The response mechanism of mandarin fish (Siniperca chuatsi) astrocyte-like cells to SCRV infection: Insights from Transcriptome Sequencing.

Abstract

A novel cell line, designated SCAC01 (Siniperca chuatsi Astrocyte clone 01), was established from the brain of mandarin fish (S. chuatsi). SCAC01 cell line highly expressed the astrocyte-specific marker gfap and could be stably passaged for more than 60 generations. The cell line exhibited high susceptibility to S. chuatsi rhabdovirus (SCRV) and supported robust viral replication accompanied by obviously cytopathic effects. Time-resolved transcriptomic analysis at 12, 24, and 36 hours post-infection (hpi) uncovered progressive and dynamic host responses to infection. SCRV infection potently activated innate immune pathways, including RIG-I-like receptor (RLR), Toll-like receptor (TLR), and NOD-like receptor (NLR) signaling, resulting in marked upregulation of type I interferon (IFN-I) and interferon-stimulated genes (ISGs). Genes associated with antigen processing and presentation, including members of MHC I and MHC II families as well as cd4 and cd74a, were also significantly upregulated. Meanwhile, cell cycle and DNA replication pathways were repressed, whereas both pro-apoptotic and pro-survival signals were triggered. Notably, 1017 differentially expressed long non-coding RNAs (DE-lncRNAs) were identified, and their predicted target genes were mostly enriched in immune-related pathways. Among the 15 trim25-like genes annotated in the mandarin fish genome, trim25 (LOC122872559) and trim25-l (LOC122874279) were significantly up-regulated upon SCRV infection. Functional assays showed that both TRIM25 and TRIM25-L activated IFN-I signaling and inhibited SCRV replication in a manner dependent on their E3 ligase activity. Collectively, these findings demonstrate that SCAC01 serves as a valuable in vitro model for investigating SCRV infection and host antiviral immunity.