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Transcriptional Differential Analysis of Nitazoxanide-Mediated Anticanine Parvovirus Effect in F81 Cells
Xia Su1, Hongzhuan Zhou1, Ziwei Han1,2
1Beijing Key Laboratory for Prevention and Control of Infectious Diseases in Livestock and Poultry, Institute of Animal Husbandry and Veterinary Medicine, Beijing Academy of Agriculture and Forestry Sciences, Beijing 100097, China.
Abstract:
Canine parvovirus (CPV) is a single-stranded DNA virus that can cause typical hemorrhagic enteritis, and it is one of the common canine lethal viruses. In previous studies, we screened the Food and Drug Administration (FDA)'s drug library and identified nitazoxanide (NTZ), which has anti-CPV capabilities. To investigate the potential antiviral mechanisms, we first reconfirmed the inhibitory effect of NTZ on the CPV by inoculating with different doses and treating for different lengths of time. Then, the differences in the transcription levels between the 0.1%-DMSO-treated virus group and the NTZ-treated virus group were detected using RNA-seq, and a total of 758 differential expression genes (DEGs) were finally identified. Further Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of the DEGs revealed that these genes are involved in a variety of biological processes and/or signaling pathways, such as cell cycle, mitosis and cell proliferation and differentiation. A protein-protein interaction (PPI) analysis further identified hub genes associated with cell cycle and division among the DEGs. In addition, the expression levels of some of the enriched genes were detected, which were consistent with the high-throughput sequencing results. Moreover, when the cell cycle was regulated with cell cycle checkpoint kinase 1 (Chk1) inhibitor MK-8776 or Prexasertib HCl, both inhibitors inhibited the CPV. In summary, the transcriptome differential analysis results presented in this paper lay the foundation for further research on the molecular mechanism and potential targets of NTZ anti-CPV.
Insights
Nitazoxanide (NTZ) inhibits canine parvovirus (CPV) by targeting cell cycle and mitosis pathways. This study identified 758 differential genes, revealing potential molecular mechanisms for NTZ
Area of Science:
- Veterinary Virology
- Molecular Biology
- Antiviral Drug Discovery
Background:
- Canine parvovirus (CPV) is a significant cause of lethal hemorrhagic enteritis in dogs.
- Nitazoxanide (NTZ) was previously identified as a potential antiviral agent against CPV.
- Understanding NTZ's antiviral mechanisms is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the antiviral mechanisms of nitazoxanide (NTZ) against canine parvovirus (CPV).
- To identify host genes and pathways affected by NTZ treatment during CPV infection.
- To explore potential therapeutic targets for CPV by analyzing gene expression changes.
Main Methods:
- Reconfirmation of NTZ's inhibitory effect on CPV through dose- and time-dependent treatment.
- RNA sequencing (RNA-seq) to analyze differential gene expression between NTZ-treated and control groups.
- Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction (PPI) analyses to identify affected pathways and hub genes.
Main Results:
- NTZ demonstrated a dose- and time-dependent inhibitory effect on CPV.
- RNA-seq identified 758 differentially expressed genes (DEGs) between NTZ-treated and control groups.
- Enrichment analyses revealed NTZ's impact on cell cycle, mitosis, and proliferation pathways, with key hub genes identified.
Conclusions:
- NTZ exhibits antiviral activity against CPV by modulating host cell cycle and division processes.
- The study provides a foundation for further research into NTZ's molecular mechanisms against CPV.
- Targeting cell cycle regulators like Chk1 with inhibitors like MK-8776 or Prexasertib HCl also showed CPV inhibition, suggesting potential therapeutic strategies.
