Porcine rotavirus (PoRV) is a significant enteric pathogen causing gastroenteritis in piglets, which causes huge economic loss to the Chinese pig industry. In this study, six porcine rotavirus A strains were isolated from three adjacent sow farms belonging to the same company within one year, which suffered severe diarrhea outbreaks. AHBZ2303 (G11P[7]) and AHBZ2305 (G9P[23]), AHBZ2304 (G9P[23]) and AHBZ2312 (G4P[6]), AHBZ2310 (G9P[23]) and AHBZ2402 (G5P[23]) were isolated from Farm A, B and C, respectively. All six isolates were related to human rotavirus through complete genome analysis, suggesting the potential cross–species infection between humans and pigs. Evolutionary analysis revealed that AHBZ2303 and AHBZ2304 likely emerged simultaneously in Farm A and B, and then AHBZ2304 was introduced to Farm A and C, leading to the emergence of AHBZ2305 and AHBZ2310. Recombination and large variation were identified for AHBZ2312 and AHBZ2402. These findings provided insights into the transmission and evolution of PoRV among farms and underscored the need for enhanced monitoring to mitigate the risk of outbreaks from novel variants.

Pseudorabies virus (PRV), an alphaherpesvirus, causes severe neurological and respiratory diseases in multiple mammalian species and poses an emerging threat to public health. Increasing evidence suggests that virus-induced inflammatory cell death plays a pivotal role in shaping host immune responses and disease outcomes. PANoptosis, a newly defined inflammatory programmed cell death pathway integrating pyroptosis, apoptosis, and necroptosis, has been implicated in host defense against diverse pathogens. However, whether PRV infection induces PANoptosis and contributes to inflammatory pathology remains largely unexplored. In this study, we demonstrate that PRV efficiently replicates in Human Acute Monocytic Leukemia Cells (THP-1)-derived macrophages and robustly induces PANoptosis, characterized by the concurrent activation of Gasdermin D, caspase-3, and Mixed Lineage Kinase Domain-Like (MLKL). Pharmacological inhibition of PANoptosis markedly attenuated PRV-induced inflammatory cytokine production in vitro. Furthermore, intranasal inoculation of PRV in Balb/c mice resulted in productive lung infection accompanied by pronounced pulmonary inflammation. Lung tissues from PRV-challenged mice exhibited molecular and histopathological hallmarks of PANoptosis. Importantly, drug-mediated suppression of PANoptosis significantly reduced lung inflammation and inflammatory cytokine expression in vivo. Collectively, our findings identify PANoptosis as a critical mechanism underlying PRV-induced inflammatory responses and suggest that targeting PANoptosis may represent a promising therapeutic strategy for PRV-associated inflammatory diseases.

Porcine epidemic diarrhea virus (PEDV) poses a persistent threat to the global swine industry through the continual emergence of variants driven by mutation and recombination. Here, we report the isolation and genomic characterization of PEDV2−5, an inter-subgenotypic recombinant isolated from clinical samples collected in Jiangxi Province, China. Phylogenetic analysis based on both the complete genome and the full-length S gene placed PEDV2−5 within the GIIb subgenotypes, clustering closely with FL201 and GD-1. Recombination detection using seven independent algorithms in RDP5, corroborated by SimPlot and phylogenetic incongruence analysis, identified PEDV2−5 as a recombinant between a GIIa major parental-like (PEDV-LY) and a GIIb minor parental-like (GD-1), generating a 7931-nucleotide fragment (nt 20060–27990) that spans the complete structural protein cassette (S, ORF3, E, M, N) and the 3′-terminal portion of ORF1b. The recombinant has replication-competent Vero-E6 cells, reaching a peak titer of 5.03 log10 TCID₅₀/mL at 36 h post-infection. Amino acid analysis revealed 98.49% identity between the PEDV2−5 S protein and the GIIb strain AJ1102, together with 13 unique substitutions and a “KKKG” insertion (residues 361–364), including two substitutions within neutralizing epitopes (A517F in COE and Y1374C in 2C10). Relative to AJ1102, the neutralizing epitopes were nearly completely conserved, whereas extensive divergence was observed against the classical GIa strain CV777. These findings highlight the importance of continued whole-genome surveillance for monitoring the emergence and spread of recombinant PEDV lineages and for informing future vaccine antigen-selection strategies.