Infection of MA-104 cells with the OSU strain of rotavirus induced an increase in Na and a decrease in K intracellular concentrations, starting at 4 h post-infection. These changes were not related to an inhibition of the Na/K pump since ouabain-sensitive Rb uptake was augmented in rotavirus-infected cells compared to control cells, whereas the [H]ouabain binding and Na/K ATPase activity in the cell homogenate were unaffected. Furosemide-sensitive Rb uptake (Na/K/2Cl cotransport) was not modified by the infection. Passive Rb efflux and Na influx were augmented in infected cells suggesting an increase in the plasma membrane permeability. The increase in intracellular Na concentration might be responsible for the observed stimulation of the Na/K pump. This effect was dependent upon the synthesis of viral proteins because it was abolished by addition of cycloheximide up to 4 h post-infection. Prevention of the increase in intracellular Na by the use of low Na-containing media did not modify the pattern of protein synthesis. This suggests that changes in intracellular Na and K concentrations were not related to shutoff of cellular protein synthesis. Alterations of ion contents in the rotavirus-infected enterocytes might impair intestinal absorptive capacity before the appearance of histopathological lesions.


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