Archives of Virology

, Volume 124, Issue 3, pp 321–332

Coxsackie B 1 virus-induced changes in cell membrane-associated functions are not responsible for altered sensitivity to bacterial invasiveness

  • K. Modalsli
  • G. Bukholm
  • S. O. Mikalsen
  • M. Degré
Original Papers

DOI: 10.1007/BF01309812

Cite this article as:
Modalsli, K., Bukholm, G., Mikalsen, S.O. et al. Archives of Virology (1992) 124: 321. doi:10.1007/BF01309812

Summary

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.

Copyright information

© Springer-Verlag 1992

Authors and Affiliations

  • K. Modalsli
    • 1
  • G. Bukholm
    • 1
  • S. O. Mikalsen
    • 2
  • M. Degré
    • 1
  1. 1.Kaptein W. Wilhelmsen og Frues Bakteriologiske InstituttUniversity of OsloOsloNorway
  2. 2.Laboratory for Environmental and Occupational Cancer, Institute for Cancer ResearchThe Norwegian Radium HospitalOsloNorway