Laboratory of Cell Biology and Virology, Institute of Molecular Biology of NAS RA, Yerevan 0014, Armenia.
Experimental Laboratory, Yerevan State Medical University after Mkhitar Heratsi, Yerevan 0025, Armenia.
Viruses. 2022 Jul 22;14(8):1593. doi: 10.3390/v14081593.
African swine fever virus manipulates the cell cycle of infected G0 cells by inducing its progression via unblocking cells from the G0 to S phase and then arresting them in the G2 phase. DNA synthesis in infected alveolar macrophages starts at 10-12 h post infection. DNA synthesis in the nuclei of G0 cells is preceded by the activation of the viral genes K196R, A240L, E165R, F334L, F778R, and R298L involved in the synthesis of nucleotides and the regulation of the cell cycle. The activation of these genes in actively replicating cells begins later and is less pronounced. The subsequent cell cycle arrest at the G2 phase is also due to the cessation of the synthesis of cellular factors that control the progression of the cell cycle-cyclins. This data describes the manipulation of the cell cycle by the virus to gain access to the nucleotides synthesized by the cell. The genes affecting the cell cycle simply remain disabled until the beginning of cellular DNA synthesis (8-9 hpi). The genes responsible for the synthesis of nucleotides are turned on later in the presence of nucleotides and their transcriptional activity is lower than that during virus replication in an environment without nucleotides.
非洲猪瘟病毒通过解除 G0 期细胞向 S 期的阻滞并将其阻滞在 G2 期,从而操纵感染的 G0 细胞的细胞周期。感染肺泡巨噬细胞中的 DNA 合成始于感染后 10-12 小时。G0 细胞中 DNA 合成之前,与核苷酸合成和细胞周期调控相关的病毒基因 K196R、A240L、E165R、F334L、F778R 和 R298L 被激活。在活跃复制的细胞中,这些基因的激活较晚且不明显。随后在 G2 期的细胞周期阻滞也归因于控制细胞周期进程的细胞因子——周期蛋白的合成停止。这些数据描述了病毒对细胞周期的操纵,以获取细胞合成的核苷酸。影响细胞周期的基因在细胞 DNA 合成开始之前(8-9 hpi)简单地保持失活。在存在核苷酸的情况下,负责核苷酸合成的基因被打开,但它们的转录活性低于在没有核苷酸的环境中进行病毒复制时的转录活性。