Due to the minimal interaction of the secretory L-fucose to VP8*, the authors of this study hypothesize that this glycan moiety has a low contribution to binding affinity and that a strong interaction would be expected for the unfucosylated H1 precursor, explaining the epidemiological studies that do not correlate the FUT2 status to infection by P[4] and P[6] genotypes [22]. This evidence concerns the gene FUT2 and infection.