Comparative analysis of transcriptomics and metabolomics provides insights into the mechanisms of VPAHPND invasion and hepatopancreatic damage in Litopenaeus vannamei

Abstract

Acute hepatopancreatic necrosis disease (AHPND) poses significant threats to the global shrimp farming industry; however, its molecular mechanisms remain largely unknown. Previous research has primarily focused on comparisons between infected and non-infected states, limiting our understanding of VPAHPND mechanisms. We integrated transcriptomic and metabolomic analyses to investigate the pathogenic mechanism underpinning AHPND in highly vulnerable post-larvae (PL) stage shrimp. By comparing shrimp infected with VPAHPND, those infected with non-VPAHPND, and uninfected shrimp (controls), we identified different VPAHPND infection responses, including significant cytoskeleton and metabolic reprogramming changes. Specifically, VPAHPND infection disturbed lipid, glutathione, and bile acid metabolism, while a key regulatory factor Farnesoid X Receptor (FXR) in these pathways was down-regulated. These findings suggest that VPAHPND manipulates host metabolism to enhance infectivity, leading to severe and irreparable hepatopancreas damage. Our study highlights the molecular interactions between VPAHPND and shrimp, and provides potential targets to mitigate the impact of AHPND in aquaculture.