Viruses, host cell protein synthesis affected

Apparently related to the problem of host cell protein synthesis inhibition by viruses is the phenomenon of viral interference. In some cases, superinfection of a cell already infected with one virus does not affect the yield of the original virus. In other cases, however, the superinfecting virus completely inhibits translation of the original viral mRRA. Such is the case for superinfection of vesicular stomatitis virus (VSV)-infected cells by poliovirus (32). The kinetics and general properties of the shut-off of VSY protein synthesis appear to be the same as the shut-off of cellular protein synthesis after poliovirus infection... 

Ribosomes phosphorylated vitro show no alteration in their translational activity (5, ) Trivial explanations such as the possibility that the ribosomes are dephosphorylated in the translation assay seem to have been eliminated. It is, of course, possible that current assay methods are inadequate to detect subtle changes caused by phosphorylation, but it is equally valid to draw the strai tforward conclusion that phosphorylation does not affect the activity of ribosomes. This is in accord with the fact that changes in the phosphorylation state of ribosomes vivo do not appear to correlate with alterations in the efficiency of the ribosomes in protein biosynthesis. The one possible exception is the phosphorylation of one of the small ribosomal subunit proteins (S2) that occurs after infection by vaccinia virus (8). The timing of the phosphorylation of S2 seems however to be related neither to the shut-off of host cell protein synthesis nor to the switch from early viral protein synthesis to late gene expression, and it remains to be proven whether the phosphorylation has any material effect on ribosome activity or specificity. 

Deletion Mutants - Another approach has been the construction of deletion mutants by the judicious use of restriction enz3mies and appropriate exonucleases. The sites of the deletions were mapped in some Instances they were widely separated but still affected a single protein. The functional ability of the mutants was then determined. The results, while at an early stage, are in agreement with the conclusions reached with the temperature-sensitive mutants. The early proteins must be functional to effect DNA replication, stimulation of host cell DNA synthesis and cell transformation. Interestingly, not all three of the late proteins appear to be required for virus production. Much more will surely come from these studies. 

Rifampicin is also an inhibitor of the synthesis of a number of phages and viruses. It has been demonstrated that the RNA polymerase, which transcribes phage p 22 following infection of Bacillus subtilis, retains the rifampicin sensitivity of the host cell enzyme , Rifampicin also inhibits the formation of infectious vaccinia virus and viral particles. Whereas virion formation is completely inhibited neither the synthesis of RNA and protein nor the activity of in vitro RNA polymerase associated to the virion is affected lt>, Rifampicin inhibits the multiplication of poxvirus in vitro and in vivo. The side chain of this antibiotic derivative appears to be essential for the anti-viral effect and anti-trachomal activity found in... 

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