GII.6 norovirus major capsid protein VP1 derived from distinct clusters induce cross-blocking effects

IF 2.6 4区医学 Q3 INFECTIOUS DISEASES

Infection Genetics and Evolution Pub Date : 2024-06-08 DOI:10.1016/j.meegid.2024.105617

Jie Ma, Jinjin Liu, Chaohong Fu, Yuqi Huo

{"title":"GII.6 norovirus major capsid protein VP1 derived from distinct clusters induce cross-blocking effects","authors":"Jie Ma, Jinjin Liu, Chaohong Fu, Yuqi Huo","doi":"10.1016/j.meegid.2024.105617","DOIUrl":null,"url":null,"abstract":"<div><p>Unlike pandemic GII.4 norovirus, GII.6 norovirus shows limited sequence variation in its major capsid protein VP1. In this study, we investigated the VP1 expression profiles, binding abilities, and cross-blocking effects of three GII.6 norovirus strains derived from three distinct variants. Norovirus VP1 was expressed using a recombinant baculovirus expression system and characterized by transmission electron microscopy, mass spectrometry, salivary histo-blood group antigen (HBGA)-virus like particles (VLPs) binding and binding blockade assays. Mass spectrometry revealed the expected molecular weight (MW) of full-length proteins and degraded or cleaved fragments of all three VP1 proteins. Peptide mapping showed loss of 2 and 3 amino acids from the N- and C-terminus, respectively. Further, the co-expression of VP1 and VP2 proteins did not lead to extra fragmentation during mass spectrometry. Salivary HBGA-VLP binding assay revealed similar binding patterns of the three GII.6 VP1 proteins. Salivary HBGA-VLP binding blockade assay induced cross-blocking effects. Our results demonstrate similar binding abilities against salivary HBGAs and specific cross-blocking effects for GII.6 norovirus strains derived from distinct variants, suggesting that fewer GII.6 strains from different evolutionary variants are needed for the development of norovirus vaccines.</p></div>","PeriodicalId":54986,"journal":{"name":"Infection Genetics and Evolution","volume":"122 ","pages":"Article 105617"},"PeriodicalIF":2.6000,"publicationDate":"2024-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1567134824000686/pdfft?md5=a20e6ff365a060e85aae767bd8ccfa1f&pid=1-s2.0-S1567134824000686-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infection Genetics and Evolution","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1567134824000686","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"INFECTIOUS DISEASES","Score":null,"Total":0}

引用次数: 0

Abstract

Unlike pandemic GII.4 norovirus, GII.6 norovirus shows limited sequence variation in its major capsid protein VP1. In this study, we investigated the VP1 expression profiles, binding abilities, and cross-blocking effects of three GII.6 norovirus strains derived from three distinct variants. Norovirus VP1 was expressed using a recombinant baculovirus expression system and characterized by transmission electron microscopy, mass spectrometry, salivary histo-blood group antigen (HBGA)-virus like particles (VLPs) binding and binding blockade assays. Mass spectrometry revealed the expected molecular weight (MW) of full-length proteins and degraded or cleaved fragments of all three VP1 proteins. Peptide mapping showed loss of 2 and 3 amino acids from the N- and C-terminus, respectively. Further, the co-expression of VP1 and VP2 proteins did not lead to extra fragmentation during mass spectrometry. Salivary HBGA-VLP binding assay revealed similar binding patterns of the three GII.6 VP1 proteins. Salivary HBGA-VLP binding blockade assay induced cross-blocking effects. Our results demonstrate similar binding abilities against salivary HBGAs and specific cross-blocking effects for GII.6 norovirus strains derived from distinct variants, suggesting that fewer GII.6 strains from different evolutionary variants are needed for the development of norovirus vaccines.

查看原文本刊更多论文

来自不同簇的 GII.6 诺如病毒主要囊膜蛋白 VP1 可产生交叉阻断效应。

与大流行的 GII.4 诺如病毒不同，GII.6 诺如病毒的主要囊膜蛋白 VP1 的序列变异有限。在本研究中，我们研究了三种不同变种的 GII.6 诺如病毒株的 VP1 表达谱、结合能力和交叉阻断效应。我们使用重组杆状病毒表达系统表达了诺如病毒 VP1，并通过透射电子显微镜、质谱分析、唾液组织血型抗原（HBGA）-类病毒颗粒（VLPs）结合和结合阻断实验对其进行了表征。质谱分析表明，所有三种 VP1 蛋白的全长蛋白和降解或裂解片段都达到了预期的分子量（MW）。肽图显示，N 端和 C 端分别损失了 2 个和 3 个氨基酸。此外，VP1 和 VP2 蛋白的共同表达不会导致质谱分析过程中出现额外的片段。唾液 HBGA-VLP 结合试验显示，三种 GII.6 VP1 蛋白的结合模式相似。唾液 HBGA-VLP 结合阻断试验产生了交叉阻断效应。我们的研究结果表明，来自不同变种的 GII.6 诺如病毒毒株与唾液 HBGA 的结合能力相似，并具有特异性交叉阻断效应，这表明诺如病毒疫苗的开发需要更少来自不同进化变种的 GII.6 毒株。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Infection Genetics and Evolution 医学-传染病学

CiteScore

8.40

自引率

0.00%

发文量

215

审稿时长

82 days

期刊介绍： (aka Journal of Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases -- MEEGID) Infectious diseases constitute one of the main challenges to medical science in the coming century. The impressive development of molecular megatechnologies and of bioinformatics have greatly increased our knowledge of the evolution, transmission and pathogenicity of infectious diseases. Research has shown that host susceptibility to many infectious diseases has a genetic basis. Furthermore, much is now known on the molecular epidemiology, evolution and virulence of pathogenic agents, as well as their resistance to drugs, vaccines, and antibiotics. Equally, research on the genetics of disease vectors has greatly improved our understanding of their systematics, has increased our capacity to identify target populations for control or intervention, and has provided detailed information on the mechanisms of insecticide resistance. However, the genetics and evolutionary biology of hosts, pathogens and vectors have tended to develop as three separate fields of research. This artificial compartmentalisation is of concern due to our growing appreciation of the strong co-evolutionary interactions among hosts, pathogens and vectors. Infection, Genetics and Evolution and its companion congress [MEEGID](http://www.meegidconference.com/) (for Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases) are the main forum acting for the cross-fertilization between evolutionary science and biomedical research on infectious diseases. Infection, Genetics and Evolution is the only journal that welcomes articles dealing with the genetics and evolutionary biology of hosts, pathogens and vectors, and coevolution processes among them in relation to infection and disease manifestation. All infectious models enter the scope of the journal, including pathogens of humans, animals and plants, either parasites, fungi, bacteria, viruses or prions. The journal welcomes articles dealing with genetics, population genetics, genomics, postgenomics, gene expression, evolutionary biology, population dynamics, mathematical modeling and bioinformatics. We also provide many author benefits, such as free PDFs, a liberal copyright policy, special discounts on Elsevier publications and much more. Please click here for more information on our author services .