Effect of 8-Azaguanine on Encephalomyocarditis Virus Multiplication.

Abstract

Summary The effect of azaG on EMC virus multiplication was investigated. It was found that the analog induces a delay in the onset of virus growth and slows the growth rate. This effect seems to be independent of host cells macromolecular synthesis, and indirect evidence suggests that it is also independent of incorporation into viral RNA. There is evidence that the synthesis of various virus-directed proteins may be primarily affected. It is suggested that an azaG-substi-tuted GTP cofactor may interfere in the transfer capacity of s-RNA. This hypothesis could explain the ability of azaG to inhibit EMC replication at low intracellular concentration of azaG products as it would be expected in azaG-R cells which lack IMP-GMP pyrophosphorylases. A known secondary mechanism for the formation of azaG nucleotides could provide sufficient amounts of an azaG-cofactor to inhibit viral multiplication in this system.