Epidemiological surveys revealed that 33 of the 93 samples were positive for FHV-1, with the gD gene of these 33 samples exhibiting low variation, high homology, and no critical amino acid mutation. Feline herpesvirus type 1 (FHV-1), also known as feline viral rhinotracheitis (FVR) virus, is one of the main causes of URT disease in cats. All cats can become hosts of FHV-1, and the spread of this disease affects the protection of rare feline animals. Nasal swabs from cats with URT disease were collected at five veterinary clinics in Yanji City from 2022 to 2024. The purpose of this study was to isolate and investigate the epidemiology of FHV-1. The gD gene of the FHV-1 strain was cloned and inserted into the pMD-18T vector and transformed into a competent Escherichia coli strain. Subsequently, the gD gene of the positive samples was sequenced and phylogenetic analysis was performed to determine the genetic evolution relationship between the strains. We successfully isolated the FHV-1 strain YBYJ-1 in Yanji City for the first time. The diameter of the virus is approximately 150–160 nm. After 48 h of virus inoculation, the cells were round, isolated, and formed grape-like clusters. The gD gene of the virus was sequenced, and the length was 1125 bp, which proved the isolate was FHV-1. This study found that the genetic evolution of the FHV-1 gD gene was stable, expanding the molecular epidemiological data on FHV-1 in cats in Yanji City.

Feline panleukopenia (FP) is a severe viral illness caused by the feline panleukopenia virus (FPV), putting sectors like companion cat breeding and endangered feline conservation at risk. The virus has a high morbidity and fatality rate and is found all over the world. We created a novel FPV assay using nanoPCR technology and assessed the method’s specificity and sensitivity. The approach amplified a 345 bp nucleic acid fragment with a minimum detection limit of 7.97 × 10² copies/μL, which is about 100 times greater than traditional PCR. We collected anal swabs from 83 cats suspected of FPV infection for practical application, and the FPV-positive rate determined by the nanoPCR approach was 77.1%. In conclusion, the approach is more sensitive than conventional PCR and more convenient and cost-effective than qPCR methodology and may be utilized for the clinical detection of FPV.

Bovine infectious rhinotracheitis (IBR), caused by bovine alphaherpesvirus 1 (BoAHV1), poses significant challenges to the global cattle industry due to its high contagiousness and economic impact. In our study, we successfully isolated a BoAHV1 strain from suspected infected bovine nasal mucus samples in Yanji city, revealing genetic similarities with strains from Sichuan, Egypt, and the USA, while strains from Xinjiang, Beijing, Hebei, and Inner Mongolia showed more distant associations, indicating potential cross-border transmission. Additionally, our investigation of BoAHV1 infection dynamics within host cells revealed early upregulation of gB, which is critical for sustained infection, while the expression of gC and gD showed variations compared to previous studies. These findings enhance our understanding of BoAHV1 diversity and infection kinetics, underscoring the importance of international collaboration for effective surveillance and control strategies. Furthermore, they lay the groundwork for the development of targeted therapeutics and vaccines to mitigate the impact of IBR on the cattle industry.

CPV is a highly pathogenic virus that enters host cells via the TFR, but its pathogenic mechanisms are not fully understood. In this study, we demonstrated that CPV infection induces ferroptosis in CRFK cells, characterized by elevated lipid peroxidation, increased intracellular ferrous iron, a reduced GSH/GSSG ratio, and mitochondrial damage. At the molecular level, CPV downregulated the ferroptosis-inhibiting proteins GPX4 and FTH1 while upregulating NCOA4 and Drp1. Notably, treatment with the iron chelator DFO both inhibited viral replication and attenuated CPV-induced ferroptosis. Collectively, our findings identify ferroptosis as a critical pathogenic mechanism of CPV infection and highlight the therapeutic potential of DFO in controlling CPV by restoring iron homeostasis. These insights provide a mechanistic basis for the development of ferroptosis-targeted antiviral strategies against CPV.