Towards a human rotavirus disease model

While the clinical importance of human rotavirus (RV) disease is well recognized and potent vaccines have been developed, our understanding of how human RV causes diarrhoea, vomiting and death remains unresolved. The fact that oral rehydration corrects electrolyte and water loss, indicates that enterocytes in the small intestine have a functional sodium-glucose co-transporter. Moreover, RV infection delays gastric emptying and loperamide appears to attenuate RV diarrhoea, thereby suggesting activation of the enteric nervous system. Serotonin (5-HT) receptor antagonists attenuate vomiting in young children with gastroenteritis while zinc and enkephalinase inhibitors attenuate RV-induced diarrhoea. In this review we discuss clinical symptoms, pathology, histology and treatment practices for human RV infections and compile the data into a simplified disease model.

► Clinical symptoms, pathology, histology and treatment practices for human RV infections are discussed.
► 5-HT3 receptor antagonists in treatment of vomiting in children with acute gastroenteritis, suggest involvement of nerves.
► Loperamide treatment reduces RV-diarrhoea indicating activation of the myenteric nerve plexus.
► Racecadotril and zinc treatment reduce RV-diarrhoea, suggesting secretory driven diarrhoea.
► ORT is effective in RV treatment, indicating functional enterocyte absorption capacity.