Emergence of Novel Human Norovirus GII.17 Strains Correlates With Changes in Blockade Antibody Epitopes
| Autor: | Jacob Kocher, Excel W Swann, Michael L. Mallory, Lisa C. Lindesmith, Kari Debbink, Paul D. Brewer-Jensen, Ralph S. Baric, Eric F. Donaldson |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Models Molecular Antigenicity Protein Conformation viruses Amino Acid Motifs Guinea Pigs Biology Antibodies Viral Neutralization Virus Epitope 03 medical and health sciences Epitopes Mice Major Articles and Brief Reports fluids and secretions Antigen Immunology and Allergy Animals Humans Amino Acid Sequence Antibodies Blocking Caliciviridae Infections Antiserum Norovirus virus diseases Genetic Variation Virology Antigenic Variation Disease Models Animal 030104 developmental biology Infectious Diseases Capsid biology.protein Capsid Proteins Immunization Rabbits Antibody Protein Binding |
| Zdroj: | The Journal of infectious diseases. 216(10) |
| ISSN: | 1537-6613 |
| Popis: | Background Human norovirus is a significant public health burden, with >30 genotypes causing endemic levels of disease and strains from the GII.4 genotype causing serial pandemics as the virus evolves new ligand binding and antigenicity features. During 2014–2015, genotype GII.17 cluster IIIb strains emerged as the leading cause of norovirus infection in select global locations. Comparison of capsid sequences indicates that GII.17 is evolving at previously defined GII.4 antibody epitopes. Methods Antigenicity of virus-like particles (VLPs) representative of clusters I, II, and IIIb GII.17 strains were compared by a surrogate neutralization assay based on antibody blockade of ligand binding. Results Sera from mice immunized with a single GII.17 VLP identified antigenic shifts between each cluster of GII.17 strains. Ligand binding of GII.17 cluster IIIb VLP was blocked only by antisera from mice immunized with cluster IIIb VLPs. Exchange of residues 393–396 from GII.17.2015 into GII.17.1978 ablated ligand binding and altered antigenicity, defining an important varying epitope in GII.17. Conclusions The capsid sequence changes in GII.17 strains result in loss of blockade antibody binding, indicating that viral evolution, specifically at residues 393–396, may have contributed to the emergence of cluster IIIb strains and the persistence of GII.17 in human populations. |
| Databáze: | OpenAIRE |
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