International Journal of Molecular Veterinary Research 2024, Vol.14, No.1, 1-8 http://animalscipublisher.com/index.php/ijmvr 2 analyses, we hope to provide comprehensive treatment and prevention guidance for FCV infections, reducing the negative impact on cat population health and provide scientific basis and practical guidelines for veterinary clinical practice. Through this work, we hope to contribute to overcoming FCV infection, protecting animal welfare, and public health safety. 1 Basic Biology and Pathology of FCV 1.1 Structure and genotypic diversity of FCV Feline calicivirus (FCV), a member of the Caliciviridae family, is a non-enveloped virus with a particle diameter of approximately 30-40 nm. The genome of FCV consists of a single-stranded positive-sense RNA, with a length of about 7.7 kilonucleotides, encoding various viral proteins, including structural and non-structural proteins. One of its distinctive features is the diversity in genotypes, primarily attributed to the high error rate of the RNA-dependent RNA polymerase, leading to frequent occurrences of mutations and recombination events. This genetic diversity enables FCV to adapt to different hosts and environmental conditions, posing challenges to vaccine development and virus control. 1.2 Infection pathways and clinical manifestations FCV is primarily transmitted through direct contact, including saliva, eye secretions, and nasal secretions of infected cats, as well as contact with contaminated objects (such as food bowls, bedding). Airborne droplets may also serve as a potential transmission route. Typical clinical manifestations include acute upper respiratory tract disease, oral ulcers, conjunctivitis, and nasal discharge. While most cats exhibit mild symptoms, in immunocompromised or unvaccinated cats, FCV can lead to more severe diseases, including pneumonia, systemic viral infections, and even death. 1.3 Pathological mechanisms FCV infection initially occurs in the epithelial cells of the oral cavity or upper respiratory tract. Virus particles enter cells by binding to receptors on the host cell surface, initiating the replication cycle (Li et al., 2022). Viral replication results in cell damage and death, triggering an inflammatory response. Behind oral ulcers and upper respiratory symptoms lies the disruption of mucosal epithelial cells and the integrity of submucosal capillaries by the virus, leading to local tissue inflammation and ulcer formation. In addition to direct cell damage, FCV can further contribute to tissue injury by activating the host's immune response. For instance, the infiltration of inflammatory cells and the release of cytokines can exacerbate local and systemic inflammatory reactions. Interestingly, FCV also demonstrates some immune escape capabilities, such as evading host neutralizing antibody responses through mutation (Tian et al., 2020). Moreover, the virus may induce latent infections in some hosts, leading to sustained immune activation and chronic inflammatory states (Wang, 2023). The pathological mechanisms of FCV are diverse and complex, and the unique viral structure and genetic diversity present additional challenges for therapy development and disease control. Therefore, a profound understanding of these fundamental biological and pathological mechanisms is crucial for the development of effective prevention and treatment strategies. 2 Modern Treatment Approaches 2.1 Antiviral therapy The primary challenge in treating feline calicivirus (FCV) lies in its high variability and the lack of specific drugs. Currently, antiviral drug use primarily focuses on two categories: nucleoside analogs and RNA polymerase inhibitors. Nucleoside analogs, such as ribavirin, disrupt the virus's replication process by mimicking nucleotides in viral RNA. RNA polymerase inhibitors, on the other hand, act by inhibiting a key enzyme in virus replication. These drugs can interfere with virus replication at different stages of the viral lifecycle, thereby alleviating symptoms (Wang, 2023).
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