Canine parvovirus (CPV-2) was first identified in the late 1970s and has since become one of the most significant infectious agents affecting dogs. CPV-2 causes severe diseases such as hemorrhagic gastroenteritis and myocarditis, posing a major threat to canine health, particularly with a high mortality rate in puppies. It is globally recognized as a highly contagious and lethal pathogen. CPV is prone to rapid mutation, leading to the emergence of new variants. Despite widespread vaccination efforts, CPV remains one of the primary causes of acute gastroenteritis and death in young and juvenile dogs. Furthermore, the detection of CPV in swine populations has introduced additional challenges to its control. This review summarizes the current epidemiological status of CPV, highlighting recent advancements in diagnostic techniques and vaccine development. Additionally, it discusses the latest research on the pathogenesis of the virus and the development of antiviral agent research and proposes prevention and control suggestions for CPV under the One Health concept. In particular, there is a need to enhance surveillance of viral dynamics, accelerate the development of novel vaccines, and deepen the exploration of the underlying pathogenic mechanisms. This review aims to provide a scientific foundation for effective control of CPV and to guide future research directions.

The global burden of tuberculosis (TB), exacerbated by the rise of drug-resistant Mycobacterium tuberculosis (M. tuberculosis), underscores the need for alternative intervention strategies. One promising approach is to block the infection at its earliest stage—bacterial adhesion to host cells—thereby preventing colonization and transmission without exerting selective pressure. Adhesins, surface-exposed molecules mediating this critical interaction, have therefore emerged as attractive targets for early prevention. This review outlines the infection process driven by bacterial adhesion and describes the architecture of the M. tuberculosis outer envelope, emphasizing components that contribute to host interaction. We comprehensively summarize both non-protein and protein adhesins, detailing their host receptors, biological roles, and experimental evidence. Recent progress in the computational prediction of adhesins, particularly neural network-based tools like SPAAN, is also discussed, highlighting its potential to accelerate adhesin discovery. Additionally, we present a detailed, generalized workflow for predicting M. tuberculosis adhesins, which synthesizes current approaches and provides a comprehensive framework for future studies. Targeting bacterial adhesion presents a therapeutic strategy that interferes with the early stages of infection while minimizing the risk of developing drug resistance. Consequently, anti-adhesion strategies may serve as valuable complements to conventional therapies and support the development of next-generation TB vaccines and treatments.

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.

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.

Helicobacter pylori (Hp) is a major pathogenic bacterium responsible for gastritis, peptic ulcers, and gastric cancer. The prevention and control of Hp infection pose significant global health challenges, particularly due to the rising antibiotic resistance alongside the current absence of an effective vaccine. This review synthesizes the key elements governing successful model establishment, including strain characteristics, animal host species selection, pre-treatment methods, and infection protocols. It further elaborates on the methods for detecting and quantifying Hp in animal models, including invasive and non-invasive detection techniques for model validation, and explores the potential applications of spatial transcriptomics in this field. Furthermore, the review outlines current progress and limitations in Hp infection modeling. Aimed at supporting preclinical research, this review serves as a practical reference for establishing stable and reproducible animal models that mimic human infection and disease progression, thereby facilitating the evaluation of novel therapeutics and vaccine candidates.