miR-24-3p通过抑制血红素加氧酶1的表达促进猪繁殖与呼吸综合症病毒的感染
发布时间：2018-09-08 08:36
【摘要】：猪繁殖与呼吸综合征(PRRS)是一种对全球养猪业造成极大危害的猪的传染病,给养猪业造成了巨大的经济损失。课题组前期研究表明PRRSV能够下调HO-1(一种与细胞保护有关的酶)的表达,HO-1的诱导表达和过表达均能有效的抑制PRRSV的复制。Mirco RNAs能在转录后水平调控基因的表达,最近的研究显示,mi RNAs在病原体和宿主的相互作用中起到非常重要的作用。Micro RNAs能通过转录后调控病毒基因或者宿主基因的表达,从而调控病毒感染。血红素加氧酶1(HO-1)对一些病毒具有抵抗作用,例如埃博拉病毒、丙型肝炎病毒、艾滋病病毒和我们所研究的PRRS病毒。那么,是否有mico RNAs调控HO-1的表达,进而调控PRRSV的复制,尚不清楚。通过生物信息学预测和实验验证,我们发现mi R-24-3p这个mi RNA可以调控HO-1的表达,并且利用不同的方法确定了它和HO-1 m RNA存在直接的相互作用。mi R-24-3p的过表达可以显著的降低HO-1的m RNA水平和蛋白水平。用HO-1表达的特异性诱导剂Co PP处理细胞,会导致mi R-24-3p表达量的下降,暗示着mi R-24-3p与HO-1可能存在着某种负相关的关系。另外,我们发现PRRSV的感染能够诱导mi R-24-3p的表达从而促进病毒的复制,在Marc145和PAM细胞中,mi R-24-3p的过表达都能够逆转Co PP诱导HO-1上调表达对PRRSV复制的抑制作用。上述结果表明,PRRSV感染可以诱导mi R-24-3p的表达,而mi R-24-3p通过m RNA降解和翻译抑制的方式抑制HO-1的表达进而促进PRRSV复制。该研究揭示了PRRSV能够利用细胞内的micro RNAs来调控宿主体内的抗病毒因子的表达,从而有利于病毒自身的复制和增殖,这为我们深入了解PRRSV感染过程中病毒与宿主的相互作用,以及病毒的防控提供了全新的视角和策略。
[Abstract]:Porcine reproductive and respiratory syndrome (PRRS) is an infectious disease of pigs which has caused great harm to the global pig industry and has caused huge economic losses to the pig industry. Our previous studies have shown that PRRSV can down-regulate the expression of HO-1 (an enzyme related to cell protection) induced and overexpression of PRRSV. Mirco RNAs can effectively inhibit the expression of genes at the post-transcriptional level. Recent studies have shown that RNAs plays a very important role in the interaction between pathogen and host. Micro RNAs can regulate virus infection through post-transcriptional regulation of virus gene or host gene expression. Heme oxygenase 1 (HO-1) is resistant to viruses such as Ebola, hepatitis C, HIV and the PRRS virus we study. It is not clear whether mico RNAs regulates the expression of HO-1 and thus the replication of PRRSV. Through bioinformatics prediction and experimental verification, we found that mi R-24-3p, a mi RNA, can regulate the expression of HO-1. Furthermore, it was determined by different methods that the direct interaction. Mi R-24-3p expression with HO-1 m RNA could significantly reduce the m RNA level and protein level of HO-1. Treatment with Co PP, a specific inducer of HO-1 expression, led to a decrease in the expression of mi R-24-3p, suggesting that there might be a negative correlation between mi R-24-3p and HO-1. In addition, we found that PRRSV infection could induce the expression of mi R-24-3p and promote the replication of the virus. The overexpression of Marc145 and PAM cells could reverse the up-regulation of HO-1 induced by Co PP and inhibit the replication of PRRSV. These results suggest that PRRSv infection can induce the expression of mi R-24-3p, while mi R-24-3p inhibits the expression of HO-1 through m RNA degradation and translation inhibition and promotes PRRSV replication. This study reveals that PRRSV can use intracellular micro RNAs to regulate the expression of antiviral factors in the host, thus facilitating the replication and proliferation of the virus itself, which provides us with an in-depth understanding of the interaction between the virus and the host during the process of PRRSV infection. And the prevention and control of the virus provides a new perspective and strategy.
【学位授予单位】：西北农林科技大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：S855.3
本文编号：2230000
[Abstract]:Porcine reproductive and respiratory syndrome (PRRS) is an infectious disease of pigs which has caused great harm to the global pig industry and has caused huge economic losses to the pig industry. Our previous studies have shown that PRRSV can down-regulate the expression of HO-1 (an enzyme related to cell protection) induced and overexpression of PRRSV. Mirco RNAs can effectively inhibit the expression of genes at the post-transcriptional level. Recent studies have shown that RNAs plays a very important role in the interaction between pathogen and host. Micro RNAs can regulate virus infection through post-transcriptional regulation of virus gene or host gene expression. Heme oxygenase 1 (HO-1) is resistant to viruses such as Ebola, hepatitis C, HIV and the PRRS virus we study. It is not clear whether mico RNAs regulates the expression of HO-1 and thus the replication of PRRSV. Through bioinformatics prediction and experimental verification, we found that mi R-24-3p, a mi RNA, can regulate the expression of HO-1. Furthermore, it was determined by different methods that the direct interaction. Mi R-24-3p expression with HO-1 m RNA could significantly reduce the m RNA level and protein level of HO-1. Treatment with Co PP, a specific inducer of HO-1 expression, led to a decrease in the expression of mi R-24-3p, suggesting that there might be a negative correlation between mi R-24-3p and HO-1. In addition, we found that PRRSV infection could induce the expression of mi R-24-3p and promote the replication of the virus. The overexpression of Marc145 and PAM cells could reverse the up-regulation of HO-1 induced by Co PP and inhibit the replication of PRRSV. These results suggest that PRRSv infection can induce the expression of mi R-24-3p, while mi R-24-3p inhibits the expression of HO-1 through m RNA degradation and translation inhibition and promotes PRRSV replication. This study reveals that PRRSV can use intracellular micro RNAs to regulate the expression of antiviral factors in the host, thus facilitating the replication and proliferation of the virus itself, which provides us with an in-depth understanding of the interaction between the virus and the host during the process of PRRSV infection. And the prevention and control of the virus provides a new perspective and strategy.
【学位授予单位】：西北农林科技大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：S855.3
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，本文编号：2230000
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