Peng Qi, Dong Yingying, Jia Mingzhu, Liu Qiannv, Bi Yuhai, Qi Jianxun, Shi Yi
Beijing Life Science Academy, Beijing, China.
CAS Key Laboratory of Pathogen Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Nat Commun. 2024 Dec 3;15(1):10524. doi: 10.1038/s41467-024-54994-5.
Nipah virus (NiV) is a non-segmented, negative-strand (NNS) RNA virus, belonging to Paramyxoviridae. The RNA polymerase complex, composed of large (L) protein and tetrameric phosphoprotein (P), is responsible for genome transcription and replication by catalyzing NTP polymerization, mRNA capping and cap methylation. Here, we determine the cryo-electron microscopy (cryo-EM) structure of fully bioactive NiV L-P polymerase complex at a resolution of 3.19 Å. The L-P complex displays a conserved architecture like other NNS RNA virus polymerases and L interacts with the oligomerization domain and the extreme C-terminus region of P tetramer. Moreover, we elucidate that NiV is naturally resistant to the allosteric L-targeting inhibitor GHP-88309 due to the conformational change in the drug binding site. We also find that the non-nucleotide drug suramin can inhibit the NiV L-P polymerase activity at both the enzymatic and cellular levels. Our findings have greatly enhanced the molecular understanding of NiV genome replication and transcription and provided the rationale for broad-spectrum polymerase-targeted drug design.
尼帕病毒(NiV)是一种不分节段的负链(NNS)RNA病毒,属于副粘病毒科。由大(L)蛋白和四聚体磷蛋白(P)组成的RNA聚合酶复合物,通过催化NTP聚合、mRNA加帽和帽甲基化来负责基因组转录和复制。在此,我们以3.19 Å的分辨率确定了具有完全生物活性的NiV L-P聚合酶复合物的冷冻电子显微镜(cryo-EM)结构。L-P复合物呈现出与其他NNS RNA病毒聚合酶相似的保守结构,并且L与P四聚体的寡聚化结构域和极端C末端区域相互作用。此外,我们阐明由于药物结合位点的构象变化,NiV对变构L靶向抑制剂GHP-88309天然耐药。我们还发现非核苷酸药物苏拉明在酶促和细胞水平上均可抑制NiV L-P聚合酶活性。我们的研究结果极大地增强了对NiV基因组复制和转录的分子理解,并为广谱聚合酶靶向药物设计提供了理论依据。