Access Restriction

Author Mizzen, Lee ♦ Macintyre, T. Georgina ♦ Wong, Fred ♦ Anderson, Robert
Source CiteSeerX
Content type Text
File Format PDF
Subject Domain (in DDC) Computer science, information & general works ♦ Data processing & computer science
Subject Keyword Mhv-infected Cell ♦ Mouse Hepatitis Virus Infection ♦ Translational Regulation ♦ Altered Intracellular Ion Concentration ♦ Infected Cell ♦ Host Cell Protein Synthesis ♦ Possible Occurrence ♦ Sodium Ion ♦ Cell Fusion ♦ Normal Influx ♦ Mhv-mediated Cell Fusion ♦ Mouse Hepatitis Virus ♦ Mhv Infection ♦ Final Concentration ♦ Similar Change ♦ Intracellular Ionic Environment ♦ Sodium Influx ♦ Mouse L-2 Fibroblast ♦ Sodium Chloride ♦ Virus System ♦ Intracellular Na ♦ Normal Inhibition ♦ Nac1 Concentration ♦ Translational Control ♦ Monoclonal Antibody ♦ Monoclonal Anti-e_ ♦ Mhv-induced Shut-offof Host Translation ♦ Strong Inhibition ♦ Viral Cellular Protein Synthesis ♦ Intracellular Na Concentration ♦ Membrane Permeability ♦ Na Influx ♦ Little Effect ♦ Cellular Protein Synthesis
Abstract Infection of mouse L-2 fibroblasts with mouse hepatitis virus (MHV) results in strong inhibition of host cell protein synthesis. Since it has been suggested in other virus systems that translational control is modulated by changes in the intracellular ionic environment, we investigated the possible occurrence of similar changes during MHV infection. Membrane permeability to extracellular sodium ions was measured by culturing MHV-infected cells in the presence of 22Na+. Sodium influx into MHV-infected cells rose dramatically from 4 to 6 h post-infection. This influx correlated chronologically with the expression of MHV-mediated cell fusion. Cell fusion was blocked by the addition of a monoclonal antibody against he MHV E 2 glycoprotein. This addition also resulted in a reduction in the normal influx of 22Na+, suggesting that E 2 expression was responsible, directly or indirectly, for the increased permeability to sodium ions in infected cells. Cultures of MHV-infected cells were labelled with [35S]methionine in the presence of medium supplemented with sodium chloride at final concentrations ranging from 150 mM to 350 mM. Incorporation of radiolabel into proteins decreased with increasing NaC1 concentration; however, the ratio of viral to cellular protein synthesis remained relatively constant. Similarly, alteration of intracellular Na + and K + levels by treatment of infected cells with ouabain had little effect on the pattern of viral/cellular protein synthesis. Using monoclonal anti-E_, antibody to inhibit Na + influx, we demonstrated normal inhibition of host cell protein synthesis. We therefore conclude that MHV-induced shut-offof host translation is not mediated by changes in intracellular Na + concentrations.
Educational Role Student ♦ Teacher
Age Range above 22 year
Educational Use Research
Education Level UG and PG ♦ Career/Technical Study
Publisher Date 1987-01-01