Porcine reproductive and respiratory syndrome virus (PRRSV) poses a severe threat to the health of pigs globally. Host factors play a critical role in PRRSV replication. Using PRRSV as a model for genome-scale CRISPR knockout (KO) screening, we identified a host factor critical to PRRSV infection: sphingomyelin phosphodiesterase acid-like 3B (SMPDL3B). Our findings show that SMPDL3B restricted PRRSV attachment, entry, replication, and secretion and that its depletion significantly inhibited PRRSV proliferation, indicating that SMPDL3B plays a positive role in PRRSV replication. Our data also show that SMPDL3B deficiency resulted in an accumulation of intracellular lipid droplets (LDs). The expression level of key genes (ACC, SCD-1, and FASN) involved in lipogenesis was increased, whereas the fundamental lipolysis gene, ATGL, was inhibited when SMPDL3B was knocked down. Overall, our findings suggest that SMPDL3B deficiency can effectively inhibit viral infection through the modulation of lipid metabolism.

Feline panleukopenia virus (FPV), the etiological agent of a highly contagious multispecies disease, demonstrates concerning phylogenetic divergence that compromises vaccine cross-protection. This study aimed to characterize a novel FPV strain through integrated virological and molecular analyses to assess epidemiological implications. From seven clinical specimens obtained from feline hosts with panleukopenia in Henan Province, China, we isolated FPV ZZ202303 using an F81 cell culture coupled with PCR verification, demonstrating potent cytopathic effects (TCID₅₀: 10^−5.72/0.1 mL) and rapid replication kinetics (viral peak at 12–24 h post-infection). Comparative virulence assessments revealed a 1.8- to 2.3-fold greater pathogenicity versus contemporary field strains (2021–2023). Phylogenetic reconstruction based on complete VP2 gene sequences positioned FPV ZZ202303 within an emerging clade sharing 97.5–98.2% identity with canine parvovirus strains versus 98.8–99.7% with FPV references, forming a distinct cluster (bootstrap = 94%) diverging from vaccine lineages. Critical structural analysis identified a prevalent I101T mutation (89.13% prevalence) in the VP2 capsid protein’s antigenic determinant region, with molecular modeling predicting altered surface charge distribution potentially affecting host receptor binding. Our findings substantiate FPV ZZ202303 as an evolutionarily divergent strain exhibiting enhanced virulence and unique genetic signatures that may underlie vaccine evasion mechanisms, providing critical data for updating prophylactic strategies against this economically impactful pathogen.

Porcine reproductive and respiratory syndrome virus (PRRSV), an enveloped single-stranded positive-sense RNA virus, poses a significant threat to global swine production. Despite the availability of modified live virus and inactivated vaccines, their limited efficacy and safety concerns highlight the urgent need for novel antiviral therapeutics. This study aimed to investigate the molecular mechanisms by which lycopene inhibits PRRSV replication. Initial assessments confirmed that lycopene did not adversely affect cellular viability, cell cycle progression, or apoptosis. Using fluorescence microscopy, flow cytometry, immunoblotting, quantitative real-time PCR (qRT-PCR), and viral titration assays, lycopene was shown to exhibit potent antiviral activity against PRRSV. Mechanistic studies revealed that lycopene suppresses reactive oxygen species (ROS) production, which is critical for PRRSV proliferation. Additionally, lycopene attenuated PRRSV-induced inflammatory responses, as demonstrated by immunoblotting, ELISA, and qRT-PCR assays. These findings suggest that lycopene inhibits PRRSV replication by modulating ROS levels and mitigating inflammation, offering a promising avenue for the development of antiviral therapeutics. This study provides new insights and strategies for combating PRRSV infections, emphasizing the potential of lycopene as a safe and effective antiviral agent.

This study investigated a suspected Feline calicivirus (FCV) outbreak at a veterinary facility in Zhengzhou, Henan Province, China. RT-PCR analysis confirmed the FCV presence, with subsequent CRFK cell culture propagation leading to the isolation and characterization of strain ZZ202306. Immunofluorescence and Western blot analyses validated the specificity of monoclonal antibodies targeting the FCV VP1 capsid protein. Transmission electron microscopy revealed non-enveloped virions of ~40 nm in diameter, exhibiting typical caliciviral architecture. Viral replication kinetics demonstrated exponential growth between 6 and 18 h post-inoculation, reaching a peak titer of 10^7.96 TCID₅₀/0.1 mL. Genomic sequencing coupled with phylogenetic reconstruction of the VP1 gene revealed a close genetic relation to domestic Chinese strains and international variants, while maintaining distinct evolutionary divergence from other calicivirus genera.