Mengovirus-induced, double-stranded RNA (RF) is infective, but its infectivity, unlike that of mengovirus, is strictly dependent upon host cell macromolecular synthesis. The treatment of cells with actinomycin D, α-amanitin or cordycepin 1 h before infection with mengovirus RF results in a drastic reduction of virus yield, whereas the same treatment has no effect on mengovirus infectivity. The kinetics of sensitivity to inhibitors suggest that the cellular macromolecule necessary for RF to initiate its infective cycle is involved only during the very early steps of replication, and probably has a very rapid turn-over. The cellular uptake of the infecting molecule seems not to be alterated by actinomycin treatment. Analysis of the intracellular distribution of [H]- or [P]-labelled mengovirus RF indicates that up to 40% of incoming molecules accumulate within the nuclear fraction (4 to 5% in nucleoli). Sedimentation velocity analyses of labelled RF recovered from each subcellular compartment show that the input molecule becomes heavier and polydisperse in gradients as the cycle of infection proceeds. A replication mechanism is proposed in which infective RF is transformed into replicative intermediate (RI), by a cellular RNA polymerase transcribing the first virus messenger RNAs with RF as abnormal template.


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