Copenhagen Hepatitis C Program, Department of Infectious Diseases and Clinical Research Centre, Copenhagen University Hospital, Hvidovre, and Department of International Health, Immunology, and Microbiology, University of Copenhagen, Copenhagen, Denmark.
J Virol. 2013 Feb;87(3):1385-99. doi: 10.1128/JVI.00684-12. Epub 2012 Nov 14.
The hepatitis C virus (HCV) envelope proteins E1 and E2 play a key role in host cell entry and represent important targets for vaccine and drug development. Here, we characterized HCV recombinants with chimeric E1/E2 complexes in vitro. Using genotype 1a/2a JFH1-based recombinants expressing 1a core-NS2, we exchanged E2 with functional isolate sequences of genotypes 1a (alternative isolate), 1b, and 2a. While the 1a-E2 exchange did not impact virus viability, the 2a-E2 recombinant was nonviable. After E2 exchange from three 1b isolates, long delays were observed before spread of infection. For recovered 1b-E2 recombinants, single E2 stem region amino acid changes were identified at residues 706, 707, and 710. In reverse genetic studies, these mutations increased infectivity titers by ~100-fold, apparently without influencing particle stability or cell binding although introducing slight decrease in particle density. In addition, the 1b-E2 exchange led to a decrease in secreted core protein of 25 to 50%, which was further reduced by the E2 stem region mutations. These findings indicated that compensatory mutations permitted robust infectious virus production, without increasing assembly/release. Studies of E1/E2 heterodimerization showed no differences in intracellular E1/E2 interaction for chimeric constructs with or without E2 stem region mutations. Interestingly, the E2 stem region mutations allowed efficient entry, which was verified in 1a-E1/1b-E2 HCV pseudoparticle assays. A CD81 inhibition assay indicated that the mutations influenced a late step of the HCV entry pathway. Overall, this study identified specific amino acids in the E2 stem region of importance for HCV entry and for production of infectious virus particles.
丙型肝炎病毒(HCV)包膜蛋白 E1 和 E2 在宿主细胞进入中发挥关键作用,是疫苗和药物开发的重要靶点。在这里,我们在体外对具有嵌合 E1/E2 复合物的 HCV 重组体进行了表征。使用基于基因型 1a/2a JFH1 的重组体表达 1a 核心-NS2,我们用基因型 1a(替代株)、1b 和 2a 的功能性分离株序列交换 E2。虽然 1a-E2 交换不影响病毒活力,但 2a-E2 重组体是无活力的。在从三个 1b 分离株交换 E2 后,观察到感染传播之前出现长时间的延迟。对于恢复的 1b-E2 重组体,在残基 706、707 和 710 处鉴定到单个 E2 茎区氨基酸变化。在反向遗传学研究中,这些突变将感染性滴度提高了约 100 倍,显然不会影响颗粒稳定性或细胞结合,尽管略微降低了颗粒密度。此外,1b-E2 交换导致分泌的核心蛋白减少 25%至 50%,而 E2 茎区突变进一步降低了核心蛋白的表达。这些发现表明,补偿性突变允许产生强大的感染性病毒,而不会增加组装/释放。E1/E2 异二聚体研究表明,对于具有或不具有 E2 茎区突变的嵌合构建体,细胞内 E1/E2 相互作用没有差异。有趣的是,E2 茎区突变允许有效的进入,这在 1a-E1/1b-E2 HCV 假病毒测定中得到了验证。CD81 抑制测定表明,这些突变影响 HCV 进入途径的后期步骤。总的来说,这项研究确定了 E2 茎区对 HCV 进入和感染性病毒颗粒产生很重要的特定氨基酸。