Longworth Steven, Damania Blossom
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
J Med Virol. 2025 Jan;97(1):e70157. doi: 10.1002/jmv.70157.
The cell cycle is governed by kinase activity that coordinates progression through a series of regulatory checkpoints, preventing the division of damaged cells. The Kaposi's sarcoma-associated herpesvirus (KSHV) encodes multiple genes that modulate or co-opt the activity of these kinases, shaping the cellular environment to promote viral persistence. By advancing the cell cycle, KSHV facilitates latent replication and subsequent transmission of viral genomes to daughter cells, while also contributing to the establishment of multiple cancer types. Conversely, during viral lytic replication, KSHV extends the resting phase of the cell cycle to prevent cellular DNA synthesis that would otherwise compete for essential replication precursors. This review will examine the mechanisms KSHV has evolved to control the kinase activity regulating host cell cycle progression.
细胞周期受激酶活性调控,激酶活性协调细胞通过一系列调控检查点的进程,防止受损细胞分裂。卡波西肉瘤相关疱疹病毒(KSHV)编码多个基因,这些基因可调节或利用这些激酶的活性,塑造细胞环境以促进病毒持续存在。通过推进细胞周期,KSHV促进病毒基因组的潜伏复制及随后向子代细胞的传播,同时也促成多种癌症类型的发生。相反,在病毒裂解复制期间,KSHV延长细胞周期的静止期,以防止细胞DNA合成,否则细胞DNA合成会竞争必需的复制前体。本综述将探讨KSHV为控制调节宿主细胞周期进程的激酶活性而进化出的机制。