International Journal of Molecular Veterinary Research, 2025, Vol.15, No.1, 22-31 http://animalscipublisher.com/index.php/ijmvr 25 4 Host Adaptation and Cross-Species Transmission Mechanisms of Pathogens 4.1 Differences in receptor recognition and host cell entry mechanisms Host range and interspecies transmission of disease-producing organisms are often an issue of the ability to recognize and bind host cell receptors. Canine parvovirus-2 (CPV-2), for example, prevents host switching by specific amino acid changes in its capsid protein VP2 that alter binding affinity to transferrin receptors (TfR) between species. Mutations at sites such as 426E/D, 305H/D, and 297S, and receptor-binding loop site mutations, also have crucial roles for CPV-2 infection in a broad host range, with the highly conserved character of significant TfR residues showing the potential of transmission even to humans (Chen et al., 2024). As in canine distemper virus (CDV), amino acid change within the hemagglutinin (H) protein, residues 530 and 549, controls attachment to host SLAM (CD150) and nectin-4 receptors and enables adaptation to new species. 4.2 Replication dynamics and immune evasion strategies in different hosts Pathogens employ a variety of mechanisms to evade host immune detection and optimize replication. Viruses, including CDV and poxviruses, are able to camouflage or mask their nucleic acids, interfere with host pattern recognition receptors (PRRs), degrade or sequester immune signal molecules to escape detection. In bacterial pathogens like Brucella canis, canine macrophage infection results in time-dependent TLR and cytokine expression, reflecting sequential immune mechanism and immune mechanism avoidance to that of other Brucella species (Park et al., 2023). Parasitic infections like Echinococcus granulosus in canine animals result in upregulation of PRR and host immune signaling pathways within host intestinal cells, reflecting dynamic host-pathogen interactions (Wang et al., 2024). 4.3 Adaptive mutations and environmental factors influencing host shifts Viral surface protein adaptive mutations are especially central to host transitions. Rabies virus experimental and natural host switching demonstrates that only a subset of mutations accrued during adaptation is retained in nature and indicates a multifactorial, complex process (Bonnaud et al., 2019). For CDV, host adaptation and emergence into new species is linked with genetic diversity in the H gene and recombination. Ecological overlap, anthropogenic changes, and increased contact between free-ranging and domestic animals further enhance cross-species pathogen transmission of diseases such as Giardia duodenalis and vector-borne pathogens (Kuthyar et al., 2021) (Figure 1). Figure 1 Analysis of RABV genetic variation in intra- and inter-host comparisons and in specific organs (Adopted from Bonnaud et al., 2019) 4.4 Molecular basis and risk assessment of cross-species transmission Comparative genomics and phylogenetics reveal cross-species transmission is associated with certain molecular signatures, i.e., amino acid substitution in receptor-binding proteins and host-generalist genotypes (Pagnossin et
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