Alterations in mitochondrial morphology and function induced by Enterocytozoon hepatopenaei (EHP) infection in ridgetail white prawn Exopalaemon carinicauda

Enterocytozoon hepatopenaei (EHP) is an obligate intracellular microsporidian parasite that poses a major threat to the sustainability of shrimp aquaculture. Although host mitochondria are known to be essential for microsporidian survival and proliferation, the specific morphological and functional alterations in host mitochondria following EHP infection remain largely unknown. In this study, EHP-infected shrimp were divided into a low-infection group (LG, < 10³ copies/50 ng hpDNA) and a high-infection groups (HG, > 10⁴ copies/50 ng hpDNA). Hepatopancreas samples from uninfected shrimp were used as controls. Shrimp from both EHP-infected groups and control group were collected for morphological observation of mitochondria, mRNA expression analysis of mitochondria and metabolism-related genes, examination of metabolic enzyme activities, detection of reactive oxygen species (ROS) levels and apoptosis. Results revealed that EHP infection induced mitochondrial structural damage and disrupted mitochondrial dynamic balance, which led to excessive ROS accumulation and mitochondrial dysfunction. Genes and corresponding enzymes involved in glycolysis and lipid metabolism were differentially expressed between the low-infection and high-infection groups, indicating stage-specific regulation of host metabolic pathways during EHP infection. Furthermore, examination of apoptosis-related genes revealed significantly increased mRNA levels of PI3K , AKT and the anti-apoptotic gene BCL2 in the LG group, whereas the expression of the pro-apoptotic gene BAX and caspase genes (Caspase 3, 8, 9) was dramatically upregulated only in the HG group. This study delineates the effects of EHP infection on mitochondrial homeostasis, metabolism and apoptosis. This study provides a deeper understanding of host-pathogen dynamics and elucidates the molecular interaction mechanisms between the host and EHP pathogen. Not applicable.