The role of monovalent cation transport in Sindbis virus maturation and release

Alterations in intracellular monovalent cation concentrations in Sindbis virus-infected avian cells result, in part, from a reduction in Na +/K + ATPase (Na + pump) activity. Inhibition of Na + pump activity was shown previously to temporally correlate with the appearance of viral envelope proteins on the cell surface and the release of virus particles. Cells infected with envelope-defective temperature-sensitive mutants exhibited reduced Na + pump activity at the nonpermissive temperature, where viral particles are not released. By contrast, Na + pump activity was not inhibited in Sindbis virus-infected cells treated with tunicamycin or with antiviral serum, which block virus maturation and release. Diuretic-sensitive transport of 86Rb +, a K + tracer, was stimulated in cells which express virus envelope proteins, but fail to release virus particles. In these cells, the furosemide-sensitive 86Rb + influx exhibited an increase in Vmax and was responsive to changes in the extracellular concentration of NaCL Furosemide inhibited the rapid release of virus from low salt-inhibited cells after shift to isotonic conditions. Alterations in ion transport during alphavirus infection may, therefore, facilitate the efficient release of progeny virus particles.