<HashMap><database>iProX</database><scores/><additional><omics_type>Proteomics</omics_type><submitter>Mengjun Wu</submitter><species>Sus Scrofa</species><species>Sus Scrofa Domesticus</species><full_dataset_link>http://www.iprox.org/page/project.html?id=IPX0015897000</full_dataset_link><submitter_email>wumengjun93@163.com</submitter_email><submitter_affiliation>Wuhan Polytechnic University</submitter_affiliation><sample_protocol></sample_protocol><repository>iProX</repository><data_protocol></data_protocol><pubmed_abstract>Porcine epidemic diarrhea (PED) is a severe viral disease caused by the porcine epidemic diarrhea virus (PEDV), leading to huge economic losses in the swine industry. Identifying therapeutic targets has long been a critical challenge in preventing and controlling PED through nutritional interventions. In the present study, 100 seven-day-old crossbred (Duroc × Landrace × Large White) healthy piglets from seven independent trials were selected for the experiment. The transcriptomics, proteomics, and metabolomics analyses were conducted on the small intestine and blood of piglets infected with PEDV, and the combined multiple batches of data were subsequently subjected to integrated analysis. Our findings revealed that PEDV infection significantly affected intestinal cell metabolism, especially lipid metabolism. Among those, sphingolipid and lysophospholipid metabolism could be potential pathways for preventive and therapeutic interventions. Additionally, retinol metabolism, mineral absorption, amino acid metabolism, and pyrimidine metabolism were remarkably altered following PEDV infection. Subsequently, candidate hub genes involved in the core pathways, such as apolipoprotein C3 (APOC3), cytochrome P450 family 3 subfamily A member 22 (CYP3A22), and intestinal alkaline sphingomyelinase (ENPP7), were identified and validated. In conclusion, the present study suggests that PEDV infection leads to the reprogramming of enterocyte lipid metabolism. Furthermore, manipulating lipid metabolism may influence the outcome of viral infection, highlighting potential targets for preventive and therapeutic interventions in managing viral infections.&lt;h4>Importance&lt;/h4>Porcine epidemic diarrhea (PED) is a severe viral disease caused by the porcine epidemic diarrhea virus (PEDV), leading to huge economic losses in the swine industry. Identifying therapeutic targets has long been a critical challenge in preventing and controlling PED through nutritional interventions. The present study suggests that PEDV infection leads to the reprogramming of enterocyte lipid metabolism. Furthermore, manipulating lipid metabolism may influence the outcome of viral infection. The study also highlights potential targets for preventive and therapeutic interventions in managing viral infections.</pubmed_abstract><pubmed_title>Metabolic reprogramming in the enterocytes of neonatal piglets infected with porcine epidemic diarrhea virus: integrated omics and multi-batch analysis highlight alterations in lipid metabolism and potential therapeutic targets.</pubmed_title><pubmed_authors>Wu Mengjun M, Zhang Qian Q, Shi Xintao X, Li Peng P, Song Zhuan Z, Li Zhonghua Z, Zhang Yanyan Y, Wang Lei L, Zhao Di D, Wu Tao T, Yi Dan D, Hou Yongqing Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Metabolic Reprogramming in the Enterocytes of Neonatal Piglets Infected with Porcine Epidemic Diarrhea Virus: Integrated Omics and Multi-Batch Analysis Highlight Alterations in Lipid Metabolism and Potential Therapeutic Targets</name><description>Our research team recently investigated the role of PEDV on piglet intestinal metabolism. We conducted several independent animal experiments and collected the samples for transcriptomics and proteomics. Our purpose is to identify and validate prospective targets for both diagnostic and therapeutic purposes in the context of PEDV. Importantly, this study offers a novel perspective for understanding the pathogenesis of PEDV and provides new insights into its prevention and control.</description><dates><publication>Fri Feb 27 00:00:00 GMT 2026</publication></dates><accession>PXD075013</accession><cross_references><TAXONOMY>9825</TAXONOMY><TAXONOMY>9823</TAXONOMY><pubmed>42059391</pubmed></cross_references></HashMap>