研究显示，pDC细胞可经TLR7信号通路产生大量I型IFN，在HCV引发的免疫应答中发挥重要的抗病毒作用。TLR7数量、结构和功能的改变会对宿主清除HCV及感染的慢性化产生重要影响。目前尚未见从pDC细胞、TLR7表达水平及其信号通路上探讨其基因多态性与HCV感染慢性化关系的研究报道。本研究在已有工作基础上，利用高危人群随访资料进行病例-对照和病例-病例研究设计。通过比较HCV持续感染组、感染自限清除组和健康对照组的TLR7分子表达水平及其基因多态性，分析、筛选三组人群体内TLR7的主要SNPs，从群体水平探讨TLR7水平及基因多态性与HCV感染慢性化的关系；并从分子水平探讨不同SNPs的pDC对HCV的识别能力及其引发先天免疫应答水平差异，特别是对诱导I型IFN产生的影响；采用生物信息学方法分析基因-免疫-环境因素之间的交互作用，为早期阻断或减缓HCV慢性化进程以及免疫治疗提供科学依据。

Previous studies have demonstrated that alpha interferon (IFN-α) highly-produced by plasmacytoid dendritic cells( pDCs) plays a role in the natural course of HCV infection. The signalling pathways that lead to the production of IFN-α and the expression of Toll-like receptor 7(TLR7) on pDCs may affect the immune response against HCV. However, there is little information available about the association between single nucleotide polymorphisms(SNPs) of TLR7 gene and pDCs level, chronic HCV infection by exploring TLR7 signalling pathways. So we will conduct a case-control/case-case study in Chinese population. This study will emphasize on the relationship of the TLR7 SNPs, IFN-α and pDCs levels with the outcome of HCV infection and the interaction of the host(gene)-immune-environment by exploring the risk factors and mechanisms of HCV infection at the molecular level. It will offer a novel interpretation for the molecular basis of the role of the TLR7 gene variations, IFN-α and pDCs levels on the development of HCV infection and also offer an approach to immune treatment or other measures protecting from the progression of persistent HCV infection.