人博卡病毒（HBoV）是继B19病毒之后在全球广泛流行的与人类疾病有关的细小病毒。现已证明HBoV1感染与婴幼儿呼吸道综合征有密切联系, 但迄今对其致病机理知之甚少。前期实验中我们发现HBoV1复制中产生一种非编码RNA（ncRNA），且发现该RNA可以抑制NF-κB的活化。我们推测HBoV1可能利用其编码的ncRNA来抑制NF-κ B信号通路，最终实现其对宿主天然免疫抗病毒反应的抑制。为此，我们将利用HBoV1的感染性克隆构建缺失ncRNA编码区的病毒，转染后比较ncRNA对病毒复制和天然免疫反应的影响，同时我们将通过确认ncRNA细胞内的作用靶点，以及其影响NF-κB 活化的具体事件，最终建立HBoV1 ncRNA调控NF-κB信号通路的具体模式。本项目将阐明HBoV1 ncRNA抑制天然免疫的分子机制，最终揭示病毒ncRNA调节天然免疫新机制，为解析HBoV1的致病机理提供理论数据。

Human Boca virus (HBoV) is a parvovirus associated with human disease that is widely prevalent in the world after the B19 virus. HBoV1 infection has been shown to be closely associated with infant respiratory syndrome, but so far little is known about its pathogenesis. In the previous experiments, we found that HBoV1 produced a non-coding RNA during replication and found that the RNA could inhibit the activation of NF-κB. We speculate that human Bocca virus may use its encoded non-coding RNA to inhibit NF-κB signaling pathway, and ultimately suppress innate antiviral immune respones. To this end, we will use HBoV1 infectious clones to construct non-coding RNA-deficient human Boca virus, and compared their effects on viral replication and innate immune response. Additionally, we will identify the cellular target of the non-coding RNA. Moreve, together with the finding that specific events in NF-κB activation targeted by the HBOV non-coding RNA, we will ultimately establish a specific pattern of HBoV1 non-coding RNA regulation of NF-κB signaling pathway. The successful implementation of this project will elucidate the molecular mechanism of HBoV1 ncRNA inhibition of innate immunity, and finally reveal a new mechanism of ncRNA regulation of innate immunity, and provide theoretical data to analyze the pathogenesis of HBoV1 .