Pineda-Tenor Daniel, Jiménez-Sousa María A, Rallón Norma, Berenguer Juan, Soriano Vicente, Aldámiz-Echevarria Teresa, García-Álvarez Mónica, Diez Cristina, Fernández-Rodríguez Amanda, Benito Jose Miguel, Resino Salvador
1 Servicio de Laboratorio Clínico, Hospital Universitario de Fuenlabrada , Madrid, Spain .
2 Unidad de Infección Viral e Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III , Majadahonda, Madrid, Spain .
AIDS Res Hum Retroviruses. 2016 Mar;32(3):226-31. doi: 10.1089/AID.2015.0223. Epub 2015 Dec 1.
The immune response against HIV and hepatitis C virus (HCV) infection partly depends on chemokine-mediated recruitment of specific T cells. CXCL12 polymorphisms have been associated with AIDS progression and survival, but there are no data related to HCV infection. The aim of this study was to determine whether CXCL12 polymorphisms are related so as to achieve sustained virological response (SVR) after HCV therapy with pegylated-interferon-alpha/ribavirin (pegIFN-α/ribavirin) in HIV/HCV-coinfected patients. We carried out a retrospective study in 319 naive patients who started HCV treatment. The CXCL12 (rs266093, rs1029153, and rs1801157) and IL28B (rs12980275) polymorphisms were genotyped by using the GoldenGate assay. Genetic data were analyzed under an additive inheritance model. The overall rates of the SVR were 54.9% (175/319) and 41.5% (90/217) in GT1/4 patients and 83.2% (84/101) in GT2/3 patients. Patients with a favorable CXCL12 rs1029153 T allele had higher SVR rates than patients with the rs1029153 CC genotype (44% CC, 49% CT, and 61.3% TT; p = 0.025). No significant results for the rs266093 and rs1801157 polymorphisms were found. Patients harboring the favorable rs1029153 T allele had significantly increased odds of achieving SVR [adjusted odds ratio (aOR) = 1.55; 95% confidence interval (95% CI) = 1.01; 2.40; p = 0.047]. Moreover, no significant association was found when the study population was stratified by HCV genotype (data not shown), possibly due to the low number of patients in each group. In conclusion, in this study we found that the favorable CXCL12 rs1029153 T allele seems to be related so as to achieve an SVR in HIV/HCV-coinfected patients on pegIFN-α/ribavirin therapy.
针对人类免疫缺陷病毒（HIV）和丙型肝炎病毒（HCV）感染的免疫反应部分取决于趋化因子介导的特定T细胞募集。CXCL12基因多态性与艾滋病进展和生存有关，但尚无与HCV感染相关的数据。本研究的目的是确定在接受聚乙二醇化干扰素-α/利巴韦林（pegIFN-α/利巴韦林）治疗的HIV/HCV合并感染患者中，CXCL12基因多态性是否与实现持续病毒学应答（SVR）相关。我们对319例开始HCV治疗的初治患者进行了一项回顾性研究。使用金标准检测法对CXCL12（rs266093、rs1029153和rs1801157）和IL28B（rs12980275）基因多态性进行基因分型。遗传数据在加性遗传模型下进行分析。GT1/4患者的SVR总体发生率为54.9%（175/319），GT2/3患者为83.2%（84/101）。携带有利的CXCL12 rs1029153 T等位基因的患者的SVR率高于rs1029153 CC基因型患者（CC型为44%，CT型为49%，TT型为61.3%；p = 0.025）。未发现rs266093和rs1801157基因多态性有显著结果。携带有利的rs1029153 T等位基因的患者实现SVR的几率显著增加[调整优势比（aOR）= 1.55；95%置信区间（95%CI）= 1.01；2.40；p = 0.047]。此外，当研究人群按HCV基因型分层时未发现显著关联（数据未显示），可能是由于每组患者数量较少。总之，在本研究中我们发现，有利的CXCL12 rs1029153 T等位基因似乎与接受pegIFN-α/利巴韦林治疗的HIV/HCV合并感染患者实现SVR相关。
