It is widely known that most viruses belonging to genus Enterovirus utilize “canyon” as their binding site to cells surface receptors, which is formed by outer capsid proteins including VP1, VP2 and VP3 . Several studies of other enteroviruses revealed that sequences of the VP1 coding region are responsible for the phenotype of viruses; some amino acid substitutions in this region altered the pathogenicity and cell tropism of the viruses [32–34]. Although the cell surface receptor to BEV has not been identified, it is likely that the capsid proteins, including VP1, may be responsible for the phenotype of BEVs, as their capsid proteins also form a “canyon” on the outer side of the virion, and a strain isolated from cattle with severe symptoms contained specific amino acid substitutions in the capsid regions [27, 35]. To elucidate the determinants of BEV virulence in hosts, genomic information of BEVs must be determined.