Rotavirus infects the Caco-2 cells
of the human intestinal epithelial cell line. The explanation
for rotavirus-associated diarrhea is thought to be
associated with increased chloride ion secretion and
cytotoxic tissue damage.4 Based on an in vitro model,
the pathophysiology of rotaviral diarrhea occurs in a
two-phase process. In the early phase, with a peak time
of 2–3 h after infection, infected Caco-2 cells show
increased tissue ion conductance of chloride.
A second phase, starting 24 h after infection, demonstrated
enterotoxic damage, as evidenced by damaged
epithelial integrity. The addition of human IgG to rotavirus-infected
cells was effective at inhibition of both
increased ion secretion and decreased transepithelial
resistance.