<p>Largemouth bass virus (LMBV), a pathogenic iridovirus, causes severe economic losses in aquaculture. This study characterized a novel LMBV strain isolated from diseased largemouth bass, and the virus showed high virulence. Histopathology revealed systemic infection with hepatic vacuolization, gill hyperplasia, and splenic lesions. Whole-genome sequencing identified a 99,190&#xa0;bp genome encoding 102 proteins. Comparative genomic analysis identified three highly variable regions that may contribute to viral adaptation. Functional annotation revealed enrichment in genes related to nucleotide metabolism, lipid metabolism, and immune evasion. Transcriptomic profiling of infected spleen tissue uncovered dynamic host responses: early infection (2 dpi) was marked by metabolic reprogramming including altered amino acid and cysteine metabolism, mid-infection (4 dpi) showed activation of DNA replication pathways and innate immune responses, while late infection (6 dpi) was characterized by adaptive immune activation. Crucially, we discovered LMBV exploits host lipid droplets (LDs) for replication. Infection upregulated lipid synthesis genes and increased LD accumulation in <i>epithelioma papulosum cyprini</i> (EPC) cells. Palmitic acid-induced LD formation enhanced viral replication, while inhibition of lipogenesis suppressed it. Our findings provide new insights into LMBV pathogenesis and identify potential therapeutic targets through lipid metabolism intervention.</p>

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Characterization of a novel isolated largemouth bass virus (LMBV) strain: genomic insights, host transcriptional responses, and lipid droplet-dependent viral replication

  • Xiangyu Yao,
  • Luqian Xu,
  • Jian Shen,
  • Zekai Xu,
  • Yiheng Zhang,
  • Yongqi Sun,
  • Zetao Wei,
  • Tao Zhang,
  • Pengfei Chu

摘要

Largemouth bass virus (LMBV), a pathogenic iridovirus, causes severe economic losses in aquaculture. This study characterized a novel LMBV strain isolated from diseased largemouth bass, and the virus showed high virulence. Histopathology revealed systemic infection with hepatic vacuolization, gill hyperplasia, and splenic lesions. Whole-genome sequencing identified a 99,190 bp genome encoding 102 proteins. Comparative genomic analysis identified three highly variable regions that may contribute to viral adaptation. Functional annotation revealed enrichment in genes related to nucleotide metabolism, lipid metabolism, and immune evasion. Transcriptomic profiling of infected spleen tissue uncovered dynamic host responses: early infection (2 dpi) was marked by metabolic reprogramming including altered amino acid and cysteine metabolism, mid-infection (4 dpi) showed activation of DNA replication pathways and innate immune responses, while late infection (6 dpi) was characterized by adaptive immune activation. Crucially, we discovered LMBV exploits host lipid droplets (LDs) for replication. Infection upregulated lipid synthesis genes and increased LD accumulation in epithelioma papulosum cyprini (EPC) cells. Palmitic acid-induced LD formation enhanced viral replication, while inhibition of lipogenesis suppressed it. Our findings provide new insights into LMBV pathogenesis and identify potential therapeutic targets through lipid metabolism intervention.