Two porcine variants of human coxsackievirus B5 and B4 emerged via independent recombination events, sharing 88% similarity in the 3D protein coding region.
This review details the emergence of swine vesicular disease viruses from human coxsackieviruses via recombination events.
In this review, we examine the occurrence of two independent, single recombination events which occurred between human enteroviruses (Picornaviridae, Enterovirus, Enterovirus betacoxsackie). These recombination events contributed to the emergence of two viruses which adapted to pigs. These viruses have caused epizootics of swine vesicular disease (SVD) for many years. As was shown previously, the classical SVD virus (SVDV-1) originated from human coxsackievirus B5. The strain T75 (SVDV-2) emerged from human coxsackievirus B4 in the Tambov region of Russia, where it circulated from 1975 to 1977. A high percentage of similarity between both types of the SVD virus was found in the 3D protein coding region (88%). In our previous work, analysis of the VP1 gene dates the appearance of the SVDV-2 precursor to between 1954 and 1975. In this work, the origin of the genome region encoding non-structural proteins was analyzed and is believed to be a result of multiple recombination events between human enteroviruses (hypothetically, E1, E9, E11 and coxsackievirus A9). The recombination breakpoint between the region of structural CVB4 proteins and non-structural T75 proteins is located in region 2A. This mini-review also represents the historical research of SVDV-1 and SVDV-2 strains (O72(USS/6/72) and T75, respectively) isolated in the former Soviet Union.
Lomakina et al. (Sat,) conducted a review in Swine vesicular disease. Two porcine variants of human coxsackievirus B5 and B4 emerged via independent recombination events, sharing 88% similarity in the 3D protein coding region.