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Untargeted metabolomics reveals bovine viral diarrhea virus infection reprogram host nucleotide and amino acid metabolism in MDBK Cells

ABSTRACT:

Bovine viral diarrhea virus (BVDV) is a highly adapted intracellular parasite that depends entirely on the host cell's metabolic resources and energy for the synthesis of viral components. However, the mechanisms by which BVDV remodels host lipid metabolism remain unclear. In this study, we explored the metabolic impact of BVDV infection in MDBK cells using untargeted metabolomics. The differential metabolite (DEMs) analysis identified 249 and 147 differential metabolites in positive and negative ion modes. These DEMs have been demonstrated to be considerably enriched in a number of critical metabolic pathways, including purine metabolism, ABC transporters, alanine, aspartate, and glutamate metabolism, according to KEGG enrichment analysis. The up-regulated DEMs (Guanine, Xanthine, Xanthosine 5'-monophosphate and Uric acid) were notably focused on purine metabolism, indicating that BVDV infection triggers the host purine de novo and remedial synthesis pathways. In contrast to the up-regulated metabolites supporting viral replication, the down-regulated DEMs (Adenosine 5'-monophosphate, Guanosine 5'- monophosphate and Adenosine) were primarily involved in metabolism and the cGMP-PKG signaling pathway. The down-regulation of several important metabolites demonstrated how BVDV achieves immune escape and persistent infection by undermining the host defense system. However, more experimental confirmation is needed to determine the molecular mechanism by which BVDV uses host metabolic resources to support its own replication. Our metabolomics data provide crucial insights into the infection-induced metabolic perturbations, thereby serving as a valuable data resource for elucidating the mechanism of BVDV-driven host metabolic reprogramming.

INSTRUMENT(S): Liquid Chromatography MS - positive - HILIC, Liquid Chromatography MS - negative - HILIC

PROVIDER: MTBLS13126 | MetaboLights | 2025-10-12

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS13126_LC-MS_negative_hilic_metabolite_profiling.txt	Txt
	a_MTBLS13126_LC-MS_positive_hilic_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS13126_LC-MS_negative_hilic_metabolite_profiling_v2_maf.tsv	Tabular
	m_MTBLS13126_LC-MS_positive_hilic_metabolite_profiling_v2_maf.tsv	Tabular

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Project description:Background: Histomonas meleagridis is an anaerobic, intercellular parasite that infects the Galliformes such as turkeys and chickens. In recent years, the reemergence of Histomoniasis has caused serious economic losses as drugs to treat the disease have been banned. At present, studies on H. meleagridis mainly focus on virulence, gene expression analysis, and the innate immunity of the host. However, there are no studies on differential expression of miRNAs (DEMs) in host immune and inflammatory response induced by H. meleagridis infection in chickens. In this study, the expression profile of cecum miRNA at 10 and 15 days post-infection (DPI) with Chinese JSYZ-F strain H. meleagridis was studied by high-throughput sequencing. Results: Compared with the control group, 94 and 127 DEMs were found in the cecum of infected chickens at 10 DPI (CE vs CC) and 15 DPI (CEH vs CCH), respectively, of which 60 DEMs were shared at two-time points. Gene Ontology (GO) enrichment analysis of the target genes of DEMs showed that 881 and 1027 GO terms were significantly enriched at 10 and 15 DPI. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of the target genes of DEMs showed that only 5 and 3 pathways were significantly enriched at 10 and 15 DPI, respectively. The integrated analysis of miRNA–gene network revealed that the DEMs played important roles in the host immune and inflammatory responses to H. meleagridis infection by dynamically regulating the expression of immune and inflammation-related cytokines. Conclusion: Our results not only suggested that host miRNA expression was dynamically altered by H. meleagridis and host, but also revealed that more miRNAs and genes were involved in the later stage of the disease. In addition, host and H. meleagridis regulated the expression of immune and inflammation-related cytokines to respond to H. meleagridis infection. Our results will contribute to future research on miRNA-target interaction during H. meleagridis infection in chickens and provide new ideas for H. meleagridis control.

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Untargeted metabolomics reveals bovine viral diarrhea virus infection reprogram host nucleotide and amino acid metabolism in MDBK Cells

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