J-Lat cell lines and which have a latent HIV provirus in which GFP replaces Nef coding sequence and ACH-2 and T cell-derived and U1 promonocyte-derived cell lines with full-length provirus. We found that Aza-CdR plus TNFa activated HIV at least twice as well as TNFa alone for almost all J-Lat cells as previously described but not for J-Lat in which TNFa plus Aza-CdR moderately decreased activation compared to TNFa alone. Surprisingly a much greater reduction of TNFa-stimulated activation with Aza-CdR was .

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