Abstract
Seneca Valley virus (SVV) is a non-encapsulated single-stranded positive-strand RNA virus whose transmission routes have not yet been fully elucidated. Exosomes have been implicated in the intercellular transport of a variety of materials, such as proteins, RNA, and liposomes. However, whether exosomes can mediate SVV intercellular transmission remains unknown. In this study, we extracted exosomes from SVV-infected IBRS-2 cells to investigate intercellular transmission. Our results suggest that the intercellular transmission of SVV is mediated by exosomes. The results of co-localization and RT-qPCR studies showed that exosomes harbor SVV and enable the virus to proliferate in both susceptible and non-susceptible cells. Furthermore, the replication of SVV was inhibited when IBRS-2 cells were treated with interfering RNA Rab27a and exosome inhibitor GW4869. Finally, neutralization experiments were performed to further verify whether the virus was encapsulated by the exosomes that mediated transmission between cells. It was found that exosome-mediated intercellular transmission was not blocked by SVV-specific neutralizing antibodies. This study reveals a new transmission route of SVV and provides clear evidence regarding the pathogenesis of SVV, information which can also be useful for identifying therapeutic interventions.
Highlights
The Seneca Valley virus (SVV) is a single-stranded positive-strand RNA virus that belongs to the Senecavirus genus and Picornaviridae family
Isolation and characterization of exosomes extracted from SVV‐infected IBRS‐2 cells IBRS-2 cells were infected with SVV, and exosomes were extracted from those infected cells (SVV-exo), as well as the non-infected cells (Mock-exo)
The results showed that SVV-exo contained the exosome-associated proteins Alix, CD9, and CD63 (Figure 1B)
Summary
The Seneca Valley virus (SVV) is a single-stranded positive-strand RNA virus that belongs to the Senecavirus genus and Picornaviridae family. SVV has a typical icosahedral symmetry and a genome 7.2 kb in length [1]. SVV was first discovered in 2002 in the PER.C6 cell line in Maryland, USA [2]. SVV mainly infects pigs, newborn piglets, fattening pigs, and other pigs of all ages; neutralizing antibodies have been found in other animals, such as cattle and sheep [3, 4]. The clinical presentation is very similar to that of foot-and-mouth disease (FMD). The main symptoms are blisters and ulceration in the hoof and nose, as well as fever and anorexia [5].
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