The study identifies that a defective function in the replication complex is involved in the restrictive event of EMC virus replication in semi-permissive monkey and monkey-mouse hybrid cells.
Should not yet inform antiviral strategies; leaves open replication complex targeting in EMC virus research.
Encephalomyocarditis (EMC) virus replication was investigated in permissive mouse MKS cells, semi-permissive monkey CV1 cells, and in somatic monkey-mouse MKCVIII hybrid cells whose permissiveness is under the negative control of the simian genome. We found that in CV1 cells the synthesis of both single- and double-stranded virus RNAs was restricted. In contrast, in semi-permissive hybrid Cl4/3 cells only the single-stranded virus RNA was synthesized in small amounts, whereas the double-stranded virus RNA accumulated late after infection. The synthesis of virus polyribosomes and virus polypeptides was lowered in semipermissive conditions. In the presence of quaternary ammonium ions, the synthesis of EMC virus was partially relieved in CV1 cells. Thus, it can be postulated that a defective function in the replication complex is involved in the restrictive event.
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M.-F. Dubois (1977) studied this question.
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