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  • Oral presentation
  • Open Access

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

Retrovirology201411 (Suppl 1) :O52

https://doi.org/10.1186/1742-4690-11-S1-O52

  • Published:

Keywords

  • Reactive Oxygen Species
  • Arsenic
  • Reactive Oxygen Species Production
  • Stress Granule
  • Oxidative Stress Inducer

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.

Authors’ Affiliations

(1)
Division of Virology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan

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