Transcriptomic analysis reveals dynamic host-pathogen interactions and potential antiviral targets during infectious myonecrosis virus infection in Litopenaeus vannamei

Infectious myonecrosis virus (IMNV), first identified in 2003, predominantly infects the shrimp species Litopenaeus vannamei and has caused significant economic losses in major shrimp farming regions in Brazil and Southeast Asia. However, the infection mechanisms of IMNV has not been elucidated. In this study we have investigated the molecular mechanisms of IMNV-shrimp interaction and identified potential antiviral key genes to provide a theoretical reference for developing new control technologies. Transcriptome sequencing of control and infected shrimp groups at 30 (early), 60 (mid), and 90 days (late) post-infection identified 695, 2411, and 401 differentially expressed genes (DEGs), respectively. Early infection analysis revealed IMNV promotes colonization and spread by inhibiting hemagglutination and apoptosis-related genes while activating antiviral pathways like JAK-STAT, indicating it evades host defenses by interfering with the innate immune response. During mid-stage infection, glucose and amino acid metabolism pathways were enriched, suggesting IMNV induces host metabolic reprogramming to support viral replication. Late-stage analysis showed downregulated apoptosis and autophagy pathways, and upregulated cytoskeleton and extracellular matrix genes, indicating the host mitigates viral tissue damage by regulating cell fate and repair mechanisms. This transcriptomics study uncovers dynamic shrimp gene expression changes induced by IMNV infection, identifying multiple immune and metabolic pathways involved in the antiviral response. It elucidates IMNV's pathogenic mechanism and identifies key regulatory genes in pathways like PI3K-Akt-mTOR and JAK-STAT. These findings enhance our understanding of IMNV-shrimp host interaction and could inform novel antiviral strategy development. • Early infection: IMNV inhibits hem-agglutination and JAK-STAT, evading host defenses by suppressing innate immunity. • Mid-stage infection: IMNV induces host metabolic reprogramming in glucose and amino acid pathways to support replication. • Late-stage: Host downregulates apoptosis, autophagy, and upregulates cytoskeleton and ECM genes to mitigate viral damage.