Epigenetic Control of Kaposi's Sarcoma-Associated Herpesvirus Latency and Reactivation

• 作 者: JiguoChen;
• 机 构: Department of Biological Sciences Mississippi State University P.O.Box GY USA
• 出 处: BIT‘s2nd Annual World Cancer Congess-2009 (2009第二届癌症大会)
• 发表日期: 2009年期

　　A key unresolved question in tumor virology is why a benign viral infection for one individual turns to be a lethal cancer for another.Kaposis sarcoma-associated herpesvirus (KSHV) is believed to be an etiologic agent strictly necessary for the development of Kaposis sarcoma, yet very few infected people ever develop cancer.Primary to answering these questions is the development of experimental cellular and animal models to study virus-host cell interactions.One of these cellular models we established is used to elucidate genetic switch on/off mechanisms.In this cellular model, a recombinant luciferase reporter virus was constructed and introduced into its host cells using Bacterial Artificial Chromosome (BAC) technology.In previous studies, we demonstrated that DNA methylation in the RTA promoter regulated its expression and demethylation was an important first step towards lytic re-activation.