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瑞德西韦抑制埃博拉病毒 RNA 依赖的 RNA 聚合酶的机制。

Mechanism of Inhibition of Ebola Virus RNA-Dependent RNA Polymerase by Remdesivir.

机构信息

Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, AB T6G 2E1, Canada.

Li Ka Shing Institute of Virology at University of Alberta, Edmonton, AB T6G 2E1, Canada.

出版信息

Viruses. 2019 Apr 4;11(4):326. doi: 10.3390/v11040326.

Abstract

Remdesivir (GS-5734) is a 1'-cyano-substituted adenosine nucleotide analogue prodrug that shows broad-spectrum antiviral activity against several RNA viruses. This compound is currently under clinical development for the treatment of Ebola virus disease (EVD). While antiviral effects have been demonstrated in cell culture and in non-human primates, the mechanism of action of Ebola virus (EBOV) inhibition for remdesivir remains to be fully elucidated. The EBOV RNA-dependent RNA polymerase (RdRp) complex was recently expressed and purified, enabling biochemical studies with the relevant triphosphate (TP) form of remdesivir and its presumptive target. In this study, we confirmed that remdesivir-TP is able to compete for incorporation with adenosine triphosphate (ATP). Enzyme kinetics revealed that EBOV RdRp and respiratory syncytial virus (RSV) RdRp incorporate ATP and remdesivir-TP with similar efficiencies. The selectivity of ATP against remdesivir-TP is ~4 for EBOV RdRp and ~3 for RSV RdRp. In contrast, purified human mitochondrial RNA polymerase (h-mtRNAP) effectively discriminates against remdesivir-TP with a selectivity value of ~500-fold. For EBOV RdRp, the incorporated inhibitor at position i does not affect the ensuing nucleotide incorporation event at position i+1. For RSV RdRp, we measured a ~6-fold inhibition at position i+1 although RNA synthesis was not terminated. Chain termination was in both cases delayed and was seen predominantly at position i+5. This pattern is specific to remdesivir-TP and its 1'-cyano modification. Compounds with modifications at the 2'-position show different patterns of inhibition. While 2'-C-methyl-ATP is not incorporated, ara-ATP acts as a non-obligate chain terminator and prevents nucleotide incorporation at position i+1. Taken together, our biochemical data indicate that the major contribution to EBOV RNA synthesis inhibition by remdesivir can be ascribed to delayed chain termination. The long distance of five residues between the incorporated nucleotide analogue and its inhibitory effect warrant further investigation.

摘要

瑞德西韦(GS-5734)是一种 1'-氰基取代的腺苷核苷酸类似物前药,对几种 RNA 病毒表现出广谱抗病毒活性。该化合物目前正在开发用于治疗埃博拉病毒病(EVD)。虽然在细胞培养和非人类灵长类动物中已经证明了抗病毒作用,但瑞德西韦抑制埃博拉病毒(EBOV)的作用机制仍有待充分阐明。埃博拉病毒 RNA 依赖性 RNA 聚合酶(RdRp)复合物最近被表达和纯化,使相关三磷酸(TP)形式的瑞德西韦及其假定靶标能够进行生化研究。在这项研究中,我们证实瑞德西韦-TP 能够与三磷酸腺苷(ATP)竞争掺入。酶动力学研究表明,EBOV RdRp 和呼吸道合胞病毒(RSV)RdRp 以相似的效率掺入 ATP 和瑞德西韦-TP。ATP 对瑞德西韦-TP 的选择性约为 EBOV RdRp 的 4 倍,RSV RdRp 的 3 倍。相比之下,纯化的人线粒体 RNA 聚合酶(h-mtRNAP)有效地将瑞德西韦-TP 区分开来,选择性值约为 500 倍。对于 EBOV RdRp,在位置 i 掺入的抑制剂不会影响位置 i+1 随后的核苷酸掺入事件。对于 RSV RdRp,我们测量到位置 i+1 的抑制约为 6 倍,尽管 RNA 合成没有终止。在两种情况下,链终止均被延迟,并且主要在位置 i+5 处观察到。这种模式是瑞德西韦-TP 及其 1'-氰基修饰所特有的。在 2'-位进行修饰的化合物表现出不同的抑制模式。虽然 2'-C-甲基-ATP 不被掺入,但ara-ATP 作为非必需的链终止子起作用,并阻止位置 i+1 的核苷酸掺入。总之,我们的生化数据表明,瑞德西韦抑制 EBOV RNA 合成的主要贡献可以归因于延迟的链终止。掺入的核苷酸类似物与其抑制作用之间相隔五个残基的长距离需要进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0178/6520719/36965e500e5b/viruses-11-00326-g001.jpg

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