Chaetocin reactivates the lytic replication of Epstein-Barr virus from latency via reactive oxygen species

• Published in: Science China. Life sciences 2017, Vol.60 (1), p.66-71
• Main Authors: Zhang, Shilun, Yin, Juan, Zhong, Jiang
• Format: Article
• Language: English
• Subjects: Acetylcysteine - pharmacology; Animals; Antigens, Viral - genetics; Antigens, Viral - metabolism; B-Lymphocytes - drug effects; B-Lymphocytes - metabolism; B-Lymphocytes - virology; Biomedical and Life Sciences; Blotting, Western; Callithrix; Cell Line, Transformed; DNA复制; Dose-Response Relationship, Drug; EB病毒; Epstein-Barr virus; Free Radical Scavengers - pharmacology; Gene Expression Regulation - drug effects; Glutathione Peroxidase - genetics; Glutathione Peroxidase - metabolism; Herpesvirus 4, Human - drug effects; Herpesvirus 4, Human - genetics; Herpesvirus 4, Human - physiology; Histones - metabolism; Host-Pathogen Interactions - drug effects; Humans; Life Sciences; Lysine - metabolism; Methylation - drug effects; N-乙酰半胱氨酸; NADH Dehydrogenase - genetics; NADH Dehydrogenase - metabolism; Piperazines - pharmacology; Reactive Oxygen Species - antagonists & inhibitors; Reactive Oxygen Species - metabolism; Research Paper; Reverse Transcriptase Polymerase Chain Reaction; Trans-Activators - genetics; Trans-Activators - metabolism; Virus Activation - drug effects; Virus Activation - genetics; Virus Latency - drug effects; Virus Latency - genetics; Virus Replication - drug effects; Virus Replication - genetics; 复活; 延迟; 感染细胞; 活性氧; 裂解
• ISSN: 1674-7305; 1869-1889
• DOI: 10.1007/s11427-016-0286-7

Oxidative stress, regarded as a negative effect of free radicals in vivo, takes place when organisms suffer from harmful stimuli. Some viruses can induce the release of reactive oxygen species （ROS） in infected cells, which may be closely related with their pathogenicity. In this report, chaetocin, a fimgal metabolite reported to have antimicrobial and cytostatic activity, was studied for its effect on the activation of latent Epstein-Barr virus （EBV） in B95-8 cells. We found that chaetocin remarkably up-regulated EBV lytic transcription and DNA replication at a low concentration （50 nmol L-l）. The activation of latent EBV was accompanied by an increased cellular ROS level. N-acetyl-L-cysteine （NAC）, an ROS inhibitor, suppressed chaetocin-induced EBV activation. Chaetocin had little effect on histone H3K9 methylation, while NAC also significantly reduced H3K9 methylation. These results suggested that chaetocin reactivates latent EBV primarily via ROS pathways.