%0 Journal Article
%T Cotranscriptional Chromatin Remodeling by Small RNA Species: An HTLV-1 Perspective
%A Nishat Aliya
%A Saifur Rahman
%A Zafar K. Khan
%A Pooja Jain
%J Leukemia Research and Treatment
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/984754
%X 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. 1. Introduction In the myriad interactions between viruses and host cells, there is a constant struggle for survival that causes both sides to adopt strategies counteracting each other¡¯s effect. More often than not, the error-prone replication of viruses offers them an advantage of selective pressure enabling them to accumulate genetic mutations over time that helps evade host immune defense mechanisms. Most chronic viruses seem to have an edge in this struggle in that they evolve means to manipulate and exploit host molecular pathways to persist in the hostile cellular environment and remain hidden from immune surveillance [1]. In this regard, retroviruses have succeeded in establishing latent infection and developing drug resistance through escape mutants like very few other chronic viruses. One of the strategies utilized by retroviruses is the modulation of chromatin structure and regulation of the rate at which transcription occurs in the target cell. Chromatin remodeling in the context of retroviral infection is being explored as a potent means of long-term persistence. Many studies have shown that the exercise of chromatin modulation in retroviral infection begins with the proviral integration into the host
%U http://www.hindawi.com/journals/lrt/2012/984754/