tailieunhanh - Báo cáo y học: "Chromatin, gene silencing and HIV latency"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Chromatin, gene silencing and HIV latency. | Review Chromatin gene silencing and HIV latency Hoi-Ping Mok and Andrew ML Lever Address Department of Medicine University of Cambridge Addenbrooke s Hospital Cambridge CB2 2QQ UK. Correspondence Andrew ML Lever. Email amll1@ Published 23 November 2007 Genome Biology 2007 8 228 doi gb-2007-8-ll-228 The electronic version of this article is the complete one and can be found online at http 2007 8 ll 228 2007 BioMed Central Ltd Abstract One of the cellular defenses against virus infection is the silencing of viral gene expression. There is evidence that at least two gene-silencing mechanisms are used against the human immunodeficiency virus HIV . Paradoxically this cellular defense mechanism contributes to viral latency and persistence and we review here the relationship of viral latency to gene-silencing mechanisms. To succeed all long-term relationships require some degree of compromise from both partners. This is no less true for persistent virus infections and their hosts. Unrestricted replication of the parasite may be to the detriment of the health of the host and shorten its life span thus depriving the parasite of its niche. Equally no replication at all is a dead end for the parasite. The pathogen thus constrains its replication and the host given that it has effectively lost the battle to eliminate the invader makes the best of a bad job and controls it when it gets out of hand. Restricting replication quantitatively or temporally so that the virus reproduces just sufficiently or at particularly strategic times for example pregnancy to achieve transmission while remaining silent at other times latency are techniques used by several viral families of which the herpesviruses are the best studied. The human immunodeficiency virus HIV the causative agent of AIDS is also postulated to become latent when it infects a T lymphocyte T cell that has ceased to divide and where levels of transcription factors that both cell .

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