限制因子能够负调控HIV-1的复制，同时病毒会通过多种途径拮抗限制因子帮助自身逃逸宿主的调控。miRNA在病毒与宿主的相互调控中的作用受到广泛的关注。课题组通过基因芯片分析发现miRNA10及其前体在HIV-1感染的T细胞中显著上调，且临床样品检测结果证明其与病毒滴度成正相关；靶标分析发现miRNA210能够与限制因子APOBEC3F（A3F）的3’UTR区相结合，且其过表达明显减弱A3F的蛋白水平，暗示了miRNA可能通过抑制A3F协助病毒复制。前期研究初步证实了miRNA210受HIV-1感染诱导及其对A3F的靶向作用。本课题拟进一步深入研究HIV-1感染诱导miRNA210及影响A3F表达的分子机制；最后应用真病毒感染系统对上述机制进行验证，以期揭示miRNA210在病毒拮抗宿主调控中的作用机理。将对理解病毒逃逸宿主调控提供新的见解，为控制HIV-1感染复制提供新的思路。

Host cells express a series of restriction factors to suppress HIV-1 replication. Conversely, viral proteins take advantage of different escape methods to complete a successful infection. Attention to the role of miRNA as a viral regulated protein has grown exponentially recently. We noticed that miRNA210 increased remarkably in HIV-1 infected MT-4 cells in an miRNA Array analysis, and showed a positive correlation with virus titer in HIV-1 infected clinical samples. All of these made sure that HIV-1 infection can induce the increasing of miRNA210. Target protein analysis showed that miRNA210 maybe can bind 3’UTR of APOBEC3F (A3F), and the expression of A3F was incredibly decreased in miRNA210 overexpressed cells, which indicated that miRNA210 could assist HIV-1 replication by suppressing the function of A3F. Our finding has primarily demonstrated that miRNA210 was induced by HIV-1 and targeted A3F to affect virus replication during infection. To uncover the role of miRNA210 in virus defending host restriction, we are supposed to explore the exact mechanism that miRNA210 is induced by HIV-1 and influence the expression of A3F with infective HIV-1.Our study will offer novel insights into virus escaping host regulation, and bring up new ideas to interfering HIV-1 infection.