近年来研究发现，HCV核心蛋白与宿主细胞中的一些转录因子，如NF-κB、AP-1、Sp1、Elk-l、NF-AT等，相互作用，在细胞信号转导、凋亡、转录调控、转化、膜重排及免疫逃逸等中起重要的调节作用，从而影响基因转录、细胞增殖和凋亡。进而这些关键基因的激活可能影响不同基因型HCV感染转归的结局。但迄今很少有涉及NF-κB基因结合病原-宿主-环境交互作用与HCV感染结局关系的研究。基于以上背景，本研究结合免疫学、分子生物学、流行病学和生物统计学等技术方法，采用大样本病例-对照，病例-病例研究设计，比较HCV持续性感染者、自限性清除者和健康对照者之间NF-κB的多态性；基于HCV基因型和环境因素的异同，对HCV慢性化的危险因素进行探讨，着重分析NF-κB基因多态性在HCV感染转归中的作用机制，为阐明HCV感染转归的生物学机制和个体化治疗提供新思路。

Recent studies found that HCV core protein can interact with some transcription factors in the host cell, such as NF-κB, AP-1, Sp1, Elk-l, NF-AT, etc. They play very important roles in the cell signal transduction, apoptosis, gene transcription regulation, cell membrane rearrangements and immune escape, thus the the activation of the key genes may influence the various outcomes of the patients infected with different genotypes of HCV. However, to date, little research has focused on the association of the NF-κB gene, combined with the interaction of host, pathogen, and environment, with the outcomes of HCV infection. Based on the above background, combining the technologies and the methods, such as immunology, molecular biology, epidemiology and biostatistics, etc., this study will adopt a large-sample case-control, case-case study design to compare the NF-κB gene polymorphisms among the patients with chronic HCV infection, the subjects with spontaneous HCV clearance and un-infected healthy controls, then explore the potential risk factors for chronic hepatitis C on basis of the difference of HCV genotypes and the environmental factors. This study will focus on the the mechanisms of the actions of genetic variants of NF-κB in the outcomes of HCV infection and may provide new insights into elucidating the biological mechanisms of the clinical outcomes and the individualized treatment of HCV infection.