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Stress granules inhibit apoptosis by reducing ROS production, but this phenomenon is nullified by HTLV-1 Tax

Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia (ATL), and the viral oncoprotein Tax plays key roles in immortalization of human T-cells and leukemogenesis. Here, we identified the ubiquitin-specific protease 10 (USP10) as a Tax-interactor in T-cells. Upon an exposure to arsenic, an oxidative stress inducer, USP10 was recruited into stress granules (SGs), which are the anti-stress machinery. USP10-knockout indicated that USP10, through augmenting formation of SGs, reduced reactive oxygen species (ROS) production and inhibited ROS-dependent apoptosis. Tax mutants and USP10-knockdown indicated that Tax inhibits arsenic-induced SG formation, stimulates ROS production and augments ROS-dependent apoptosis, and they are all dependent on interactions of Tax with USP10. These findings suggest that USP10 is a host factor that controls stress-induced ROS production and apoptosis in HTLV-1-infected T-cells. A clinical trial showed that a combination therapy containing arsenic is effective against some forms of ATL. Thus, these findings may also be relevant to chemotherapy against ATL.

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Correspondence to Masahiko Takahashi.

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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.

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Takahashi, M., Higuchi, M. & Fujii, M. Stress granules inhibit apoptosis by reducing ROS production, but this phenomenon is nullified by HTLV-1 Tax. Retrovirology 11 (Suppl 1), O52 (2014).

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