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Picornaviridae are non-enveloped ssRNA viruses that cause diseases such as poliomyelitis, hand-foot-and-mouth disease (HFMD), hepatitis A, encephalitis, myocarditis, and foot-and-mouth disease (FMD). Virus-like particles (VLPs) vaccines mainly comprise particles formed through the self-assembly of viral capsid proteins (for enveloped viruses, envelope proteins are also an option). They do not contain the viral genome. On the other hand, the nanoparticles vaccine (NPs) is mainly composed of self-assembling biological proteins or nanomaterials, with viral antigens displayed on the surface. The presentation of viral antigens on these particles in a repetitive array can elicit a strong immune response in animals. VLPs and NPs can be powerful platforms for multivalent antigen presentation. This review summarises the development of virus-like particle vaccines (VLPs) and nanoparticle vaccines (NPs) against picornaviruses. By detailing the progress made in the fight against various picornaviruses such as poliovirus (PV), foot-and-mouth disease virus (FMDV), enterovirus (EV), Senecavirus A (SVA), and encephalomyocarditis virus (EMCV), we in turn highlight the significant strides made in vaccine technology. These advancements include diverse construction methods, expression systems, elicited immune responses, and the use of various adjuvants. We see promising prospects for the continued development and optimisation of VLPs and NPs vaccines. Future research should focus on enhancing these vaccines' immunogenicity, stability, and delivery methods. Moreover, expanding our understanding of the interplay between these vaccines and the immune system will be crucial. We hope these insights will inspire and guide fellow researchers in the ongoing quest to combat picornavirus infections more effectively.

Senecavirus A (SVA) is a positive-sense single-stranded RNA virus that belongs to the Senecavirus genus within the Picornaviridae family. The virus has been silently circulating in pig herds of the USA since 1988. However, cases of senecavirus-associated vesicular disease were reported in Canada in 2007 and in the USA in 2012. Since late 2014 and early 2015, an increasing number of senecavirus outbreaks have been reported in pigs in different producing categories, with this virus being detected in Brazil, China, and Thailand. Considering the novel available data on senecavirus infection and disease, 2015 may be a divisor in the epidemiology of the virus. Among the aspects that reinforce this hypothesis are the geographical distribution of the virus, the affected pig-producing categories, clinical signs associated with the infection, and disease severity. This review presents the current knowledge regarding the senecavirus infection and disease, especially in the last two years. Senecavirus epidemiology, pathogenic potential, host immunological response, diagnosis, and prophylaxis and control measures are addressed. Perspectives are focused on the need for complete evolutionary, epidemiological and pathogenic data and the capability for an immediate diagnosis of senecavirus infection. The health risks inherent in the swine industry cannot be neglected.

Vesicular disease caused by Seneca Valley virus infection occurred in pigs from 5 outdoor pig farms in England during June-September 2022. Clinical signs resembled notifiable vesicular diseases, such as foot-and-mouth disease. Full genome sequences shared a common ancestor with a virus circulating in the United States.

Ducks can shed and disseminate viruses and thus play a role in cross-species transmission. In the current study, we detected and characterised various avian parvoviruses and picornaviruses from wild Pacific black ducks, Chestnut teals, Grey teals and Wood ducks sampled at multiple time points from a single location using metagenomics. We characterised 46 different avian parvoviruses belonging to three different genera Dependoparvovirus, Aveparvovirus and Chaphamaparvovirus, and 11 different avian picornaviruses tentatively belonging to four different genera Sicinivirus , Anativirus , Megrivirus and Aalivirus . Most of these viruses were genetically different from other currently known viruses from the NCBI dataset. The study showed that the abundance and number of avian picornaviruses and parvoviruses varied considerably throughout the year, with the high number of virus reads in some of the duck samples highly suggestive of an active infection at the time of sampling. The detection and characterisation of several parvoviruses and picornaviruses from the individual duck samples also suggests co-infection, which may lead to the emergence of novel viruses through possible recombination. Therefore, as new and emerging diseases evolve, it is relevant to explore and monitor potential animal reservoirs in their natural habitat.

Seneca Valley virus (SVV), a new member of Picornaviridae , causes idiopathic vesicular symptoms in pregnant sows and acute death in neonatal piglets, considerably damaging the swine industry. The viral protease 3C (3C pro ) cleaves host immune-related molecules to create a favorable environment for viral replication. In this study, we found that mRNA decapping enzyme 1A (DCP1A) is a novel antiviral effector against SVV infection that targets 3D viral RNA-dependent RNA polymerase for OPTN-mediated autophagic degradation. To counteract this effect, SVV 3C pro targets DCP1A for cleavage at glutamine 343 (Q343), resulting in the cleaved products DCP1A (1–343) and DCP1A (344–580), which lose the ability to restrict SVV replication. In contrast, the 3C cleavage-resistant DCP1A-Q343A mutant exhibited stronger antiviral effects than the wild-type DCP1A. Additionally, the degradation of the viral 3D protein targeted by DCP1A was abolished after its cleavage by SVV 3C pro . In conclusion, our study demonstrated that SVV 3C pro is a pivotal ISG antagonist that cleaves DCP1A. These results offer novel insight into how viruses evade host immunity.

Rosavirus is a newly discovered member of the family Picornaviridae that was initially detected in wild rodents and subsequently in children with diarrhoea. Nevertheless, there is a significant gap in our understanding of the geographical distribution, phylogenetic relationships, evolutionary patterns, and transmission of rosaviruses. To address these issues, we analysed 434 rodents and shrews from five different species that were collected in southern China. Using PCR screening of faecal samples, we detected rosaviruses in Norway rats ( Rattus norvegicus ) and identified two previously undocumented host species: tanezumi rats ( Rattus tanezumi ) and Asian house shrews ( Suncus murinus ). Rosaviruses were particularly common in these animals, with an overall prevalence rate of 32.49% (141/434). For genetic and evolutionary analyses, we selected six representative positive samples to amplify the complete genomes of rosaviruses. Bayesian phylogenetic analysis suggested that our sequences clustered within the genus Rosavirus, where genotype B sequences are the closest relatives. The elevated nonsynonymous-to-synonymous ratios observed in rosavirus B may be attributed to relaxed selection pressures driven by virus spillover events. On the basis of the available data, it is hypothesized that the genus Rosavirus may have originated from Norway rats around the year 1339. In summary, these findings provide valuable insights into the complex evolutionary history of rosaviruses and underscore the urgent need for ongoing surveillance of this virus.

Enteric diseases in swine are often caused by different pathogens and thus metagenomics are a useful tool for diagnostics. The capacities of nanopore sequencing for viral diagnostics were investigated here. First, cell culture-grown porcine epidemic diarrhea virus and rotavirus A were pooled and sequenced on a MinION. Reads were already detected at 7 seconds after start of sequencing, resulting in high sequencing depths (19.2 to 103.5X) after 3 h. Next, diarrheic feces of a one-week-old piglet was analyzed. Almost all reads (99%) belonged to bacteriophages, which may have reshaped the piglet’s microbiome. Contigs matched Bacteroides , Escherichia and Enterococcus phages. Moreover, porcine kobuvirus was discovered in the feces for the first time in Belgium. Suckling piglets shed kobuvirus from one week of age, but an association between peak of viral shedding (10 6.42 –10 7.01 copies/swab) and diarrheic signs was not observed during a follow-up study. Retrospective analysis showed the widespread (n = 25, 56.8% positive) of genetically moderately related kobuviruses among Belgian diarrheic piglets. MinION enables rapid detection of enteric viruses. Such new methodologies will change diagnostics, but more extensive validations should be conducted. The true enteric pathogenicity of porcine kobuvirus should be questioned, while its subclinical importance cannot be excluded.

In this study, two novel picornaviruses (eagle/WE6/HUN/2014, PV454551-PV454552 and avocet/PA12/HUN/2018, PV454553) were detected in white-tailed eagle ( Haliaeetus albicilla ) and pied avocet ( Recurvirostra avosetta ) in Hungary, and characterized by next generation sequencing, RT-PCR and Sanger sequencing methods. The complete polyprotein coding genomes were 6,573 and 6,567 nt long and had the genome organization 5′UTR IRES-III -[VP4-VP2-VP3-VP1-2A-2B-2C hel -3A-3B VPg -3C pro -3D pol ]-3′UTR-poly(A)n. The P1 and the 3C pro proteins of the eagle/WE6/HUN/2014 showed 47.9% and 62.4% aa sequence identities to the corresponding proteins of the picornavirus (MT138036) from a little egret metagenome, respectively. The 2C hel /3D pol had 44.1%/41% aa identity to the corresponding proteins of bat-origin picornaviruses (OR867633 and KX420952). The P1 protein of the avocet/PA12/HUN/2018 had 53% aa sequence identity to the P1 protein of crane70contig328 (OQ423840) from red-crowned crane metagenome; the 2C hel , 3C pro proteins had 52.6%, 52.3% aa sequence identity to the corresponding proteins of picornavirus (MT138035) from bird metagenome and 3D pol had 43.2% aa identity to the 3D pol of the picornavirus (MT138036) from a little egret metagenome, respectively. The 3’UTR of avocet/PA12/HUN/2018 contained two repetitive nt sequence motifs (the 17-nt-long Motif-1 at five times forming a secondary RNA structure and the 9-nt-long Motif-2 at two times). The eagle/WE6/HUN/2014 and avocet/PA12/HUN/2019 represent the founding members of two potential novel bird-origin picornavirus species and even genera in the subfamily Heptrevirinae (family Picornaviridae ).

Senecavirus A (SVA) is an emerging pathogen that causes idiopathic vesicular infections in pig herds, posing a potential threat to their production performance. Heat shock protein 70 (Hsp70) is a molecular chaperone that plays an important role in host homeostasis under both physiological and stress conditions. However, the effects of Hsp70 on SVA infection and its underlying regulatory mechanisms remain unclear. Here, we confirmed that Hsp70 expression promotes SVA infection, as evidenced by the expression of viral proteins, viral titers, and the number of rSVA-eGFP-infected cells. This positive regulatory role of Hsp70 is mainly involved in post-entry stages of SVA. Viral proteins that interacted with Hsp70 were screened, and co-immunoprecipitation (co-IP) shows an interaction between Hsp70 and SVA L and 3D proteins. Subsequently, we determined that the expression of Hsp70 is beneficial for the stability of the SVA L and 3D proteins. Additionally, the substrate-binding domain (SBD) of Hsp70 plays an important role in the interaction between Hsp70 and SVA L or 3D proteins; and the deletion of this domain results in the loss of the stabilizing effect of Hsp70 on SVA L and 3D proteins and the positive regulatory effect of Hsp70 on SVA replication. These results reveal that Hsp70 promotes SVA infection by stabilizing viral L and 3D proteins and provides a strategy for preventing and controlling SVA infection.

Seneca Valley virus (SVV) infection has recently disseminated across pig farms in Canada, America, and China. The SVV has been identified in humans, rodents, and houseflies. Although cross‐species transmission events may lead to limited subsequent transmission, sustained outbreaks have been observed in new mammalian hosts. Thus, in our study, we utilized molecular characteristics, pathological examination, and the immune response to ascertain whether mink could serve as a novel mammalian host for SVV. Here, our study utilized a porcine strain of SVV to infect minks orally, resulting in pathological changes in the intestines. In addition, SVV could stimulate a specific neutralizing antibody response. The neutralizing antibody against SVV has also been found in mink through an epidemiological investigation in Heilongjiang Province. This study highlights the role of SVV infection in minks as an impetus for viral evolution, which poses potential threats to livestock, public health, and economic prosperity.