Key result
Recombinant EMC viral RNA with a complete poly(C) tract induces diabetes in ~90% of mice.
Why the study?
Does recombinant chimeric RNA with a long poly(C) tract produce pathogenic progeny virus in vivo?
Does recombinant chimeric RNA with a long poly(C) tract produce pathogenic progeny virus in vivo?
This method provides a novel technique for constructing full-length infectious clones of RNA viruses with long poly(C) tracts, overcoming a major technical barrier in virology.
The murine cardioviruses and bovine aphthoviruses are distinguished from other (+) strand RNA viruses by their long poly(C) tract in the 5'-noncoding region. The presence of this poly(C) tract has long hampered the construction of full-length cDNA with the complete poly(C) tract, because long poly(dC-dG) homopolymer-containing plasmids are difficult to amplify in bacterial systems. To overcome this problem, we constructed a chimeric RNA by joining the poly(C) region of the viral RNA to the 5'-truncated RNA transcript of the encephalomyocarditis (EMC) virus cDNA. The non-chimeric, recombinant EMC virus with a short poly(C) tract produces recombinant progeny virus, but this is not pathogenic in vivo. On the other hand, the EMC viral RNA chimera with the complete poly(C) tract produces recombinant progeny virus that is pathogenic in vivo. This method of viral RNA construction will be invaluable for functional studies of other cardioviruses and aphthoviruses, as well as for recombinant RNA manipulations.
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Bae et al. (1993) studied Preclinical model (viral diabetogenicity). Chimeric RNA with complete poly(C) tract (EMC virus) vs. Uninfected mice or wild type/short poly(C) viruses was evaluated on Diabetogenicity (blood glucose index >248 mg/dl). The EMC viral RNA chimera with the complete poly(C) tract produced recombinant progeny virus that was pathogenic in vivo, inducing diabetes in 90% of inoculated SJL/J male mice.
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