Choi Young Bong, Harhaj Edward William
Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns HopkinsSchool of Medicine, Baltimore, MD 21287, USA.
Front Biol (Beijing). 2014 Dec;9(6):423-436. doi: 10.1007/s11515-014-1332-0.
Between 15-20% of human cancers are associated with infection by oncogenic viruses. Oncogenic viruses, including HPV, HBV, HCV and HTLV-1, target mitochondria to influence cell proliferation and survival. Oncogenic viral gene products also trigger the production of reactive oxygen species which can elicit oxidative DNA damage and potentiate oncogenic host signaling pathways. Viral oncogenes may also subvert mitochondria quality control mechanisms such as mitophagy and metabolic adaptation pathways to promote virus replication. Here, we will review recent progress on viral regulation of mitophagy and metabolic adaptation and their roles in viral oncogenesis.
15%至20%的人类癌症与致癌病毒感染有关。致癌病毒，包括人乳头瘤病毒（HPV）、乙肝病毒（HBV）、丙肝病毒（HCV）和人类嗜T淋巴细胞病毒1型（HTLV-1），靶向线粒体以影响细胞增殖和存活。致癌病毒基因产物还会触发活性氧的产生，活性氧可引发氧化性DNA损伤并增强致癌的宿主信号通路。病毒癌基因也可能破坏线粒体质量控制机制，如线粒体自噬和代谢适应途径，以促进病毒复制。在此，我们将综述病毒对线粒体自噬和代谢适应的调控及其在病毒致癌作用中的作用的最新进展。
