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Relationship between membrane integrity and the inhibition of host translation in virus-infected mammalian cells. Comparative studies between encephalomyocarditis virus and poliovirus.

The inhibition of host protein synthesis after picornavirus infection, and its relationship to the modification of membrane permeability has been studied. In encephalomyocarditis (EMC)-virus-infected L cells, cellular protein synthesis is reduced from the third hour after infection, at which time an inhibition in 86Rb+ uptake by the infected cell was observed. The bulk of viral protein synthesis takes place in a cell in which a profound modification in the ionic concentration has occurred. This is in agreement with the idea that optimal viral translation requires a higher concentration of monovalent ions as compared to cellular protein synthesis. 
 
 
 
A parallel measurement of (a) protein synthesis, (b) 86Rb+ content, (c) membrane potential and (d) modification of permeability to hygromycin B in EMC-virus-infected and poliovirus-infected HeLa cells, indicates that in EMC-virus-infected cells a correlation exists between membrane alterations and the inhibition of host protein synthesis. This correlation was not apparent in poliovirus-infected cells, suggesting that in this system other factors, different from monovalent ion alterations, are involved in the shut-off. However, in this system, the synthesis of viral proteins also takes place when the cell membrane has been modified and permeability to ions is altered. 
 
 
 
The analysis of the shut-off of protein synthesis and permeability modification in different cell lines infected with EMC virus or poliovirus indicates that the kinetic pattern of the shut-off is variable and depends on the cell line used and the multiplicity of infection used in each experiment. 
 
 
 
The ATP content of picornavirus-infected cells was examined throughout infection. A decrease of this nucleotide in the infected cells was apparent from the third hour post-infection and this factor could perhaps contribute to the inhibition of viral protein synthesis that occurs late in infection. Another factor that could influence this inhibition is the transport of amino acids. For instance, the transport of glycine decreased from the beginning of the infection in EMC-virus-infected cells and a leakage of methionine was also observed late in infection. These modifications in membrane permeability could contribute to the development of the cytopathic effect observed in virus-infected cells.