Abstract：
The genetic diversity of killer cell immunoglobulin-like receptors (KIRs) and human leukocyte antigen (HLA) genes influences the host\'s immune response to viral pathogens. This study aims to explore the impact of five single nucleotide polymorphisms (SNPs) in KIR3DL2 and HLA-A genes on hepatitis C virus (HCV) infection. A total of 2251 individuals were included in the case-control study. SNPs including KIR3DL2 rs11672983, rs3745902, rs1654644, and HLA-A rs3869062, rs12202296 were genotyped. By controlling various confounding factors using a modified logistic regression model, as well as incorporating stratified analysis, joint effects analysis, and multidimensional bioinformatics analysis, we analyzed the relationship between SNPs and HCV infection. The logistic regression analysis showed a correlation between KIR3DL2 rs11672983 AA, KIR3DL2 rs3745902 TT, and increased HCV susceptibility (p < 0.01). Stratified analysis indicated that KIR3DL2 rs1654644 and HLA-A rs3869062 also heightened HCV susceptibility in certain subgroups. A linear trend of rising HCV infection rates was observed when combining KIR3DL2 rs11672983 AA and KIR3DL2 rs3745902 TT (ptrend = 0.007). Bioinformatics analysis suggested these SNPs\' regulatory potential and their role in altering messenger RNA secondary structure, implying their functional relevance in HCV susceptibility. Our findings indicate that KIR3DL2 rs11672983 AA and KIR3DL2 rs3745902 TT are significantly associated with increased susceptibility to HCV infection.
摘要：
杀伤细胞免疫球蛋白样受体(KIRs)和人类白细胞抗原(HLA)基因的遗传多样性影响宿主对病毒病原体的免疫应答。本研究旨在探讨KIR3DL2和HLA-A基因中5种单核苷酸多态性(SNPs)对丙型肝炎病毒(HCV)感染的影响。共有2251人被纳入病例对照研究。对包括KIR3DL2rs11672983、rs3745902、rs1654644和HLA-Ars3869062、rs12202296在内的SNP进行基因分型。通过使用改进的逻辑回归模型控制各种混杂因素，以及结合分层分析，联合效应分析，和多维生物信息学分析，我们分析了SNPs与HCV感染之间的关系。Logistic回归分析显示KIR3DL2rs11672983AA，KIR3DL2rs3745902TT,增加HCV易感性(p<0.01)。分层分析表明，KIR3DL2rs1654644和HLA-Ars3869062也提高了某些亚组的HCV易感性。当组合KIR3DL2rs11672983AA和KIR3DL2rs3745902TT时，观察到HCV感染率上升的线性趋势（ptrend=0.007）。生物信息学分析提示这些SNPs的调节潜能及其在改变信使RNA二级结构中的作用,暗示它们在HCV易感性中的功能相关性。我们的发现表明KIR3DL2rs11672983AA和KIR3DL2rs3745902TT与HCV感染易感性增加显著相关。
