The study demonstrates that stably cloning long poly(C) tracts of EMC virus can be achieved using a shortened synthetic oligonucleotide cartridge, and identifies a specific point mutation affecting viral plaque size and protein mobility.
Highlights capsid residue modulating EMCV phenotype; extends picornavirus genetic mapping but remains hypothesis-generating for pathogenesis.
We constructed and characterized two infectious molecular clones of encephalomyocarditis (EMC) virus. Both constructs, pDL and pDA, were assembled from five overlapping cDNA clones derived from the diabetogenic variant of EMC virus (EMC-D) and from two synthetic oligonucleotide cartridges. pDA contained a single point mutation at position 1720 within the "puff" region of capsid protein 1AB that was derived from the nondiabetogenic variant of EMC virus (EMC-B). This point mutation resulted in an amino acid substitution of arginine (EMC-B) for lysine (EMC-D). Our construction illustrates two novel findings: (i) that the problem of stably cloning long poly(C) tracts of EMC virus can be circumvented by the use of a shortened, synthetic, poly(dC-dG) oligonucleotide cartridge, and (ii) that a single point mutation in the puff region of the capsid protein 1AB leads to change in its electrophoretic mobility and to a change in the plaque size of recombinant virus.
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Naviaux et al. (1990) studied this question.
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