A B S T R A C TFeline calicivirus (FCV) causes upper respiratory tract infections in felines and threatens the health of wild and domestic felines. Clinically, specific drugs to treat FCV have not yet been developed. Here, IgG was extracted from inactivated FCV-immunized horse sera. Equine F(ab') 2 fragments were obtained from pepsin-digested IgG and then purified by protein-G column chromatography. In our study, equine immunoglobulin F(ab') 2 fragments showed efficient neutralizing activity in vitro against FCV and had therapeutic and prophylactic effects in FCVinfected cats. The anti-FCV-specific F(ab') 2 fragment can significantly alleviate the clinical symptoms of FCVinfected cats and reduce the viral loads of the trachea, lung and spleen. These results indicate that the F(ab') 2 fragment prepared from inactivated FCV-immunized horses may be used as a prophylactic and therapeutic agent for diseases caused by FCV.

Feline calicivirus (FCV) is a highly contagious pathogen that causes acute upper respiratory infections and oral disease in cats, thus seriously endangering feline health. Recently, there have been outbreaks of particularly virulent variant strains of FCV, which can cause both acute symptoms and fatal systemic disease. The discovery of effective antiviral agents to treat FCV infection is, therefore, gradually assuming increased importance. In this study, we showed that both nitazoxanide and mizoribine had antiviral activity in F81 cells infected with different strains of FCV and also demonstrated a synergistic effect between the two drugs. Experiments in cats challenged with FCV showed that nitazoxanide significantly reduced the clinical symptoms of FCV infection, reduced viral load in the trachea and lungs, and reduced viral shedding. Our results showed that nitazoxanide and mizoribine could potentially be used as therapeutic agents to treat FCV infection.

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Background: Feline calicivirus (FCV) is a common and highly prevalent pathogen causing upper respiratory diseases in kittens and felines in recent years. Due to the substantial genetic variability of the viral genes, existing vaccines cannot provide complete protection. Therefore, research on FCV antiviral drugs has received much attention. Results: In this study, we found that copper chloride had dose-dependent antiviral effects on FCV in F81 cells. We also found that the combination of copper chloride and ribavirin had a synergistic protective effect against FCV in F81 cells. In contrast, the combination of copper chloride and horse anti-FCV immunoglobulin F (ab') 2 showed an antagonistic effect, likely because copper chloride has an effect on F (ab') 2 immunoglobulin; however, further research is needed to clarify this supposition. Conclusions: In summary, we found that copper chloride had low cytotoxicity and significant antiviral effects on FCV in F81 cells, providing a new drug candidate for the prevention and treatment of FCV infection.