Alteration of the Intracellular Energetic and Ionic Conditions by Mengovirus Infection of Ehrlich Ascites Tumor Cells and Its Influence on Protein Synthesis in the Midphase of Infection
- 1 June 1977
- journal article
- research article
- Published by American Society for Microbiology in Journal of Virology
- Vol. 22 (3) , 591-597
- https://doi.org/10.1128/jvi.22.3.591-597.1977
Abstract
Mengovirus infection of [mouse] Ehrlich ascites tumor cells caused a change of the intracellular ATP concentration. It increased by 35% within the first 3 h postinfection and then declined to zero within the next 5 h. The decrease in the ATP concentration was due, at least in part, to leakage of ATP into the medium, where it could be demonstrated by the luciferin-luciferase assay. Gross leakage of ATP was observed at 4.5 h postinfection, concomitant with the production of the 1st intracellular, infectious virus particles. A similar concentration decrease was detected for Mg2+, polyamines and K+, but an increase in the Na+ concentration was observed. The intracellular Mg2+ concentration varied synchronously with the ATP level, rising by 16% during the first 3 h postinfection and then progressively falling to lower values in the late period of the infectious cycle. After an initial slight enhancement, putrescine, spermidine and spermine concentrations declined at about 1.5 h postinfection. While the intracellular K+ concentration increased by 17% during the 1st h postinfection, the Na+ concentration diminished by the same value within the same time period, leaving the internal ionic strength unchanged early in infection. Three hours after the beginning of virus infection, there was a rapid decline of K+ and enhancement of Na+ within the cell. These alterations of the intracellular energetic and ionic conditions seem to be, at least in part, responsible for the cessation of virus-specific protein synthesis in mengovirus-infected Ehrlich ascites tumor cells commencing 3-3.5 h postinfection.This publication has 20 references indexed in Scilit:
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