ArticleMicroorganisms2025
Identification of Host-Protein Interaction Network of Canine Parvovirus Capsid Protein VP2 in F81 Cells.
Article in Microorganisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Molecular Mechanisms Between Canine Parvovirus 2 and Host Interactions: From Viruses to Innate Immune Signaling Pathways.Viruses · 2026Review
- The effects of leukocyteBMC veterinary research · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Canine Parvovirus (CPV) is a highly contagious virus that causes severe hemorrhagic enteritis and myocarditis, posing a major threat to the life and health of dogs. The molecular mechanism by which VP2, the major capsid protein of CPV, infects host cells and utilizes host cell proteins for self-replication remains poorly understood. In this study, 140 host proteins specifically binding to CPV VP2 protein were identified by immunoprecipitation combined with liquid chromatography-mass spectrometry (LC-MS/MS). Subsequently, the protein Interaction Network (PPI), the annotation of gene ontology (GO) and the database of Kyoto Encyclopedia of Genes and Genomes (KEGG) were constructed for in-depth analysis. The results showed that CPV VP2 protein participated mainly in cell metabolism, cell biosynthesis, protein folding and various signal transduction processes. According to the results of proteomics analysis, we randomly selected seven proteins for co-immunoprecipitation verification, and the experimental results were consistent with the LC-MS/MS data. In addition, our study found that the expression level of the VP2-interacting protein FHL2 mediated CPV replication. Preliminary studies have shown that knockdown of FHL2 promotes CPV replication by decreasing the expression of interferon β (IFN-β) and interferon-stimulated genes (ISGs), while overexpression of FHL2 can inhibit the replication of CPV by up-regulating the expression of IFN-β and related ISGs. This study lays the foundation for elucidating the potential function of CPV VP2 protein in the process of viral infection and proliferation which provides a theoretical basis for the design of antiviral agents and vaccines.
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Registered trials
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