DEAE-DEXTRAN AND INTERFERON PRODUCTIONmetabolizable fatty materials, viz., lipoid granulomata with gradual disappearance of oil cysts, residual collection of phagocytic cells, and final disappearance of reactions after some months. There was no evidence that adjuvant 65 would be likely to cause abscess or nodule formation. A test for teratogenicity in rabbits given adjuvant 65 emulsified preparations, or their aqueous counterparts on the eighth day of pregnancy revealed no apparent effects on fetal development.In vitro and in vivo production of interferon (IF) has been recently reported using double-stranded polynucleotides as inducers (6). The present note will describe the influence of diethylaminoethyl dextran ( DEAlEdx) on IF production by L cells treated with double-stranded synthetic polyinosinic-polycytidilic acid (1:C).Maderials and Methods. Mouse L cells (CCL-1 strain) were grown in loosely stoppered vertical 16 )( 100-mm tubes in humidified 5% COa environment at 37°C. Eagle's medium supplemented with 10% calf serum was used for the growth. The Same medium supplemented with 2% calf serum was used during the experiments. All the experiments were carried out in a COZ incubator at 37OC. The IF was titrated by plaque reduction assay using L cells and Semliki Forest virus (SFV as the challenge virus. Antiviral resistance was determined by inhibition of yield of SFV in a single growth cycle as previously reported ( 2 ) . DEAE-dx 0.015% was added to the nutrient agar over lay medium to inactive agar-inhibi,tors of SFV (3). Polyinosinic and Polycytidilic acids (Sigma Chemical Co.) were processed as indicated by Field et al. (1) in order to obtain the double-stranded complex I: C.The DEAE-dx (mol. wt. 2 X 106, Pharat Glasgow University Library on June 30, 2015 ebm.sagepub.com Downloaded from

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SUMMARYMengovirus-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, ,-amanitin or cordycepin I 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 [aH]-or [32P]-labelled mengovirus RF indicates that up to 4o % 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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