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Novel Interactions between the Human T-Cell Leukemia Virus Type 1 Antisense Protein HBZ and the SWI/SNF Chromatin Remodeling Family: Implications for Viral Life Cycle
Author(s) -
Ahlam Alasiri,
Jorge Abboud Guerr,
William W. Hall,
Noreen Sheehy
Publication year - 2019
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.00412-19
Subject(s) - biology , swi/snf , transactivation , chromatin remodeling , chromatin immunoprecipitation , chromatin , transcription factor , microbiology and biotechnology , immunoprecipitation , transcription (linguistics) , chromatin structure remodeling (rsc) complex , human t lymphotropic virus 1 , repressor , viral protein , regulation of gene expression , leukemia , gene expression , gene , genetics , virus , promoter , t cell leukemia , linguistics , philosophy
The pathogenic potential of HTLV-1 is linked to the indispensable multifaceted functions of the viral regulatory proteins Tax and HBZ, encoded by the sense and antisense viral transcripts, respectively. The interaction between Tax and the SWI/SNF family of chromatin remodeling complexes has been associated with HTLV-1 transcriptional activation. To date, the relationship between the SWI/SNF chromatin remodeling family and HBZ, the only viral protein that is consistently expressed in infected cells and ATL cells, has not been elucidated. Here, we have characterized the biological significance of the SWI/SNF family in regard to viral transcriptional repression by HBZ. This is important because it provides a better understanding of the function and role of HBZ in downregulating viral transcription and, hence, its contribution to viral latency and persistencein vivo , a process that may ultimately lead to the development of ATL.

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