Abstract：
The 871C silkworm strain exhibits a high level of resistance to Bombyx mori nucleopolyhedrovirus (BmNPV), making it a valuable variety for the sericulture industry. Understanding the underlying mechanism of its resistance holds great biological significance and economic value in addressing viral disease risks in sericulture. Initially, we infected the resistant strain 871C and its control strain 871 with BmNPV and conducted secondary infection experiments using the progeny occlusion bodies (OBs). As a result, a significant decrease in pathogenicity was observed. Electron microscopy analysis revealed that 871C produces progeny virions with defective DNA packaging, reducing virulence following BmNPV infection. Blood proteomic identification of the silkworm variety 871C and control 871 after BmNPV infection demonstrated the crucial role of the viral proteins P6.9 and VLF-1 in the production of defective viruses by impeding the proper encapsulation of viral DNA. Additionally, we discovered that BmHSP19.9 interacts with P6.9 and VLF-1 and that its expression is significantly upregulated after BmNPV infection. BmHSP19.9 exhibits strong antiviral activity, in part by preventing the entry of the proteins P6.9 and VLF-1 into the nucleus, thereby hindering viral nucleocapsid and viral DNA assembly. Our findings indicate that the antiviral silkworm strain 871C inhibits BmNPV proliferation by upregulating Bmhsp19.9 and impeding the nuclear localization of the viral proteins P6.9 and VLF-1, leading to the production of defective viral particles. This study offers a comprehensive analysis of the antiviral mechanism in silkworms from a viral perspective, providing a crucial theoretical foundation for future antiviral research and the breeding of resistant silkworm strains.
摘要：
871C家蚕品系对家蚕核型多角体病毒(BmNPV)表现出很高的抗性,使其成为蚕桑产业的宝贵品种。了解其抗性的潜在机制对于解决蚕业中的病毒性疾病风险具有重要的生物学意义和经济价值。最初，我们用BmNPV感染了耐药菌株871C及其对照菌株871，并使用后代闭塞体（OBs）进行了二次感染实验。因此,观察到致病性显著降低.电子显微镜分析显示，871C产生具有缺陷DNA包装的后代病毒体，降低BmNPV感染后的毒力。BmNPV感染后，对家蚕品种871C和对照871的血液蛋白质组学鉴定表明，病毒蛋白P6.9和VLF-1通过阻碍病毒DNA的正确封装在缺陷病毒的生产中发挥了关键作用。此外,我们发现BmHSP19.9与P6.9和VLF-1相互作用，其表达在BmNPV感染后显著上调。BmHSP19.9具有很强的抗病毒活性，部分通过阻止蛋白质P6.9和VLF-1进入细胞核，从而阻碍病毒核衣壳和病毒DNA组装。我们的发现表明，抗病毒蚕871C菌株通过上调Bmhsp19.9并阻止病毒蛋白P6.9和VLF-1的核定位来抑制BmNPV增殖，从而导致缺陷病毒颗粒的产生。本研究从病毒的角度全面分析了家蚕的抗病毒机制,为今后的抗病毒研究和家蚕抗性品系的选育提供了重要的理论基础。
