Mitochondrial damage induced by HTLV-1 infection in host cells / 中华微生物学和免疫学杂志

ABSTRACT

Objective To investigate the effects of human adult T lymphoblastic leukemia virus typeⅠ (HTLV-1) infection on the production of reactive oxygen species (ROS) and mitochondrial damage in host cells. Methods A cell model of HTLV-1 infection was established by co-culturing HTLV-1-positive cell line MT2 with HeLa cells. ROS, mitochondrial membrane potential ( MMP) and total mitochondria were detected using specific fluorescence probe labeling method. Cell apoptosis was detected by Annexin V-FITC/PI method. Western blot was performed to detect viral proteins Tax and p19, as well as mitochondrial pro-teins TIM23 and TOM20. After the treatment of MT2 cells with different concentrations of reverse transcrip-tion inhibitors ( ZDV) , relative viral loads were detected by quantitative real-time PCR and Western blot, and the mass of mitochondria was analyzed by flow cytometry. Results After co-culturing HeLa cells with MT2 cells for 24 h, the ROS level in host cells increased without obvious cell apoptosis, while the mitochon-drial membrane potential, mitochondrial protein expression and total mitochondria decreased significantly. When the replication of HTLV-1 in MT2 cells was inhibited by ZDV, the ROS level and total mitochondria increased. Conclusions HTLV-1 infection can cause oxidative stress in host cells, resulting in mitochon-drial damage. Autophagy might be activated to degrade mitochondrial damage and maintain cell homeostasis during the infection.