Abstract

An early stage of encephalomyocarditis (EMC) virus multiplication, probably the effective release of viral genome, is impaired in the majority of cells of a HeLa subline. Poliovirus, replicating or not, induces an actinomycin-sensitive conversion of the nonpermissive cells into permissive ones. These conclusions are based on the following observations. At moderate multiplicities of infection with EMC virus, only a small fraction of the cells in the population undergoes productive infection, as revealed by either infectious centers or the immunofluorescent techniques. The restriction in the majority of the cells can be overcome either by an increase in the multiplicity of infection or by coinfection with poliovirus. Replication of the helper virus RNA does not seem to be a prerequisite for the stimulation of EMC virus multiplication, since the enhancing effect can be obtained with guanidine-sensitive strains of poliovirus in the presence of guanidine or with guanidine-dependent strains in the absence of the drug. On the other hand, simultaneous coinfection with poliovirus fails to stimulate EMC virus reproduction in the presence of aurantine, a preparation of actinomycins. If, however, the cells are preinfected with the helper virus under conditions preventing its replication, the subsequent superinfection with EMC virus proceeds efficiently even in the presence of the antibiotic. Preinfection with poliovirus does not affect appreciably either adsorption and eclipse of EMC virus or the infectious center formation by EMC virus RNA.

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