Rotavirus is transmitted by feco–oral transmission.
Rotavirus survives the acidic environment in the stomach and initiates infection in the mucosal cells of the small intestine. It does not cause infection in mucosa of the stomach and large intestine. After absorption, the viruses replicate in the cytoplasm of the enterocytes and damage their transport mechanism.
Non-structural protein 4 (NSP4) of the rotavirus may act as a viral enterotoxin, which causes secretion of fluids by stimulating a signal transduction pathway. The toxin induces influx of calcium ion into enterocytes and release of neuro-nal activators, and alters sodium and glucose absorption. The resulting diarrhea is due to impaired sodium and glucose absorption, as damaged cells on the villi are replaced by nonabsorbing immature crypt cells.
The rotavirus after replicating in the cell causes damage to the cell. The damaged cells are released into the lumen of intes-tine, releasing large quantities of viruses in the diarrheic stool. It takes around 3–8 weeks for restoring the normal function of the cell. Hence, the rotavirus produces watery diarrhea similar to that seen in cholera.
Rotavirus infection is characterized by the presence of high quantity of immunoglobulin A (IgA) in the intestinal secre-tions. The IgA plays an important role in conferring the gut immunity against rotavirus. It protects newborns up to the age of 6 months. The serum antibodies usually reduce the severity of the disease, but not necessarily prevent reinfec-tion. Even a small quantity of a virus may cause infection and diarrhea in the absence of specific antibodies in the serum.