Low C-F, Syarul Nataqain B, Chee H-Y, Rozaini M Z H, Najiah M
Institute of Systems Biology, Universiti Kebangsaan Malaysia, Bangi, Selangor, Malaysia.
Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Selangor, Malaysia.
J Fish Dis. 2017 Nov;40(11):1489-1496. doi: 10.1111/jfd.12638. Epub 2017 Apr 27.
Progressive research has been recently made in dissecting the molecular biology of Betanodavirus life cycle, the causative pathogen of viral encephalopathy and retinopathy in economic important marine fish species. Establishment of betanodavirus infectious clone allows the manipulation of virus genome for functional genomic study, which elucidates the biological event of the viral life cycle at molecular level. The betanodavirus strategizes its replication by expressing anti-apoptosis/antinecrotic proteins to maintain the cell viability during early infection. Subsequently utilizes and controls the biological machinery of the infected cells for viral genome replication. Towards the late phase of infection, mass production of capsid protein for virion assembly induces the activation of host apoptosis pathway. It eventually leads to the cell lysis and death, which the lysis of cell contributes to the accomplishment of viral shedding that completes a viral life cycle. The recent efforts to dissect the entire betanodavirus life cycle are currently reviewed.
近来,在剖析经济重要海洋鱼类病毒性脑病和视网膜病的致病病原体——β-诺达病毒生命周期的分子生物学方面取得了渐进性研究进展。β-诺达病毒感染性克隆的建立使得对病毒基因组进行操作以开展功能基因组学研究成为可能,这在分子水平上阐明了病毒生命周期的生物学事件。β-诺达病毒通过表达抗凋亡/抗坏死蛋白来维持早期感染期间的细胞活力,从而规划其复制过程。随后利用并控制被感染细胞的生物机制进行病毒基因组复制。在感染后期,大量产生用于病毒粒子组装的衣壳蛋白会诱导宿主凋亡途径的激活。这最终导致细胞裂解和死亡,细胞裂解有助于完成病毒释放,从而完成病毒生命周期。本文对近期剖析整个β-诺达病毒生命周期的研究工作进行了综述。