SUMMARY: Addition of virginiamycin M or S before the virulent phage 2 C prevented from lysing, and this effect was increased 100-fold by simultaneous addition of both factors. When the antibiotics were administered at the end of the eclipse phase, the viral cycle was shortened by virginiamycin S, prolonged by factor M and halted by the two inhibitors together. Virginia-mycins also prevented the accumulation of phage particles by inhibiting the synthesis of viral precursors during the eclipse period as well as during the maturation phase.

Synthesis of cellular macromolecules was decreased (not suppressed) in after infection with phage 2C, and the degree of repression was a function of the input multiplicity. Viral inhibition of thymidine and uridine incorporation into host DNA and RNA was prevented when virginiamycin was added before infection but unaffected when addition was made at the end of the eclipse phase. Virus and virginiamycin had additive non-overlapping effects on protein synthesis. Moreover, virginia-mycins interfered with the function, not the formation, of RNA pulse-labelled after infection, and prevented its decay.

It can be concluded that virginiamycin blocks () the preferential translation of viral message, () the mechanism by which virus halts host-macro-molecule formation, and () the synthesis of viral DNA. This can be explained by an inhibitory action of virginiamycin on the synthesis and function of virus-dictated proteins.


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