It is known that infection of intestinal epithelial cells with RV causes disruption of tight junctions and loss of transepithelial resistance (TER), even in the absence of cell death [13] . Loss of TER involves alteration of tight junction proteins, mainly claudin-1, occludin, and ZO-1 as determined in human small intestine carcinoma cells (Caco2) [13] , although use of cancer cells for such mechanistic studies is not appropriate. Rotavirus infection is also associated with increased production of lactate, decreased mitochondrial oxygen consumption, and reduced cellular ATP, conditions known to reduce the integrity of epithelial tight junctions [13, 14] .