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.
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