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Absence of significant antiviral effects of beta-gamma-methylene GTP on encephalomyocarditis virus infection of L cells and mice.

Abstract
The protein synthesis inhibitor beta-gamma-methylene guanosine triphosphate (Gpp-CH2p) is shown here to be ineffective as a 'leaky membrane' antiviral agent against encephalomyocarditis virus infection of L cells and mice. Studies with GppCH2p in encephalomyocarditis virus-infected L cells indicate that the cells only become permeable to the inhibitor late in infection because the compound significantly inhibits protein synthesis only when added at 4 h p.i. At this time 50 to 70% of the new infectious virus particles have already been synthesized, and this is reflected in maximum inhibition of virus yields of only about 40%. Moreover, comparison of inhibition of protein synthesis by GppCH2p in vitro and in cell cultures indicates that the intracellular concentration attained is only 0.25% of that in the medium. The lack of antiviral activity of GppCH2p in encephalomyocarditis virus-infected mice is probably due to leakiness of infected cells occurring too late for sufficient inhibition of virus synthesis to be obtained.
AuthorsK M Dawson, A Stewart, N Stebbing
JournalThe Journal of general virology (J Gen Virol) Vol. 45 Issue 1 Pg. 237-40 (Oct 1979) ISSN: 0022-1317 [Print] England
PMID230305 (Publication Type: Journal Article)
Chemical References
  • Guanosine Triphosphate
Topics
  • Animals
  • Cell Division (drug effects)
  • Encephalomyocarditis virus (drug effects)
  • Enterovirus Infections (drug therapy)
  • Guanosine Triphosphate (analogs & derivatives, pharmacology, therapeutic use)
  • L Cells
  • Mice
  • Protein Biosynthesis
  • Time Factors

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