【摘要】：豬繁殖與呼吸綜合征(PRRS)是一種對全球養(yǎng)豬業(yè)造成極大危害的豬的傳染病,給養(yǎng)豬業(yè)造成了巨大的經(jīng)濟損失。課題組前期研究表明PRRSV能夠下調(diào)HO-1(一種與細胞保護有關(guān)的酶)的表達,HO-1的誘導(dǎo)表達和過表達均能有效的抑制PRRSV的復(fù)制。Mirco RNAs能在轉(zhuǎn)錄后水平調(diào)控基因的表達,最近的研究顯示,mi RNAs在病原體和宿主的相互作用中起到非常重要的作用。Micro RNAs能通過轉(zhuǎn)錄后調(diào)控病毒基因或者宿主基因的表達,從而調(diào)控病毒感染。血紅素加氧酶1(HO-1)對一些病毒具有抵抗作用,例如埃博拉病毒、丙型肝炎病毒、艾滋病病毒和我們所研究的PRRS病毒。那么,是否有mico RNAs調(diào)控HO-1的表達,進而調(diào)控PRRSV的復(fù)制,尚不清楚。通過生物信息學(xué)預(yù)測和實驗驗證,我們發(fā)現(xiàn)mi R-24-3p這個mi RNA可以調(diào)控HO-1的表達,并且利用不同的方法確定了它和HO-1 m RNA存在直接的相互作用。mi R-24-3p的過表達可以顯著的降低HO-1的m RNA水平和蛋白水平。用HO-1表達的特異性誘導(dǎo)劑Co PP處理細胞,會導(dǎo)致mi R-24-3p表達量的下降,暗示著mi R-24-3p與HO-1可能存在著某種負相關(guān)的關(guān)系。另外,我們發(fā)現(xiàn)PRRSV的感染能夠誘導(dǎo)mi R-24-3p的表達從而促進病毒的復(fù)制,在Marc145和PAM細胞中,mi R-24-3p的過表達都能夠逆轉(zhuǎn)Co PP誘導(dǎo)HO-1上調(diào)表達對PRRSV復(fù)制的抑制作用。上述結(jié)果表明,PRRSV感染可以誘導(dǎo)mi R-24-3p的表達,而mi R-24-3p通過m RNA降解和翻譯抑制的方式抑制HO-1的表達進而促進PRRSV復(fù)制。該研究揭示了PRRSV能夠利用細胞內(nèi)的micro RNAs來調(diào)控宿主體內(nèi)的抗病毒因子的表達,從而有利于病毒自身的復(fù)制和增殖,這為我們深入了解PRRSV感染過程中病毒與宿主的相互作用,以及病毒的防控提供了全新的視角和策略。
[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.
【學(xué)位授予單位】：西北農(nóng)林科技大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：S855.3

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