Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6141954 | Virology | 2008 | 12 Pages |
Enteroviruses can induce human myocarditis, which can be modeled in mice inoculated with group B coxsackieviruses (CVB) and in which CVB evolve to produce defective, terminally deleted genomes. The 5â² non-translated region (NTR) was enzymatically amplified from heart tissue of a fatal case of enterovirus-associated myocarditis in Japan in 2002. While no intact 5â² viral genomic termini were detected, 5â² terminal deletions ranged in size from 22 to 36 nucleotides. Sequence of the 5â² third of this viral genome is of a modern strain, closely related to CVB2 strains isolated in Japan in 2002. A CVB3 chimera containing the 5â² NTR with a 22 nt deletion produced progeny virus upon transfection of HeLa cells. When the 5â² 22 nucleotide deletion was repaired, the virus induced myocarditis in mice and replicated like wild type virus in murine heart cells. This is the first report of these naturally-occurring defective enteroviral genomes in human myocarditis.