Abstract：
Baculoviruses have been extensively studied for their potential in microbial pest control, but the mechanisms behind their mode of action still need to be addressed. Here we report differential expression of a cellular miRNA, Sfr-miR-184, from Sf9 cells in response to Autographa californica multicapsid Nucleopolyhedrovirus (AcMNPV) infection. Our results showed that Sfr-miR-184 is down-regulated in AcMNPV-infected cells but not with UV-inactivated virus. Prohibitin gene was determined as a target of the miRNA, which was up-regulated following AcMNPV infection. Using synthetic miRNA mimic, we found that oversupply of the miRNA resulted in decreased transcript levels of the target gene. Results suggest that Sfr-miR-184 negatively regulate prohibitin transcripts in the host cells. Antibody-mediated inhibition and silencing of the prohibitin gene revealed significant reductions in virus DNA replication suggesting a possible role for prohibitin in the virus-host interaction. These findings highlight another molecular mechanism used by baculovirus to manipulate host cells for its replication.
摘要：
杆状病毒在微生物害虫控制方面的潜力已得到广泛研究，但是他们行动模式背后的机制仍然需要解决。在这里，我们报告了细胞miRNA的差异表达，Sfr-miR-184，来自Sf9细胞，响应于加利福尼亚自拟多衣壳核型多角体病毒（AcMNPV）感染。我们的结果表明，Sfr-miR-184在AcMNPV感染的细胞中下调，但在UV灭活的病毒中没有下调。Prohibitin基因被确定为miRNA的靶标，在AcMNPV感染后上调。使用合成的miRNA模拟物，我们发现miRNA的过度供应导致靶基因的转录水平降低.结果表明Sfr-miR-184负调节宿主细胞中的抑制素转录本。抗体介导的阻抑素基因的抑制和沉默揭示了病毒DNA复制的显着减少，表明阻抑素在病毒-宿主相互作用中的可能作用。这些发现强调了杆状病毒用于操纵宿主细胞进行复制的另一种分子机制。
