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Updated: Jan 31, 2026

Leveraging CyVerse Resources for De Novo Comparative Transcriptomics of Underserved Non-model Organisms
Published on: May 9, 2017
Comparative transcriptomic analysis of bovine papillomatosis
Débora M Barreto1, Gerlane S Barros1, Lucas A B O Santos1
1Laboratory of Molecular Genetics and Biotechnology, Department of Biology, Center for Biological and Health Sciences, Federal University of Sergipe, São Cristóvão, Sergipe, Brazil.
Background:
Bovine papillomavirus (BPV) belongs to the Papillomaviridae family and infects epithelial cells of bovines and closely related animals, causing hyperproliferative lesions known as warts or papillomas, which may regress or progress to form benign or malignant tumors. The virus enters the host cell and interacts with it by altering the regulation of genes that are responsible for controlling the cell cycle, thus triggering lesion formation. It is not yet known which host genes are regulated by viral infection. Therefore, the objective of this study was to make use of next-generation RNA sequencing methods to identify differentially expressed genes associated with BPV infection, which might elucidate possible marker genes that could be used to control the disease.
Results:
Transcriptome analysis revealed that 1343 genes were differentially regulated (FDR < 0.05). A comparison of gene expression in infected and noninfected cows indicated that 655 genes were significantly upregulated, and 688 genes were significantly downregulated. Most differentially expressed genes were associated with BPV infection pathways, which supports the hypothesis that viral infection was the mechanism associated with this regulation.
Conclusions:
This is the first study that focused on a large-scale evaluation of gene expression associated with BPV infection, which is important to identify possible metabolic pathways regulated by host genes for lesion development. In addition, novel targets could be identified in order to find ligands that interact with BPV, with the aim of interrupting the infection cycle.
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