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Int J Mol Sci. 2022 Oct 21;23(20):12649. doi: 10.3390/ijms232012649.
RNA-dependent RNA polymerase (RdRP) is essential for the replication and expression of RNA viral genomes. This class of viruses comprise a large number of highly pathogenic agents that infect essentially all species of plants and animals including humans. Infections often lead to epidemics and pandemics that have remained largely out of control due to the lack of specific and reliable preventive and therapeutic regimens. This unmet medical need has led to the exploration of new antiviral targets, of which RdRP is a major one, due to the fact of its obligatory need in virus growth. Recent studies have demonstrated the ability of several synthetic nucleoside analogs to serve as mimics of the corresponding natural nucleosides. These mimics cause stalling/termination of RdRP, or misincorporation, preventing virus replication or promoting large-scale lethal mutations. Several such analogs have received clinical approval and are being routinely used in therapy. In parallel, the molecular structural basis of their inhibitory interactions with RdRP is being elucidated, revealing both traditional and novel mechanisms including a delayed chain termination effect. This review offers a molecular commentary on these mechanisms along with their clinical implications based on analyses of recent results, which should facilitate the rational design of structure-based antiviral drugs.
RNA 依赖性 RNA 聚合酶(RdRP)是 RNA 病毒基因组复制和表达所必需的。这类病毒包含大量高度致病的病原体,感染了包括人类在内的几乎所有动植物物种。由于缺乏特定和可靠的预防和治疗方案,这些感染经常导致流行病和大流行,而且基本上无法控制。由于 RdRP 在病毒生长中的强制性需求,这种未满足的医疗需求促使人们探索新的抗病毒靶点,其中 RdRP 是一个主要靶点。最近的研究表明,几种合成核苷类似物能够作为相应天然核苷的模拟物。这些模拟物会导致 RdRP 停滞/终止或错误掺入,从而阻止病毒复制或促进大规模致死突变。其中一些类似物已获得临床批准,并在常规治疗中使用。与此同时,它们与 RdRP 抑制相互作用的分子结构基础正在被阐明,揭示了包括传统和新型机制在内的机制,包括延迟链终止效应。基于对最近结果的分析,本综述对这些机制及其临床意义进行了分子评论,这应该有助于基于结构的抗病毒药物的合理设计。