Alterations of 86Rb+ fluxes in poliovirus-infected HeLa cells and their dependence on virus replication.
Components of the 86Rb+ influx were investigated subsequent to poliovirus infection in the presence and absence of guanidine-HCl, both under normal steady-state conditions and after Na+ preloading of the cells. Measurements of the ouabain-sensitive 86Rb+ uptake indicated a biphasic change in the activity of the Na+, K+ pump in the course of virus infection: a transient increase in the second hour postinfection, that was detectable only after Na+ preloading and inhibition after 3 hr. The enhanced activity of the Na+, K+ pump was not affected, while the decrease later was fully prevented by the antiviral agent guanidine-HCl. The piretanide-sensitive 86Rb+ uptake due to the Na+, K+, 2 Cl- cotransport system also became strongly inhibited beginning in the second hour postinfection. The inhibition of this transport system was partially antagonized by guanidine-HCl. The remaining 86Rb+ influx in the presence of ouabain and piretanide increased in the third hour postinfection. The latter change in 86Rb+ influx, indicating an increased permeability to monovalent cations was completely abolished by guanidine-HCl.
D001693:Biological Transport, Active; D002472:Cell Transformation, Viral; D004261:DNA Replication; D006367:HeLa Cells / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D017955:Poliovirus / Q000235:genetics*; D011868:Radioisotopes; D012413:Rubidium / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D014779:Virus Replication
D011868:Radioisotopes; D000254:Sodium-Potassium-Exchanging ATPase; D012413:Rubidium