IJMVR_2024v14n1

International Journal of Molecular Veterinary Research 2024, Vol.14, No.1, 23-31 http://animalscipublisher.com/index.php/ijmvr 26 course at each stage is crucial for developing early diagnosis and effective treatment strategies. In addition, understanding the recovery period can help to infer the immune response mechanism of chickens to H5N1 avian influenza virus and provide important reference for vaccine development. 2.2 Impact on production performance After being infected with H5N1, the egg production of chickens decreased significantly, which directly threatened the economic health of the poultry breeding industry (Wang et al., 2023). Reduced egg production not only affects the supply stability of the poultry and egg market, but also poses potential risks to market price fluctuations for consumers. At the same time, the quality of infected eggs may also be seriously affected, including reduced eggshell quality and abnormal internal structure, further weakening the market competitiveness of egg products. This decline in quality poses a challenge for every link in the egg industry chain, with everyone involved, from hatcheries to retailers, threatened with financial losses. Studying the specific mechanisms of egg production decline plays a decisive role. Possible mechanisms include direct virus damage to the chicken reproductive system, physiological disorders caused by immune responses, and effects on nutrient absorption and metabolism. By in-depth understanding of these mechanisms, humans can formulate more targeted management and health care measures during the epidemic to minimize the adverse impact on the egg industry. Chicken flocks infected with H5N1 show a tendency to slow down their growth rate, which poses a direct threat to the efficiency and economic benefits of broiler production. The slowed growth rate leads to the extension of the breeding cycle and increases the maintenance and feeding costs of the farm. At the same time, reduced feed efficiency due to infection is also a common problem, causing farmers to face higher investments while maintaining profitability. This not only affects the economic benefits of farmers, but may also lead to a shortage of broiler chickens on the market and affect consumers' food choices. Understanding the specific mechanisms of slowed growth and factors affecting reduced feed efficiency can enable targeted and effective development of response strategies. Possible mechanisms include the virus directly affecting the metabolic activity of chickens, increased energy consumption due to immune responses, and inhibition of feed nutrient absorption. By in-depth study of these mechanisms, researchers can better optimize the breeding environment and management measures, improve the disease resistance and production performance of chickens, thereby reducing production costs and maintaining the sustainable development of the industry. 3 Molecular Mechanism Research As the H5N1 avian influenza virus continues to spread and evolve, an in-depth understanding of its interaction with host cells has become an urgent need for scientific research and disease prevention and control. The study of molecular mechanisms is the key to solving the mystery of the life cycle of avian influenza viruses and provides a basis for designing more effective prevention and control strategies. 3.1 Virus-host interaction In-depth study of the interaction between H5N1 avian influenza virus and host cells is to fully understand how the virus replicates within the host. The mechanism by which viruses invade host cells is a complex and tightly regulated process, in which the specific binding of viral surface proteins to host cell surface receptors is the critical first step (Nuñez and Ross, 2019). This process involves the interaction of the hemagglutinin (HA) protein on the surface of the virus with the glycoprotein on the surface of the host cell, forming a connection between the virus and the cell membrane. Once the connection is made, the virus enters the host cell and releases its genetic material into the cytoplasm by fusing its envelope with the host cell membrane. In this process, the nucleoprotein (NP) and genomic RNA inside the virus play an important role. After the viral genomic RNA is released into the host cytoplasm, the virus begins to synthesize its own proteins and replicate within the host cell by utilizing the host cell's biological mechanism (Figure 1). During this process, the virus also uses the host cell's organelles and metabolic machinery to complete its life cycle.

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