Induction of reactive oxygen species by human T-cell leukemia virus type 1 tax correlates with DNA damage and expression of cellular senescence marker.
Human T-cell leukemia virus type 1 (HTLV-1) Tax affects cellular genomic stability and senescence. As yet, the mechanism(s) for these events caused by Tax is incompletely understood. Here, we show that Tax expression in primary human cells induces reactive oxygen species (ROS), which elicits DNA damage and the expression of senescence marker. Treatment with a ROS scavenger or knockdown of Tax expression by small interfering RNA (siRNA) abrogated Tax-induced DNA damage and the expression of senescence marker. Our data suggest that ROS induction explains Tax-induced cellular DNA damage and cellular senescence.
Kinjo
Takao
T
Molecular Virology Section, Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Ham-Terhune
Julia
J
Peloponese
Jean-Marie
JM
Jeang
Kuan-Teh
KT
D002478:Cells, Cultured; D016922:Cellular Senescence; D004249:DNA Damage; D055785:Gene Knockdown Techniques; D016356:Gene Products, tax / Q000037:antagonists & inhibitors / Q000502:physiology*; D042822:Genomic Instability; D054884:Host-Pathogen Interactions; D015368:Human T-lymphotropic virus 1 / Q000472:pathogenicity*; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism* / Q000633:toxicity*; D015238:Sulfotransferases / Q000096:biosynthesis*
D016356:Gene Products, tax; D017382:Reactive Oxygen Species; C514970:tax protein, Human T-lymphotrophic virus 1; D015238:Sulfotransferases; C028152:alcohol sulfotransferase