Mitochondrial damage induced by HTLV-1 infection in host cells
10.3760/cma.j.issn.0254-5101.2019.12.003
- VernacularTitle: HTLV-1病毒感染诱导宿主细胞线粒体损伤
- Author:
Xue YANG
1
;
Yecheng XIE
1
;
Yilin GUO
2
;
Xuelu LI
2
;
Huandi LIU
1
;
Liangwei DUAN
1
;
Yuna NIU
1
Author Information
1. School of Laboratory Medicine, Xinxiang Medical University, Henan Key Laboratory of Immunology and Targeted Drugs, Xinxiang 453003, China
2. Scientific Research Innovation Group, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang 453003, China
- Publication Type:Journal Article
- Keywords:
Human adult T lymphoblastic leukemia virus typeⅠ;
Reactive oxygen species;
Oxidative stress;
Mitochondrial damage
- From:
Chinese Journal of Microbiology and Immunology
2019;39(12):898-903
- CountryChina
- Language:Chinese
-
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 proteins TIM23 and TOM20. After the treatment of MT2 cells with different concentrations of reverse transcription 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 mitochondrial 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 mitochondrial damage. Autophagy might be activated to degrade mitochondrial damage and maintain cell homeostasis during the infection.
