Specificity of interferon action in protein synthesis

Journal of Virology (Impact Factor: 4.44). 10/1978; 27(3):648-58.
Source: PubMed


Inhibitors of elongation steps in protein synthesis such as cycloheximide and anisomycin mimic interferon treatment in that they specifically inhibit the synthesis of certain viral proteins. These specific effects are seen only at very low concentrations of the antibiotics, under conditions where host cellular protein synthesis, as well as cell viability, are not severely reduced. A qualitatively as well as quantitatively close correlation between the effects of the two types of agents has been established for encephalomyocarditis virus, vesicular stomatitis virus and murine leukemia virus protein synthesis. It is concluded that one of the primary mechanisms of interferon action may be a nonspecific retardation of one or more elongation steps, and that this may be sufficient to account for its effects on the replication of certain viruses such as encephalomyocarditis and vesicular stomatitis viruses.

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Available from: Peter Yau, Mar 06, 2014
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    ABSTRACT: virus mRNA andhost mRNA'sininfected cells weremeasured using twoindependent techniques. In bothcases theresults showed thatviral mRNA initiates atamuchhigher rate thanhostmRNA's. Thisdifference wasobserved midwayintheinfectious cycle, wellbefore virus-induced cytopathic effects (leakage oflow-molecular-weight metabolites, failure toexclude trypan blue) wereapparent. Theseresults confirm thatencephalomyocarditis viral mRNA isamoreefficient initiator thanhost
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    ABSTRACT: The relative initiation rates for encephalomyocarditis virus mRNA and host mRNA's in infected cells were measured using two independent techniques. In both cases the results showed that viral mRNA initiates at a much higher rate than host mRNA'S. This difference was observed midway in the infectious cycle, well before virus-induced cytopathic effects (leakage of low-molecular-weight metabolites, failure to exclude trypan blue) were apparent. These results confirm that encephalomyocarditis viral mRNA is a more efficient initiator than host mRNA's in vivo, as has previously been demonstrated in in vitro experiments.
    Journal of Virology 10/1978; 27(3):640-7. · 4.44 Impact Factor
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    ABSTRACT: SUMMARY Primary African green monkey kidney cells (GMK) treated with poly(rI).poly- (rC) in the presence of DEAE-dextran (' treated cells ') developed antiviral resistance and concomitantly released interferon into the medium. Treated and untreated cells were infected with herpes simplex virus type I (HSVI) in the presence of cyto- sine arabinoside (araC), and total RNA was isolated and hybridized with purified radio-labelled HSVI DNA. The intracellular concentration of virus-specific trans- cripts was not significantly altered in treated cells, but a smaller proportion of the genome of HSVI hybridized with the extracted RNA. Transcription was similarly restricted when protein synthesis was inhibited by cycloheximide. To analyse virus translation, proteins were radiolabelled between 6 and lo h after infection and were immunoprecipitated with a pool of human sera and run on SDS-polyacrylamide gels. No virus-specific proteins could be detected in treated cells. In contrast about 25 HSVI-induced proteins were found in infected cells and about 22 proteins in cells infected in the presence of araC. In particular, two virus proteins with apparent tool. wt. of ~28ooo and 42 5oo were immunoprecipi- tared. Since these two were also detected in cells under conditions where elongation of polypeptide chains was non-specifically retarded, it is unlikely that a similar mechanism was responsible for the impaired growth of HSVI in our treated cells. We conclude that this impairment probably resulted from regulation at the level of virus translation, probably mediated through interferon.
    Journal of General Virology 04/1980; 47(1):97-111. DOI:10.1099/0022-1317-47-1-97 · 3.18 Impact Factor
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