Feline coronavirus (FCoV) infections present as one of two forms: a mild or symptom-less enteric infection (FEC) and a fatal systemic disease termed feline infectious peritonitis (FIP). The lack of epidemiology of FCoV in central China and the reason why different symptoms are caused by viruses of the same serotype have motivated this investigation. Clinical data of 81 suspected FIP cases, 116 diarrhea cases and 174 healthy cases were collected from veterinary hospitals using body cavity effusion or fecal samples. Risk factors, sequence comparison and phylogenetic studies were performed. The results indicated that FIPV was distinguished from FECV in the average hydrophobicity of amino acids among the cleavage sites of furin, as well as the mutation sites 23,531 and 23,537. FIPV included a higher minimal R-X-X-R recognition motif of furin (41.94%) than did FECV (9.1%). The serotype of FCoV was insignificantly correlated with FIP, and the clade 1 and clade 2 strains that appeared were unique to central China. Thus, it is hypothesized that this, along with the latent variables of an antigenic epitope at positions 1058 and 1060, as well as mutations at the S1/S2 sites, are important factors affecting FCoV transmission and pathogenicity.

The global spread of lumpy skin disease (LSD), a devastating cattle disease caused by the lumpy skin disease virus (LSDV), is hampered by the lack of a practical small animal model for vaccine evaluation. Here, we established a mouse model by challenging C57BL/6 mice with goatpox virus (GTPV), a close relative of LSDV. Intranasal inoculation with a high dose (10^4.5 TCID₅₀) of GTPV induced robust infection characterized by weight loss, fever, high viral loads in the lungs and livers, and significant pulmonary pathology including immune cell infiltration and alveolar wall thickening. Infected mice mounted potent humoral immunity, with rapid IgM and sustained IgG and GTPV-specific binding antibody responses. The infection also elicited a dynamic cellular immune response, marked by biphasic IFN-γ production and dose-dependent increases in IL-17A and TNF-α. This GTPV-based murine model effectively recapitulates critical aspects of LSDV pathogenesis and immunity, providing a valuable and accessible tool for the accelerated development and preclinical assessment of novel LSDV vaccines.