ArticleVeterinary research2025
Integrated transcriptomic and metabolomic analysis identifies host response mechanisms to oncogenic Marek's disease virus in Wenchang chickens.
Article in Veterinary research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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Authors and funding
12 authors.
Funding
Abstract
Marek's disease (MD), caused by Marek's disease virus (MDV), poses a significant threat to the poultry industry worldwide by inducing neurological disorders and malignant lymphoma in infected chickens. The underlying mechanisms of the host response to MDV infection and tumorigenesis remain poorly understood. To gain insight into the host response, we analysed the transcriptomic and metabolomic profiles of the heart tissue of Wenchang chickens, an indigenous Chinese breed, using RNA sequencing and untargeted metabolomics. A total of 2470 and 2666 genes were significantly up- and down-regulated, respectively, between infected and uninfected chickens. KEGG pathway enrichment analysis revealed distinct transcriptional patterns in response to MDV infection: upregulated genes were enriched primarily in immunity-related pathways, whereas downregulated genes were associated with metabolic pathways. Among the 433 differentially expressed metabolites identified, only the caffeine metabolism pathway approached statistical significance (p = 0.067). Integrative mapping of genes and metabolites to the KEGG enzyme database highlighted L-tryptophan interactions, with KYNU, KMO, KYAT3, and AADAT as the most representative relationships. These results provide a quantitative overview of MDV-induced transcriptional and metabolic perturbations, suggesting that hosts may counteract viral infection and tumor progression by suppressing cellular metabolism to potentiate immune responses.
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