H9N2亚型流感病毒NS1蛋白位点突变对IFN-β及其诱导基因转录活性的影响

Effect of site-directed mutants of the NS1 protein of H9N2 subtype influenza virus on the transcriptional activity of IFN-beta and IFN-beta-inducible genes

利用反向遗传技术拯救了H9N2亚型流感病毒NS1蛋白效应区第114,124,202和212位的定点突变病毒。病毒感染后9 h,荧光定量PCR结果显示,当NS1蛋白发生P114S、M124V、S212P氨基酸置换后,可以显著抑制IFN-β及RIG-1、PKR、OAS1、Mx1和ISG15等干扰素刺激基因(ISGs) mRNA的转录活性。由此表明,NS1蛋白的114,124和212位点与H9N2亚型流感病毒拮抗宿主先天性免疫应答密切相关。

In this study,the reverse genetic technique was used to rescue the site-directed mutant virus at the 114,124,202,or 212 site of the NS1 protein of H9 N2 subtype influenza virus.On 9 h post virus infection,the results of fluorescent quantitative PCR showed that the transcriptional activities of IFN-beta and the interferon-stimulated genes such as RIG-1,PKR,OAS1,Mx1 and ISG15 were significantly inhibited due to the amino acid substitution of P114 S,M124 V or S212 P in NS1 protein.It suggests that the positions 114,124 and 212 of NS1 protein are closely related to the antagonism of H9 N2 subtype influenza virus to the innate immune response of host.