Receptor profile and immunogenicity of the non-epidemic norovirus GII.8 variant.

Noroviruses are causative agents of acute nonbacterial gastroenteritis epidemics worldwide. There are various genotypes, among which the non-epidemic genotype GII.8 can cause norovirus outbreaks. We previously demonstrated that the immunogenicity of GII.8 differed from that of epidemic variants. This study aimed to comprehensively compare the receptor profile and immunogenicity of the GII.8 variant with those of the epidemic variants. Using the baculovirus-insect cell expression system, we observed that recombinant capsid protein VP1 of the norovirus GII.8 GZ2017-L601 strain formed virus-like particles (VLPs) with a diameter of approximately 30 nm, as evidenced by transmission electron microscopy analysis. The GII.8 VLPs showed weak or moderate binding with all secretor histo-blood group antigens (HBGAs), but not with non-secretors, as evidenced by the HBGA-VLP binding test. The GII.8 VLP antiserum obtained from immunized BALB/c mice was tested for cross-reactivity with other norovirus genotypes (n = 28). The results showed that this antiserum demonstrated moderate cross-reactivity with GI.1, GII.3, and GII.15; however, no cross-reactivity with the epidemic variants of GII.2, GII.4, and GII.17 was observed. Additionally, the blocking-antibody activity of GII.8 antisera against GII.4 VLP-HBGAs and GII.17 VLP-HBGAs interactions and the cross-blocking of GII.8 VLP-HBGAs interactions by GI.1 and GII.4 antisera were evaluated using the HBGAs-VLP blocking test. However, no cross-blocking effect was observed. In summary, the characterization of norovirus GII.8 VLPs and derived antisera revealed that the GII.8 immunogenicity differed from that of epidemic variants.