Cotranscriptional Chromatin Remodeling by Small RNA Species: An HTLV-1 Perspective.
Cotranscriptional Chromatin Remodeling by Small RNA Species: An HTLV-1 Perspective.
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DOI：
10.1155/2012/984754
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发表时间：
2012-01-01
期刊：
影响因子：
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通讯作者：
Jain, Pooja
中科院分区：
文献类型：
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作者：
Aliya, Nishat;Rahman, Saifur;Jain, Pooja
人 T 细胞白血病病毒 1 的细胞类型特异性被认为是初级靶细胞与次级靶细胞中病毒结果不同的可能原因。通过染色质重塑，HTLV-1 反式激活蛋白 Tax 与染色体整合的病毒启动子处的细胞因子相互作用，激活下游基因并控制病毒转录。 RNA 干扰是由调节基因表达的短 RNA 种类（siRNA 或 miRNA）介导的宿主先天防御机制。细胞转录因子与 miRNA 存在密切的协同功能，以调节许多真核基因的表达，包括那些参与抑制细胞生长、诱导细胞凋亡以及抑制病毒复制和传播的基因。此外，有人认为逆转录病毒潜伏期受到 miRNA 引起的染色质改变的影响。由于 Tax 需要组装转录辅助因子来进行病毒基因表达，因此影响染色质改变的 miRNA 与 Tax 介导的 LTR 激活之间可能存在密切关联。在此，我们探讨了 HTLV-1 感染和导致染色质重组的 miRNA 途径之间可能的相互作用，这是决定不同细胞类型中 HTLV-1 细胞特异性和病毒命运的机制之一。
Cell type specificity of human T cell leukemia virus 1 has been proposed as a possible reason for differential viral outcome in primary target cells versus secondary. Through chromatin remodeling, the HTLV-1 transactivator protein Tax interacts with cellular factors at the chromosomally integrated viral promoter to activate downstream genes and control viral transcription. RNA interference is the host innate defense mechanism mediated by short RNA species (siRNA or miRNA) that regulate gene expression. There exists a close collaborative functioning of cellular transcription factors with miRNA in order to regulate the expression of a number of eukaryotic genes including those involved in suppression of cell growth, induction of apoptosis, as well as repressing viral replication and propagation. In addition, it has been suggested that retroviral latency is influenced by chromatin alterations brought about by miRNA. Since Tax requires the assembly of transcriptional cofactors to carry out viral gene expression, there might be a close association between miRNA influencing chromatin alterations and Tax-mediated LTR activation. Herein we explore the possible interplay between HTLV-1 infection and miRNA pathways resulting in chromatin reorganization as one of the mechanisms determining HTLV-1 cell specificity and viral fate in different cell types.