The first porcine sapovirus (SaV) was discovered in 1980 from a diarrheic nursing pig that was also co-infected with rotavirus and astrovirus. Its genome was determined, and it was classified as genogroup III (GIII) SaV. Since then, genetically diverse porcine SaVs have been detected in domestic pigs and are classified into eight genogroups (GIII, V–XI), with GIII the most prevalent genogroup worldwide. Although the prevalence of porcine SaVs was high, the significance of SaV infection in the pork industry is still debatable because they were often detected with similar rates in diarrheic and non-diarrheic samples, and they were rarely the sole enteric pathogen detected in a gastroenteritis outbreak. On farms, GIII SaVs were often involved in post-weaning pig gastroenteritis with high morbidity but low mortality rates. The etiology and pathogenesis of the prototype porcine SaV Cowden strain was confirmed in experimentally infected neonatal gnotobiotic pigs. It replicated in the villous epithelial cells mainly in duodenal and jejunum and caused small intestinal lesions, leading to mild–moderate diarrhea lasting for several days. Fecal virus shedding persisted for at least 7 days post-inoculation. Currently, diagnosis of porcine SaV infection is based mainly on the detection of viral nucleic acids. There are no commercial vaccines or antiviral drugs for porcine SaVs. Although porcine SaVs have not been detected in humans, the recent detection of human GI-like SaV from pigs emphasizes the importance of continuous monitoring and investigating this group of RNA viruses for both swine and human health.