Key result
Genetic differences in both coding and noncoding regions of group B coxsackieviruses determine virulence and pathogenic phenotypes, though findings from laboratory strains require wild-type confirmation.
This review highlights the importance of specific genetic changes in group B coxsackieviruses that determine virulence and pathogenic phenotypes in hosts.
Laboratory findings on coxsackievirus genetics require wild-type validation; leaves open clinical translation for myocarditis risk stratification.
The group B coxsackieviruses (CVB) are well-studied human enteroviruses that are established causes of numerous serious human diseases. Characterized differences in CVB genomes of different strains affect the ability with which specific strains induce disease in the mouse host and, by inference, in humans as well. The first hurdle is to define specific examples of CVB genetic changes that are associated with pathogenic phenotypes. Such differences have been mapped both to coding and noncoding genomic regions. Many studies have used laboratory-derived strains to identify genetic differences that are essential to phenotype expression, work that is valuable but requires confirmation from studies of wild-type isolates. Rapid viral replication is closely associated with acute disease, indicating a key role for viral damage to the host, while host-mediated responses to the viral infection and viral persistence over a longer period of time indicate other roles for the virus in pathogenesis.
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Kim et al. (2006) conducted a review in Group B coxsackievirus infection. Genetic differences in both coding and noncoding regions of group B coxsackieviruses determine virulence and pathogenic phenotypes, though findings from laboratory strains require wild-type confirmation.
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