Persistent Infection and Transmission of Senecavirus A from Carrier Sows to Contact Piglets

Abstract

Senecavirus A (SVA) is a picornavirus that causes acute vesicular disease (VD), that is clinically indistinguishable from foot-and-mouth disease (FMD), in pigs. Notably, SVA RNA has been detected in lymphoid tissues of infected animals several weeks following resolution of the clinical disease, suggesting that the virus may persist in select host tissues. Here, we investigated the occurrence of persistent SVA infection and the contribution of stressors (transportation, immunosuppression, or parturition) to acute disease and recrudescence from persistent SVA infection. Our results show that transportation stress leads to a slight increase in disease severity following infection. During persistence, transportation, immunosuppression, and parturition stressors did not lead to overt/recrudescent clinical disease, but intermittent viremia and virus shedding were detected up to day 60 postinfection (p.i.) in all treatment groups following stress stimulation. Notably, real-time PCR and in situ hybridization (ISH) assays confirmed that the tonsil harbors SVA RNA during the persistent phase of infection. Immunofluorescence assays (IFA) specific for double-stranded RNA (dsRNA) demonstrated the presence of double-stranded viral RNA in tonsillar cells. Most importantly, infectious SVA was isolated from the tonsil of two animals on day 60 p.i., confirming the occurrence of carrier animals following SVA infection. These findings were supported by the fact that contact piglets (11/44) born to persistently infected sows were infected by SVA, demonstrating successful transmission of the virus from carrier sows to contact piglets. Results here confirm the establishment of persistent infection by SVA and demonstrate successful transmission of the virus from persistently infected animals. IMPORTANCE Persistent viral infections have significant implications for disease control strategies. Previous studies demonstrated the persistence of SVA RNA in the tonsil of experimentally or naturally infected animals long after resolution of the clinical disease. Here, we showed that SVA establishes persistent infection in SVA-infected animals, with the tonsil serving as one of the sites of virus persistence. Importantly, persistently infected carrier animals shedding SVA in oral and nasal secretions or feces can serve as sources of infection to other susceptible animals, as evidenced by successful transmission of SVA from persistently infected sows to contact piglets. These findings unveil an important aspect of SVA infection biology, suggesting that persistently infected pigs may function as reservoirs for SVA.

A virulent and pathogenic infectious clone of Senecavirus A

“…Interestingly, high levels of SVA RNA were observed in the tonsil of the inoculated animals on day 14 p.i. (end of acute phase of infection), suggesting that similar to the wt SVA, the rSVA SD15-26 clone was also able to establish persistence in tonsil as shown previously for wild-type SVA SD15-26 [14]. The rSVA SD15-26 clone generated here will be great platform to dissect the molecular mechanisms underlying SVA persistence.…”

“…(). Similar patterns of viremia have been observed in nursing [26] and finishing pigs [11–13], and sows [14] infected with wild-type strains of SVA. No differences in virus shedding in oral/nasal secretions and faeces between rSVA- and wt SVA SD15-26-inoculated groups were noted ().…”

“…Affected animals may shed virus in oral and nasal secretions and in faeces for up to 21–28 days p.i. [11, 14]. Later events in the course of infection involve the development of SVA-specific CD8 + T cells, culminating in the resolution of the disease [12].…”

Potent Protective Immune Responses to Senecavirus Induced by Virus-Like Particle Vaccine in Pigs

“…This virus mainly infects the host by inhibiting the production of INF-γ to escape the immune response [ 10 ]. It mainly exists the tonsils of pigs after infection [ 33 ], leading to continuous infection of the host. Therefore, increasing the immune response of Th-1 type cells is key to improving the vaccine protection rate.…”

Structures and Functions of Viral 5′ Non-Coding Genomic RNA Domain-I in Group-B Enterovirus Infections

“…RNA viruses including picornaviruses have been shown to develop persistent infections in human target tissues [120,[138][139][140]. Among human picornaviruses, polioviruses and group-B coxsackieviruses have been shown to establish persistent infections in target tissues resulting in chronic pathologies such as type 1 diabetes and DCM [120].…”