Abstract
Senecavirus A (SVA), also known as Seneca Valley virus, is a recently emerged picornavirus that can cause swine vesicular disease, posing a great threat to the global swine industry. A recombinant reporter virus (rSVA-Nluc) stably expressing the nanoluciferase (Nluc) gene between SVA 2A and 2B was developed to rapidly detect anti-SVA neutralizing antibodies and establish a high-throughput screen for antiviral agents. This recombinant virus displayed similar growth kinetics as the parental virus and remained stable for more than 10 passages in BHK-21 cells. As a proof-of-concept for its utility for rapid antiviral screening, this reporter virus was used to rapidly quantify anti-SVA neutralizing antibodies in 13 swine sera samples and screen for antiviral agents, including interferons ribavirin and interferon-stimulated genes (ISGs). Subsequently, interfering RNAs targeting different regions of the SVA genome were screened using the reporter virus. This reporter virus (rSVA-Nluc) represents a useful tool for rapid and quantitative screening and evaluation of antivirals against SVA.
Highlights
Senecavirus A (SVA), formally named Seneca Valley virus, is a single-stranded non-enveloped RNA virus and belongs to the genus Senecavirus of the family Picornaviridae (Hales et al, 2008; Adams et al, 2015)
The results showed that the rSVA-Nluc neutralization assay detecting neutralizing antibodies in SVA sera had a higher sensitivity than the conventional Cytopathic effect (CPE) assay
Porcine IFN-α (PoIFN-α) proteins were tested for anti-SVA-Nluc activities in swine testis (ST) cells
Summary
Senecavirus A (SVA), formally named Seneca Valley virus, is a single-stranded non-enveloped RNA virus and belongs to the genus Senecavirus of the family Picornaviridae (Hales et al, 2008; Adams et al, 2015). The genome of SVA is about 7.2 kb in length. It contains a unique open reading frame (ORF), flanked by a 5 untranslated region (UTR) and a short 3 UTR followed by a poly(A) tail. In 2002, a company in the United States accidentally discovered SVA in cell culture (Hales et al, 2008). SVA was originally considered a contaminant in the cell culture, presumably derived from porcine trypsin or fetal bovine serum (Reddy et al, 2007). After 2014, SVA has been associated with vesicular disease outbreaks of swine in Canada, United States, Brazil, Thailand, and China (Vannucci et al, 2015; Joshi et al, 2016; Wu et al, 2017; Xu et al, 2017; Saeng-Chuto et al, 2018)
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