Abstract Title
Molecular genetic characterization of the GII.17 norovirus strains in South Korea
Presenter
Myung-Guk Han, KDCA
Co-Author(s)
Yunhee Jo, Minji Lee, Deog-Yong Lee and Sun-Whan Park
Abstract Category
Molecular Epidemiology & Evolution
Abstract
Background
Norovirus is a leading cause of acute gastroenteritis across all age groups worldwide. Over the past two decades, the GII.4 genotype has been predominantly responsible for outbreaks. However, around the winter of 2014, a novel GII.17 variant, known as the Kawasaki 2014 strain, emerged in East Asia, leading to significant outbreaks in countries such as Japan, Hong Kong, and China. This variant exhibited unique amino acid insertions in the P2 domain of the VP1 capsid protein, which altered the virus's antigenic properties and its binding affinity to histo-blood group antigens (HBGAs). Such changes suggest a potential for this variant to replace existing strains. In South Korea, the GII.17 norovirus has also become a prevalent strain, necessitating a detailed molecular epidemiological investigation.
Methods
This study analyzed norovirus-positive samples collected through South Korea's national laboratory surveillance system, K-CaliciNet. Norovirus infections were confirmed using real-time reverse transcription polymerase chain reaction (RT-PCR). Positive samples underwent genotyping by amplifying the capsid (VP1) and RNA-dependent RNA polymerase (RdRp) genes. Next-generation sequencing (NGS) was employed to elucidate the genetic variations of the GII.17 genotype. Phylogenetic analyses were conducted using MEGA X software, and amino acid sequences were compared to identify specific mutations.
Results
Phylogenetic analysis demonstrated that the GII.17 norovirus strains detected in South Korea during 2024 were genetically distinct from the historical Kawasaki 2014 lineage, forming a newly emerging cluster designated as Cluster IV. This separation implies continuous genetic drift and local adaptation. Comparative amino acid sequence analysis revealed several notable substitutions concentrated in the VP1 capsid protein’s P2 domain, which is known for its role in host receptor binding and immune recognition. Changes were identified at positions 298, 299, 336, 352, 363, 374, 378, 388, 399, 404, and 417, and were especially prominent around residue 378, corresponding to a site critical for HBGA binding. These substitutions suggest that the re-emerged GII.17 strains may have acquired an enhanced ability to interact with a broader range of human histo-blood group antigens, contributing to immune evasion and sustained transmission in the population. Additionally, identical genetic sequences were identified in strains from severe clinical cases, highlighting potential pathogenic implications.
Conclusion
The GII.17 norovirus strains currently prevalent in South Korea, while genetically similar to the Kawasaki 2014 variant, possess unique mutations in the P2 domain of the VP1 protein. These alterations likely influence the virus's antigenicity and immune evasion capabilities, facilitating its swift rise as a dominant strain. Continuous genetic surveillance and research on GII.17 variants are imperative to inform vaccine development and establish effective preventive measures.
Norovirus is a leading cause of acute gastroenteritis across all age groups worldwide. Over the past two decades, the GII.4 genotype has been predominantly responsible for outbreaks. However, around the winter of 2014, a novel GII.17 variant, known as the Kawasaki 2014 strain, emerged in East Asia, leading to significant outbreaks in countries such as Japan, Hong Kong, and China. This variant exhibited unique amino acid insertions in the P2 domain of the VP1 capsid protein, which altered the virus's antigenic properties and its binding affinity to histo-blood group antigens (HBGAs). Such changes suggest a potential for this variant to replace existing strains. In South Korea, the GII.17 norovirus has also become a prevalent strain, necessitating a detailed molecular epidemiological investigation.
Methods
This study analyzed norovirus-positive samples collected through South Korea's national laboratory surveillance system, K-CaliciNet. Norovirus infections were confirmed using real-time reverse transcription polymerase chain reaction (RT-PCR). Positive samples underwent genotyping by amplifying the capsid (VP1) and RNA-dependent RNA polymerase (RdRp) genes. Next-generation sequencing (NGS) was employed to elucidate the genetic variations of the GII.17 genotype. Phylogenetic analyses were conducted using MEGA X software, and amino acid sequences were compared to identify specific mutations.
Results
Phylogenetic analysis demonstrated that the GII.17 norovirus strains detected in South Korea during 2024 were genetically distinct from the historical Kawasaki 2014 lineage, forming a newly emerging cluster designated as Cluster IV. This separation implies continuous genetic drift and local adaptation. Comparative amino acid sequence analysis revealed several notable substitutions concentrated in the VP1 capsid protein’s P2 domain, which is known for its role in host receptor binding and immune recognition. Changes were identified at positions 298, 299, 336, 352, 363, 374, 378, 388, 399, 404, and 417, and were especially prominent around residue 378, corresponding to a site critical for HBGA binding. These substitutions suggest that the re-emerged GII.17 strains may have acquired an enhanced ability to interact with a broader range of human histo-blood group antigens, contributing to immune evasion and sustained transmission in the population. Additionally, identical genetic sequences were identified in strains from severe clinical cases, highlighting potential pathogenic implications.
Conclusion
The GII.17 norovirus strains currently prevalent in South Korea, while genetically similar to the Kawasaki 2014 variant, possess unique mutations in the P2 domain of the VP1 protein. These alterations likely influence the virus's antigenicity and immune evasion capabilities, facilitating its swift rise as a dominant strain. Continuous genetic surveillance and research on GII.17 variants are imperative to inform vaccine development and establish effective preventive measures.