Coxsackie B 1 virus-induced changes in cell membrane-associated functions are not responsible for altered sensitivity to bacterial invasiveness
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- Modalsli, K., Bukholm, G., Mikalsen, S.O. et al. Archives of Virology (1992) 124: 321. doi:10.1007/BF01309812
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To analyze the possible mechanisms by which coxsackie B 1 virus infection affects the invasiveness ofShigella flexneri, we have studied the influence of intracellular levels of Na+ and K+, ATPase activity, cytoplasmic membrane potential, cAMP level and cell communication through gap junctions. 3 h after adsorption of viable or UV-inactivated coxsackie B 1 virus the Na+-K+ gradient of the cell collapsed, ATPase activity decreased, the cytoplasmic membranic potential-dependent tetraphosphonium ion uptake were reduced. No changes in cAMP or intercellular cell communication were observed.S. flexneri invasiveness in HEp-2 cell pretreated with viable or UV-inactivated coxsackie B 1 virus was enhanced, but bacterial invasiveness was unchanged in K+-depleted HEp-2 cells, cell cultures with high intracellular Na+ content or ouabain pre-treated cells compared to control cells. We found no correlation between the enhanced bacterial invasiveness in the early phase of coxsackie B 1 virus infection in HEp-2 cell cultures and intracellular K+ depletion, high intracellular Na+ content, inhibited Na+-K+ ATPase activity or membranic depolarization.