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Blood, 15 May 2006, Vol. 107, No. 10, pp. 3976-3982. Prepublished online as a Blood First Edition Paper on January 19, 2006; DOI 10.1182/blood-2005-11-4551. This Article Full Text (PDF) All Versions of this Article: 2005-11-4551v1 107/10/3976    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Arnold, J. Articles by Green, P. L Search for Related Content PubMed PubMed Citation Articles by Arnold, J. Articles by Green, P. L Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 17, 2005 Accepted January 7, 2006 Enhancement of infectivity and persistence in vivo by HBZ, a natural antisense coded protein of HTLV-1 Joshua Arnold, Brenda Yamamoto, Min Li, Andrew J Phipps, Ihab Younis, Michael D Lairmore, and Patrick L Green* Departments of Veterinary Biosciences and Molecular Virology Immunology, and Medical Genetics, Center for Retrovirus Research, Comprehensive Cancer Center and Solove Research Institute, The Ohio State University, Columbus, OH, USA * Corresponding author; email: green.466{at}osu.edu. Natural antisense viral transcripts have been recognized in retroviruses including HTLV-1, HIV-1, and FIV and have been postulated to encode proteins important for the infection cycle and/or pathogenesis of the virus. The antisense strand of the HTLV-1 genome encodes HBZ, a novel nuclear b-ZIP protein, that in over-expression assays down-regulates Tax oncoprotein-induced viral transcription. Herein, we investigated the contribution of HBZ to HTLV-1-mediated immortalization of primary T-lymphocytes in vitro and HTLV-1 infection in a rabbit animal model. HTLV-1 HBZ mutant viruses were generated and evaluated for viral gene expression, protein production, and immortalization capacity. Biological properties of HBZ mutant viruses in vitro were indistinguishable from wild type HTLV-1 providing the first direct evidence that HBZ is dispensable for viral replication and cellular immortalization. Rabbits inoculated with irradiated cells expressing HTLV-1 HBZ mutant viruses became persistently infected. However, these rabbits displayed a decreased antibody response to viral gene products and reduced proviral copies in PBMCs as compared to wild type HTLV-1 infected animals. Our findings indicated that HBZ was not required for in vitro cellular immortalization, but enhanced infectivity and persistence in inoculated rabbits. This study demonstrates that retroviruses utilize negative strand-encoded proteins in the establishment of chronic viral infections. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: HTLV-1 HBZ: stop making sense Gerold Feuer Blood 2006 107: 3813-3814. [Full Text] [PDF] This article has been cited by other articles: M. Halin, E. Douceron, I. Clerc, C. Journo, N. L. Ko, S. Landry, E. L. Murphy, A. Gessain, I. Lemasson, J.-M. Mesnard, et al. Human T-cell leukemia virus type 2 produces a spliced antisense transcript encoding a protein that lacks a classic bZIP domain but still inhibits Tax2-mediated transcription Blood, September 17, 2009; 114(12): 2427 - 2438. [Abstract] [Full Text] [PDF] L. Xie, M. Kesic, B. Yamamoto, M. Li, I. Younis, M. D. Lairmore, and P. L. 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