Abstract:
Background Grass carp reovirus (GCRV) is the causative agent of hemorrhagic disease in grass carp (Ctenopharyngodon idella), posing a serious threat to freshwater aquaculture in China. Establishing an infection model that mimics natural transmission is essential for elucidating the epidemiology and pathogeny of this virus.
Objective This study aims to develop a co-habitation model of GCRV infection in rare minnow (Gobiocypris rarus) to investigate its pathogenicity, viral load in tissues, and host immune responses.
Methods Rare minnows were infected with GCRV via intraperitoneal injection, and kept in the same tank with an equal number of healthy fish for up to 3 weeks. Disease progression was monitored, mortality was recorded, and survival rates were obtained. The expression levels of the viral gene (Vp5) encoding capsid protein and host antiviral gene (Mx1) in the gills, spleen, and hindgut were quantified using quantitative real-time polymerase chain reaction (qRT-PCR).
Results In the injection group, mortality was observed on day 4 post-infection, and all injected fish died on day 8. In contrast, the co-habitation group exhibited a delayed and more prolonged disease progressing, with mortality recorded on day 12 and reaching 100% on day 20. It was shown that significantly higher Vp5 expression was detected in the gills compared to the spleen and hindgut under both infection modes. Additionally, the expression of Mx1 was significantly upregulated in all examined tissues.
Conclusion A co-habitation infection model for GCRV was successfully established in rare minnow. The results indicate that gills serve as a key entry site for viral invasion. Although host antiviral defense is activated upon infection, it is insufficient to control viral replication. The co-habitation infection model provides a valuable tool for further investigation into the transmission dynamics, pathogenesis, host immune response to GCRV, and the development of control strategies.
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