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Viruses 2016, 8(2), 34; doi:10.3390/v8020034

The Role of HBZ in HTLV-1-Induced Oncogenesis

1
College of Chemistry and Life Sciences, Zhejiang Normal University, 688 Yingbin Road, Jinhua 321004, China
2
Key Lab of Wildlife Biotechnology and Conservation and Utilization of Zhejiang Province, Zhejiang Normal University, 688 Yingbin Road, Jinhua 321004, China
Academic Editor: Louis M. Mansky
Received: 28 October 2015 / Revised: 25 January 2016 / Accepted: 28 January 2016 / Published: 2 February 2016
(This article belongs to the Special Issue Recent Advances in HTLV Research 2015)
View Full-Text   |   Download PDF [1462 KB, uploaded 2 February 2016]   |  

Abstract

Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL) and chronic inflammatory diseases. HTLV-1 bZIP factor (HBZ) is transcribed as an antisense transcript of the HTLV-1 provirus. Among the HTLV-1-encoded viral genes, HBZ is the only gene that is constitutively expressed in all ATL cases. Recent studies have demonstrated that HBZ plays an essential role in oncogenesis by regulating viral transcription and modulating multiple host factors, as well as cellular signaling pathways, that contribute to the development and continued growth of cancer. In this article, I summarize the current knowledge of the oncogenic function of HBZ in cell proliferation, apoptosis, T-cell differentiation, immune escape, and HTLV-1 pathogenesis. View Full-Text
Keywords: HBZ; HTLV-1; ATL HBZ; HTLV-1; ATL
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Zhao, T. The Role of HBZ in HTLV-1-Induced Oncogenesis. Viruses 2016, 8, 34.

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