Infection of mouse fibroblasts by cardioviruses: Premature uncoating and its prevention by elevated pH and magnesium chloride

Abstract

The plating efficiencies of ME-, EMC-, MM-, Columbia SK-, and mengoviruses, collectively called “cardioviruses,” were enhanced 2- to 5-fold by conducting the virus attachment step at 22° rather than at 37°. This behavior was traced to a temperature-dependent loss of infectivity (abortive infection) following attachment of the virion to the cell. Abortive infection was virus specific; it was detectable with cardioviruses but not with poliovirus type 1 or coxsackievirus B1 and took place on both HeLa and L cells. Studies with purified, isotopically labeled ME-virus showed that loss of infectivity was accompanied by release of the RNA genome from cell-attached virions into the extracellular fluid. The coat protein initially remained attached to the cell after RNA release but subsequently dissociated from the cell in the form of 14 S subunits. Premature uncoating was inhibited by alkaline pH and by hypertonic salt solutions.