Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Department of Microbiology and Immunology, Faculty of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.
PLoS Pathog. 2022 Jun 3;18(6):e1010593. doi: 10.1371/journal.ppat.1010593. eCollection 2022 Jun.
Flaviviruses, which are globally distributed and cause a spectrum of potentially severe illnesses, pose a major threat to public health. Although Flaviviridae viruses, including flaviviruses, possess similar genome structures, only the flaviviruses encode the non-structural protein NS1, which resides in the endoplasmic reticulum (ER) and is secreted from cells after oligomerization. The ER-resident NS1 is known to be involved in viral genome replication, but the essential roles of secretory NS1 in the virus life cycle are not fully understood. Here we characterized the roles of secretory NS1 in the particle formation of flaviviruses. We first identified an amino acid residue essential for the NS1 secretion but not for viral genome replication by using protein-protein interaction network analyses and mutagenesis scanning. By using the recombinant flaviviruses carrying the identified NS1 mutation, we clarified that the mutant flaviviruses employed viral genome replication. We then constructed a recombinant NS1 with the identified mutation and demonstrated by physicochemical assays that the mutant NS1 was unable to form a proper oligomer or associate with liposomes. Finally, we showed that the functions of NS1 that were lost by the identified mutation could be compensated for by the in trans-expression of Erns of pestiviruses and host exchangeable apolipoproteins, which participate in the infectious particle formation of pestiviruses and hepaciviruses in the family Flaviviridae, respectively. Collectively, our study suggests that secretory NS1 plays a role in the particle formation of flaviviruses through its interaction with the lipid membrane.
黄病毒在全球范围内分布广泛,可引起一系列潜在严重疾病,对公共卫生构成重大威胁。尽管黄病毒科病毒(包括黄病毒)具有相似的基因组结构,但只有黄病毒编码非结构蛋白 NS1,该蛋白位于内质网(ER)中,并在寡聚化后从细胞中分泌。已知 ER 驻留的 NS1 参与病毒基因组复制,但分泌型 NS1 在病毒生命周期中的重要作用尚未完全阐明。在这里,我们研究了分泌型 NS1 在黄病毒颗粒形成中的作用。我们首先通过蛋白质-蛋白质相互作用网络分析和突变扫描鉴定了一个对 NS1 分泌而非病毒基因组复制至关重要的氨基酸残基。通过使用携带鉴定出的 NS1 突变的重组黄病毒,我们阐明了突变型黄病毒利用病毒基因组复制。然后,我们构建了一个带有鉴定出的突变的重组 NS1,并通过物理化学分析表明,突变型 NS1 无法形成适当的寡聚体或与脂质体结合。最后,我们表明,通过转染表达瘟病毒的 Erns 和参与黄病毒科瘟病毒和肝病毒感染性颗粒形成的宿主可交换载脂蛋白,可以补偿由鉴定出的突变导致的 NS1 功能丧失。总之,我们的研究表明,分泌型 NS1 通过与脂膜相互作用在黄病毒的颗粒形成中发挥作用。