Porcine epidemic diarrhea virus (PEDV) severely threatens the global swine industry and causes massive economic losses due to high morbidity and mortality in neonatal piglets. To date, key host receptors and molecular determinants regulating PEDV entry remain poorly characterized. Here, we found that overexpression of porcine interferon-induced transmembrane protein 1 (pIFITM1) in LLC-PK1, IPEC-J2, and Huh7 cells enhanced PEDV-HM infection. Conversely, knockout of endogenous pIFITM1 suppressed PEDV-HM infection, and this phenotype was rescued by pIFITM1 reconstitution. Additionally, pIFITM1 interacted with the PEDV spike, envelope, and membrane proteins and promoted PEDV attachment and internalization. As PEDV invades host cells via caveolae-mediated endocytosis, we further confirmed that pIFITM1 interacted with caveolin-1 (CAV1) and modulated plasma membrane cholesterol distribution to promote PEDV entry through this pathway. Mechanistically, deletion of the conserved intracellular loop (CIL) abolished the proviral effect of pIFITM1. Notably, site-directed mutagenesis of lysine residues K62 and K83 within the CIL abolished its proviral function, suggesting that these two residues are essential for pIFITM1-mediated promotion of PEDV entry. In summary, our study demonstrates that pIFITM1 acts as a critical proviral factor that facilitates PEDV entry by binding viral structural proteins and regulating the cholesterol–CAV1 complex. This study also identifies pIFITM1 as a promising target for developing anti-PEDV interventions.

Porcine sapelovirus (PSV), an emerging picornavirus, is increasingly recognized for its wide distribution and impact on swine health. While often subclinical, PSV can cause multisystemic disease and is frequently detected in co-infections with other porcine pathogens. However, the emergence and evolutionary dynamics of PSV in China are still not well characterized. This review consolidates recent progress on the origin and genetic evolution of PSV, with emphasis on genomic surveillance and recombination events. Studies reveal extensive genetic diversity and continuous adaptive evolution, driven largely by frequent recombination across the genome, with the 2A gene region identified as a key hotspot. This synthesis provides a timely theoretical foundation for understanding PSV evolution and informs future surveillance strategies. We emphasize the necessity of sustained genomic monitoring and call for focused research on the pathogenicity of circulating recombinants and their roles in co-infections, which is essential for developing effective countermeasures.

Porcine sapelovirus (PSV) is an emerging enteric pathogen associated with diarrheal disease in pigs, yet its epidemiological characteristics and genomic diversity in China remain inadequately characterized. In this study, we systematically compiled epidemic data on all Chinese PSV strains reported in domestic and international literature and constructed a geographic distribution map of PSV across China. Analysis of co-infection patterns revealed that PSV frequently co-occurs with PEDV, PAstV, and PKoV. A total of 74 PSV Chinese strains were retrieved from GenBank for genomic characterization. No distinct regional clustering was observed among the prevalent strains; however, a remarkably high recombination rate of 85.14% was identified, with recombination breakpoints predominantly concentrated near the 2A gene region. Temporal phylogenetic analysis indicated that avian sapeloviruses and PSV shared a similar evolutionary timeline (1985), with PSV-1 emerging earlier than PSV-2. Within the PSV-1 subtype, the German strain exhibited the earliest divergence (1997), followed by Chinese strains (1985), then Korean and American strains (2005). These findings underscore the importance of sustained genomic surveillance and highlight the need for further investigation into the pathogenicity of circulating recombinant strains and their roles in polymicrobial infections, which is critical for developing effective control strategies.

Porcine epidemic diarrhea virus (PEDV) is a major enteric coronavirus that causes severe economic losses to the global swine industry. Current vaccines suffer from weak immunogenicity, insufficient mucosal immunity, and a short duration of protection. Nanoparticle delivery systems have emerged as a promising strategy for next-generation vaccine development. In the present study, we constructed an S1-Ferritin nanoparticle vaccine using the SpyTag-SpyCatcher modular conjugation system. The morphology, particle size, and uniformity of the nanoparticle vaccine were systematically characterized by transmission electron microscopy (TEM) and dynamic light scattering (DLS). After two immunizations, the S-Ferritin nanoparticle vaccine elicited potent humoral and cellular immune responses in both mice and piglets. In piglets, at 2 weeks post booster vaccination, PEDV-specific serum IgG endpoint titers peaked at 1:2560, virus-neutralizing antibody titers reached 1:256 against the JS-2/2015 strain, and serum IFN-γ levels reached 274 pg/mL. All these immunological indicators were significantly higher than those observed in the PEDV-inactivated whole-virus vaccine group. Furthermore, challenge tests showed that the S1-Ferritin nanoparticle vaccine provided complete protection against PEDV infection and significantly reduced the severity of diarrhea and intestinal damage in piglets after challenge. These findings suggest that the S1-Ferritin nanoparticle vaccine constitutes a promising candidate against PEDV infection, though our study is only a preliminary step and subsequent field trials in pigs are still required.