Department of Biochemistry and Molecular Biology, Life Sciences Institute, University of British Columbia, Vancouver BC, V6T 1Z3, Canada.
Michael Smith Laboratories, University of British Columbia, Vancouver BC, V6T 1Z3, Melbourne, Australia.
Sci Rep. 2018 Nov 26;8(1):17353. doi: 10.1038/s41598-018-35717-5.
Viruses are classically characterized as being either enveloped or nonenveloped depending on the presence or absence of a lipid bi-layer surrounding their proteinaceous capsid. In recent years, many studies have challenged this view by demonstrating that some nonenveloped viruses (e.g. hepatitis A virus) can acquire an envelope during infection by hijacking host cellular pathways. In this study, we examined the role of exosome-like vesicles (ELVs) during infection of Drosophilia melanogaster S2 cells by Cricket paralysis virus (CrPV). Utilizing quantitative proteomics, we demonstrated that ELVs can be isolated from both mock- and CrPV-infected S2 cells that contain distinct set of proteins compared to the cellular proteome. Moreover, 40 proteins increased in abundance in ELVs derived from CrPV-infected cells compared to mock, suggesting specific factors associate with ELVs during infection. Interestingly, peptides from CrPV capsid proteins (ORF2) and viral RNA were detected in ELVs from infected cells. Finally, ELVs from CrPV-infected cells are infectious suggesting that CrPV may hijack ELVs to acquire an envelope during infection of S2 cells. This study further demonstrates the diverse strategies of nonenveloped viruses from invertebrates to vertebrates to acquire an envelope in order to evade the host response or facilitate transmission.
病毒通常根据其蛋白衣壳周围是否存在脂质双层而被分为有包膜或无包膜病毒。近年来，许多研究通过证明某些无包膜病毒（例如甲型肝炎病毒）可以通过劫持宿主细胞途径在感染过程中获得包膜，从而挑战了这一观点。在本研究中，我们研究了外泌体样小泡（ELVs）在黑腹果蝇 S2 细胞感染 Cricket 麻痹病毒（CrPV）过程中的作用。利用定量蛋白质组学，我们证明可以从 mock 感染和 CrPV 感染的 S2 细胞中分离出 ELVs，与细胞蛋白质组相比，ELVs 中含有独特的蛋白质组。此外，与 mock 相比，来自 CrPV 感染细胞的 ELVs 中 40 种蛋白质的丰度增加，表明在感染过程中特定因子与 ELVs 相关。有趣的是，来自 CrPV 衣壳蛋白（ORF2）和病毒 RNA 的肽段在感染细胞的 ELVs 中被检测到。最后，来自 CrPV 感染细胞的 ELVs 具有感染性，表明 CrPV 可能在感染 S2 细胞时劫持 ELVs 以获得包膜。本研究进一步证明了无包膜病毒从无脊椎动物到脊椎动物获得包膜的多种策略，以逃避宿主反应或促进传播。
