Hypothesis & Theory ARTICLE
Differential transforming activity of the retroviral Tax oncoproteins in human T lymphocytes
- 1Penn State Hershey Cancer Institute, Hershey, PA, USA
- 2Institute of Human Virology, School of Medicine, University of Maryland, Baltimore, MD, USA
Human T cell leukemia virus type 1 and type 2 (HTLV-1 and -2) are two closely related retroviruses. HTLV-1 causes adult T cell leukemia and lymphoma, whereas HTLV-2 infection is not etiologically linked to human disease. The viral genomes of HTLV-1 and -2 encode highly homologous transforming proteins, Tax-1 and Tax-2, respectively. Tax-1 is thought to play a central role in transforming CD4+ T lymphocytes. Expression of Tax-1 is crucial for promoting survival and proliferation of virally infected human T lymphocytes and is necessary for initiating HTLV-1-mediated oncogenesis. In transgenic mice and humanized mouse model, Tax-1 has proven to be leukemogenic. Although Tax-1 is able to efficiently transform rodent fibroblasts and to induce lymphoma in mouse model, it rarely transforms primary human CD4+ T lymphocytes. In contrast, Tax-2 efficiently immortalizes human CD4+ T cells though it exhibits a lower transforming activity in rodent cells as compared to Tax-1. We here discuss our recent observation and views on the differential transforming activity of Tax-1 and Tax-2 in human T cells.
Keywords: HTLV-1/-2, Tax, human T lymphocytes, immortalization, transformation
Citation: Ren T and Cheng H (2013) Differential transforming activity of the retroviral Tax oncoproteins in human T lymphocytes. Front. Microbiol. 4:287. doi: 10.3389/fmicb.2013.00287
Received: 30 July 2013; Accepted: 05 September 2013;
Published online: 23 September 2013.
Edited by:Umberto Bertazzoni, University of Verona, Italy
Reviewed by:Masanori Baba, Kagoshima University, Japan
Edward Harhaj, Johns Hopkins School of Medicine, USA
Masahiro Fujii, Niigata University Graduate School of Medical and Dental sciences, Japan
Copyright © 2013 Ren and Cheng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Hua Cheng, Institute of Human Virology, School of Medicine, University of Maryland, 655 West Baltimore Street, Baltimore, MD 21201, USA e-mail: firstname.lastname@example.org