Literature DB >> 29890334

The full-length genome characterization, genetic diversity and evolutionary analyses of Senecavirus A isolated in Thailand in 2016.

Kepalee Saeng-Chuto1, Christopher James Stott1, Matthew Wegner2, Pavita Kaewprommal3, Jittima Piriyapongsa3, Dachrit Nilubol4.   

Abstract

Senecavirus A (SVA) is a novel picornavirus that causes porcine idiopathic vesicular disease characterized by lameness, coronary band hyperemia, and vesicles on the snout and coronary bands. An increase in the detection rate of SVA in several countries suggests that the disease has become a widespread problem. Herein, we report the detection of SVA in Thailand and the characterization of full-length genomic sequences of six Thai SVA isolates. Phylogenetic, genetic, recombination, and evolutionary analyses were performed. The full-length genome, excluding the poly (A) tail of the Thai SVA isolates, was 7282 nucleotides long, with the genomic organization resembling other previously reported SVA isolates. Phylogenetic and genetic analyses based on full-length genome demonstrated that the Thai SVA isolates were grouped in a novel cluster, separated from SVA isolates from other countries. Although the Thai SVA isolates were closely related to 11-55910-3, the first SVA isolate from Canada, with 97.9-98.2%, but they are different. Evolutionary and recombinant analyses suggested that the Thai SVA isolates shared a common ancestor with the 11-55910-3 isolate. The positive selection in the VP4 and 3D genes suggests that the virus was not externally introduced, but rather continuously evolved in the population prior to the first detection. Addition, the presence of SVA could have been ignored due to the presence of other pathogens causing similar clinical diseases. This study warrants further investigations into molecular epidemiology and genetic evolution of the SVA in Thailand.
Copyright © 2018 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Full-length genome; Pigs; Senecavirus A; Thailand

Mesh:

Substances:

Year:  2018        PMID: 29890334     DOI: 10.1016/j.meegid.2018.06.011

Source DB:  PubMed          Journal:  Infect Genet Evol        ISSN: 1567-1348            Impact factor:   3.342


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