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No surface morphology is visible by EM. The X-ray crystallographic structure of Seneca Valley virus (SVV) has been determined at 2.3Å resolution (Venkataraman et al., 2008). The overall folds of the CPs are very similar to the corresponding proteins in other picornaviruses. Similar to cardioviruses, VP1 of SVV possesses a hydrophobic pocket without a pocket factor. However, the entrance to the hydrophobic cleft in SVV is almost completely sealed off by a number of VP1 residues. In cardioviruses the entrance is narrow while in the human rhinoviruses it is wide.
SVV is stable at pH 3.0.
Length of genome (Hales et al., 2008): c. 7,310 nt (5'-UTR: 666 nt; ORF: 6546 nt; 3'-UTR: 71 nt). 5' UTR contains a type IV IRES. The predicted folding of the 3'-UTR reveals two stem-loops with the potential to form a kissing-loop structure. This type of structure has been shown to be important in enterovirus replication. The location of the cre has not been identified.
The deduced polyprotein has a length of 2,181 aa. There is a leader polypeptide of unknown function. It lacks both catalytic residues, present in the aphtho- and erboviruses, which are necessary for proteolytic activity and zinc finger/tyrosine-phosphorylation motifs present in the cardioviruses. 1AB possesses a myristoylation signal at its amino-terminus and is cleaved to VP4 and VP2. 2A is a short FMDV-like polypeptide with NPG↓P motif.
Only a single type, Seneca Valley virus 1 (SVV-1), has been recognized.
Seneca Valley virus was first isolated from pigs in 1988 in the USA (Knowles et al., 2006). It was later serendipitously detected as a contaminant of PER.C6 cells while cultivating adenovirus-5-based vectors (Hales et al., 2008). The only known natural host is the pig but SVV was also detected in faeces and small intestine of mice and in flies. SVV can replicate and cause CPE in a wide range of cell cultures include those derived from pigs, sheep, rabbits, hamsters, monkeys and humans. Although early isolations of SVV were not linked with disease in pigs, since the late 1990s there has been an increasing association with idiopathic vesicular disease. Recently, a direct causation of vesicular disease in pigs has been established and the virus has spread to other countries (Canada, Brazil, China and Thailand). SVV has potent cytolytic activity and high selectivity for human tumour cell lines having neuroendocrine properties versus adult normal cells. Its use for treatment of human metastatic neuroendocrine cancers has been investigated.
Seneca: from Seneca Valley virus, name is derived from Seneca Creek State Park (Maryland, USA), near the laboratories that first described the virus.
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