Norovirus is a leading cause of infectious gastroenteritis that poses significant public health challenges. Beyond causing widespread outbreaks with considerable social and economic consequences, the virus can be life-threatening for high-risk groups including pediatric, geriatric, and immunocompromised patients. According to WHO estimates, the number of infections worldwide, mainly in developing countries, is about 680 million per year, and the number of deaths is 200,000 per year. Currently, no approved therapeutic treatments or vaccines are available for norovirus infection. The inability to cultivate norovirus in standard cell culture systems remains a significant barrier, necessitating the development of reliable and universally applicable propagation methods. Like many viruses, it has become clear that norovirus uses glycans to infect host cells [1]. Norovirus recognizes the histo-blood group antigen (HBGA), a type of carbohydrate-based antigen expressed on the cell surface, by the capsid protein VP1 [2, 3]. Norovirus-HBGA binding facilitates viral attachment to host cells and promotes subsequent infection (Fig. 66.1). On the other hand, there are reports of norovirus strains that do not bind to HBGA, and norovirus binds to glycans other than HBGA, such as sialoglycan, heparan sulfate, galactosylceramide, and sulfatide [4, 5], and further knowledge about the structure and function of glycans that interact with norovirus is expected in the future.