Abstract
Classical swine fever (CSF) is a highly contagious swine infectious disease and causes significant economic losses for the pig industry worldwide. The objective of this study was to determine whether small molecule metabolites contribute to the pathogenesis of CSF. Birefly, serum metabolomics of CSFV Shimen strain-infected piglets were analyzed by ultraperformance liquid chromatography/electrospray ionization time-of-flight mass spectrometry (UPLC/ESI-Q-TOF/MS) in combination with multivariate statistical analysis. In CSFV-infected piglets at days 3 and 7 post-infection changes were found in metabolites associated with several key metabolic pathways, including tryptophan catabolism and the kynurenine pathway, phenylalanine metabolism, fatty acid and lipid metabolism, the tricarboxylic acid and urea cycles, branched-chain amino acid metabolism, and nucleotide metabolism. Several pathways involved in energy metabolism including fatty acid biosynthesis and β-oxidation, branched-chain amino acid metabolism, and the tricarboxylic acid cycle were significantly inhibited. Changes were also observed in several metabolites exclusively associated with gut microbiota. The metabolomic profiles indicate that CSFV-host gut microbiome interactions play a role in the development of CSF.
Highlights
Classical swine fever (CSF) is a highly contagious swine infectious disease with high morbidity and mortality caused by CSFV, featuring high fever, severe depression, extensive hemorrhage, leucopenia, anorexia, and alternating constipation and diarrhea (Moennig et al, 2003)
Alternating constipation and diarrhea, convulsions, depression, and coma were observed in CSFV-infected piglets
Of note is that one of the infected piglets did not show any clinical signs until dpi 8, while serum samples collected at dpi 3 and 7 from this animal were included in the metabolomic analysis
Summary
Classical swine fever (CSF) is a highly contagious swine infectious disease with high morbidity and mortality caused by CSFV, featuring high fever, severe depression, extensive hemorrhage, leucopenia, anorexia, and alternating constipation and diarrhea (Moennig et al, 2003). A notifiable disease of the OIE-World Organization for Animal Health, CSF causes major economic losses in many countries worldwide. CSFV replicates in organs with leucocytes, mononuclear macrophages, as its target cells, causing malfunction or failure of multiple body components, including the immune, circulative, digestive, locomotor, reproductive, and respiratory systems (Floegel-Niesmann et al, 2003). While a detailed analysis of CSFV infection has identified various factors involved in viral replication and virulence (Ji et al, 2015), a comprehensive analysis of the host response to CSFV infection is necessary to decipher the underlying molecular mechanism of viral pathogenesis. Systems biology with high throughput techniques provides a powerful tool to reveal global changes in gene expression and metabolism associated with disease progression.
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