Baculovirus nucleocapsids egress from the nuclear membrane during infection. However, details of alternation of nuclear membrane structure during baculovirus egress are unknown. In this study, we examined the changes of lamin B receptor (LBR), a main inner nuclear membrane component, during Autographa californica nucleopolyhedrovirus (AcMNPV) infection. Firstly, the open reading frame (Orf) of Sf9 lbr was cloned by reverse transcription PCR, and the distribution of LBR in Sf9 cells were observed by fusing LBR with the red fluorescence protein mcherry. Besides, the amount of endogenous LBR during AcMNPV infection was detected by western blotting. Moreover, the distribution of LBR after AcMNPV infection was observed under the confocal fluorescence microscopy. Furthermore, the effects of protein kinase C (PKC) inhibitor on stability of LBR and release of budded virus (BVs) were determined. The results showed that Sf9 lbr contains an Orf of 2040 nucleotides (NTs), which encodes a predicted protein of 679 amino acids (AAs). Fluorescence microscopy showed that LBR is localized to the nuclear membrane. Western blotting result showed that the amount of endogenous LBR is significantly reduced after AcMNPV infection. Transfection and infection assay demonstrated that the fluorescence of LBR nearly completely disappeared after viral infection. PKC inhibitor can suppress the degradation of LBR induced by AcMNPV, resulting in the reduction of viral titer of progeny viruses. The electron microscopy analysis demonstrated that PKC inhibitor did not influence virion entry, uncoating, and assembly, but may partially protect the nuclear membrane from disruption by AcMNPV. Taken together, AcMNPV infection can distort the expression of LBR, which may promote the egress of nucleocapsids.

中文翻译：

---

加利福尼亚州Autographa californica核多角体病毒感染过程中Sf9细胞层粘连蛋白B受体的特征及其命运。

在感染过程中，杆状病毒核衣壳从核膜中逸出。然而，在杆状病毒流出期间核膜结构改变的细节是未知的。在这项研究中，我们检查了在加利福尼亚州Autographa californica核多角体病毒（AcMNPV）感染期间lamin B受体（LBR）（一种主要的内核膜成分）的变化。首先，通过逆转录PCR克隆了Sf9 lbr的开放阅读框（Orf），并通过将LBR与红色荧光蛋白融合，观察了Sf9细胞中LBR的分布。此外，通过蛋白质印迹法检测AcMNPV感染期间内源性LBR的量。此外，在共聚焦荧光显微镜下观察到AcMNPV感染后LBR的分布。此外，确定蛋白激酶C（PKC）抑制剂对LBR稳定性和芽出病毒（BVs）释​​放的影响。结果表明，Sf9 lbr包含2040个核苷酸（NTs）的Orf，其编码679个氨基酸（AAs）的预测蛋白。荧光显微镜显示，LBR位于核膜上。Western印迹结果表明，AcMNPV感染后内源性LBR的量明显减少。转染和感染试验表明，病毒感染后LBR的荧光几乎完全消失。PKC抑制剂可以抑制AcMNPV诱导的LBR降解，从而降低子代病毒的病毒滴度。电子显微镜分析表明，PKC抑制剂不影响病毒体的进入，脱膜和组装，但可以部分保护核膜免受AcMNPV的破坏。综上所述，AcMNPV感染可扭曲LBR的表达，这可能促进核衣壳的释放。