Cojohari Olesea, Burrer Christine M, Peppenelli Megan A, Abulwerdi Fardokht A, Nikolovska-Coleska Zaneta, Chan Gary C
Department of Microbiology & Immunology, SUNY Upstate Medical University, Syracuse, New York, USA.
Department of Pathology, University of Michigan, Ann Arbor, Michigan, USA.
J Virol. 2015 May;89(10):5739-46. doi: 10.1128/JVI.00236-15. Epub 2015 Mar 4.
Herpesviruses, including human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), and Kaposi's sarcoma-associated herpesvirus, establish latency by modulating or mimicking antiapoptotic Bcl-2 proteins to promote survival of carrier cells. BH3 profiling, which assesses the contribution of Bcl-2 proteins towards cellular survival, was able to globally determine the level of dependence on individual cellular and viral Bcl-2 proteins within latently infected cells. Moreover, BH3 profiling predicted the sensitivity of infected cells to small-molecule inhibitors of Bcl-2 proteins.
疱疹病毒,包括人类巨细胞病毒(HCMV)、爱泼斯坦-巴尔病毒(EBV)和卡波西肉瘤相关疱疹病毒,通过调节或模拟抗凋亡Bcl-2蛋白来建立潜伏状态,以促进载体细胞的存活。BH3分析可评估Bcl-2蛋白对细胞存活的贡献,它能够全面确定潜伏感染细胞对个体细胞和病毒Bcl-2蛋白的依赖程度。此外,BH3分析还可预测感染细胞对Bcl-2蛋白小分子抑制剂的敏感性。