This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ku, S. C. Y.
Right arrow Articles by Chao, S.-H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ku, S. C. Y.
Right arrow Articles by Chao, S.-H.

 Previous Article  |  Next Article 

Journal of Virology, May 2008, p. 4343-4353, Vol. 82, No. 9
0022-538X/08/$08.00+0     doi:10.1128/JVI.02054-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

XBP-1, a Novel Human T-Lymphotropic Virus Type 1 (HTLV-1) Tax Binding Protein, Activates HTLV-1 Basal and Tax-Activated Transcription{triangledown}

Sebastian C. Y. Ku,1 Jialing Lee,1 Joanne Lau,1 Meera Gurumurthy,1 Raymond Ng,1 Siew Hui Lwa,1 Joseph Lee,1 Zachary Klase,2 Fatah Kashanchi,2 and Sheng-Hao Chao1*

Expression Engineering Group, Bioprocessing Technology Institute, 20 Biopolis Way, #06-01 Centros, Singapore 138668, Singapore,1 Department of Biochemistry and Molecular Biology, George Washington University School of Medicine, Washington, DC 200372

Received 17 September 2007/ Accepted 11 February 2008

X-box binding protein 1 (XBP-1), a basic leucine zipper transcription factor, plays a key role in the cellular unfolded protein response (UPR). There are two XBP-1 isoforms in cells, spliced XBP-1S and unspliced XBP-1U. XBP-1U has been shown to bind to the 21-bp Tax-responsive element of the human T-lymphotropic virus type 1 (HTLV-1) long terminal repeat (LTR) in vitro and transactivate HTLV-1 transcription. Here we identify XBP-1S as a transcription activator of HTLV-1. Compared to XBP-1U, XBP-1S demonstrates stronger activating effects on both basal and Tax-activated HTLV-1 transcription in cells. Our results show that both XBP-1S and XBP-1U interact with Tax and bind to the HTLV-1 LTR in vivo. In addition, elevated mRNA levels of the gene for XBP-1 and several UPR genes were detected in the HTLV-1-infected C10/MJ and MT2 T-cell lines, suggesting that HTLV-1 infection may trigger the UPR in host cells. We also identify Tax as a positive regulator of the expression of the gene for XBP-1. Activation of the UPR by tunicamycin showed no effect on the HTLV-1 LTR, suggesting that HTLV-1 transcription is specifically regulated by XBP-1. Collectively, our study demonstrates a novel host-virus interaction between a cellular factor XBP-1 and transcriptional regulation of HTLV-1.


* Corresponding author. Mailing address: Expression Engineering Group, Bioprocessing Technology Institute, 20 Biopolis Way, #06-01 Centros, Singapore 138668, Singapore. Phone: (65) 6478-8899. Fax: (65) 6478-9561. E-mail: jimmy_chao{at}bti.a-star.edu.sg

{triangledown} Published ahead of print on 20 February 2008.


Journal of Virology, May 2008, p. 4343-4353, Vol. 82, No. 9
0022-538X/08/$08.00+0     doi:10.1128/JVI.02054-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.