Transcriptome analysis of Crandell Rees Feline Kidney (CRFK) cells infected with Feline calicivirus strain 023 (FCV 023).

Abstract

Vesivirus felis (Feline calicivirus, FCV) is a widely prevalent viral pathogen in domestic cats, commonly associated with upper respiratory tract infections. However, the transcriptomic responses of host cells to FCV infection remain largely uncharacterized. In this study, an in vitro FCV infection model was established using Crandell-Rees Feline Kidney (CRFK) cells. High-throughput RNA sequencing (RNA-Seq) was performed at 4, 8, and 12 h post-infection (hpi) to investigate the dynamics of host gene expression. Differentially expressed genes (DEGs) were identified and subjected to Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction (PPI) network analyses. A total of 829, 5,432, and 6342 DEGs were detected at 4, 8, and 12 hpi, respectively. Key enriched pathways were associated with metabolic processes, endoplasmic reticulum stress, cytoskeletal remodeling, apoptosis, and immune responses, including the activation of Ubiquitin-mediated proteolysis, Apoptosis signaling, Adherens junctions, and the MAPK, NF-κB, and Toll-like receptor signaling pathways. This study provides a comprehensive transcriptomic landscape of FCV-infected CRFK cells and identifies key molecular mechanisms involved in virus-host interactions, offering potential targets for antiviral therapy.