Update on Senecavirus A research: Epidemiology of infection, evolution of the virus and its oncolytic activity

Abstract

Senecavirus A (SVA), formerly known as Seneca valley virus (SVV) (20), is a critical pathogen causing vesicular lesions in pigs and acute death of newborn piglets, resulting in very large economic losses in the pig industry. The aim of this paper was to present the current knowledge about the epidemiology and evolution of Senecavirus A, as well as the role of the virus in oncolytic therapy. From 1988 to 2005, a number of virus isolates were sporadically recovered from pigs in various regions of the United States, but without a detailed description of the clinical signs. After 2014, a sudden increase in SVA outbreaks appeared outside the United States and Canada, and SVA infection was reported in more regions of the United States, in Brazil, China, Colombia, Thailand and Vietnam with extensive distribution. After the expansion of the SVA area, complete and partial SVA genomic sequences were determined from SVA strains in most of these regions. Therefore, advances were also possible in the molecular epidemiology of the virus. A certain genetic distance has been determined between SVA strains isolated in various countries and at different times, suggesting a constant and rapid evolvement of SVA. It was shown that a combination of evolutionary processes, such as multiple mutations at variable sites and purifying selection, drove the genetic diversity and evolution of SVA. Evolutionary changes that accumulated in the SVA genome over the years may have contributed to the increased incidence of the disease. SVA is the first oncolytic picornavirus to be tested in humans and to penetrate solid tumours through the vascular system, unlike many other oncolytic viruses. SVA has a potential cytolytic activity and high selectivity for tumour cell lines with neuroendocrine properties versus adult normal cells