HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by del Castillo, J. R. Articles by Liprandi, F. Search for Related Content PubMed PubMed Citation Articles by del Castillo, J. R. Articles by Liprandi, F. Agricola Articles by del Castillo, J. R. Articles by Liprandi, F.

Rotavirus infection alters Na⁺ and K⁺ homeostasis in MA-104 cells

¹ Laboratorio de Fisiología Gastrointestinal
and² Laboratorio de Biología de Virus, Instituto Venezolano de Investigaciones Cientificas (IVIC), Apartado 21827, Caracas 1020-A, Venezuela

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 ⁸⁶Rb uptake was augmented in rotavirus-infected cells compared to control cells, whereas the [³H]ouabain binding and Na⁺/K⁺ ATPase activity in the cell homogenate were unaffected. Furosemide-sensitive ⁸⁶Rb uptake (Na⁺/K⁺/2Cl^- cotransport) was not modified by the infection. Passive ⁸⁶Rb efflux and ²²Na 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.

Received 11 September 1990; accepted 28 November 1990.

This article has been cited by other articles:

				R. F. Ramig Pathogenesis of Intestinal and Systemic Rotavirus Infection J. Virol., October 1, 2004; 78(19): 10213 - 10220. [Full Text] [PDF]

				M. A. Cuadras, D. A. Feigelstock, S. An, and H. B. Greenberg Gene Expression Pattern in Caco-2 Cells following Rotavirus Infection J. Virol., March 27, 2002; 76(9): 4467 - 4482. [Abstract] [Full Text] [PDF]

				J. F. Pérez, M.-C. Ruiz, M. E. Chemello, and F. Michelangeli Characterization of a Membrane Calcium Pathway Induced by Rotavirus Infection in Cultured Cells J. Virol., March 1, 1999; 73(3): 2481 - 2490. [Abstract] [Full Text]