Morard Isabelle, Clément Sophie, Calmy Alexandra, Mangia Alessandra, Cerny Andrea, De Gottardi Andrea, Gorgievski Meri, Heim Markus, Malinverni Raffaele, Moradpour Darius, Müllhaupt Beat, Semela David, Pascarella Stéphanie, Bochud Pierre-Yves, Negro Franco
Division of Gastroenterology and Hepatology, University Hospitals, Geneva, Switzerland.
Division of Clinical Pathology, University Hospitals, Geneva, Switzerland.
PLoS One. 2014 Sep 5;9(9):e106424. doi: 10.1371/journal.pone.0106424. eCollection 2014.
The CCR5 receptor, expressed on Th1 cells, may influence clinical outcomes of HCV infection. We explored a possible link between a CCR5 32-base deletion (CCR5delta32), resulting in the expression of a non-functioning receptor, and clinical outcomes of HCV infection.
CCR5 and HCV-related phenotypes were analysed in 1,290 chronically infected patients and 160 patients with spontaneous clearance.
Carriage of the CCR5delta32 allele was observed in 11% of spontaneous clearers compared to 17% of chronically infected patients (OR = 0.59, 95% CI interval 0.35-0.99, P = 0.047). Carriage of this allele also tended to be observed more frequently among patients with liver inflammation (19%) compared to those without inflammation (15%, OR = 1.38, 95% CI interval 0.99-1.95, P = 0.06). The CCR5delta32 was not associated with sustained virological response (P = 0.6), fibrosis stage (P = 0.8), or fibrosis progression rate (P = 0.4).
The CCR5delta32 allele appears to be associated with a decreased rate of spontaneous HCV eradication, but not with hepatitis progression or response to antiviral therapy.
在Th1细胞上表达的CCR5受体可能会影响丙型肝炎病毒(HCV)感染的临床结局。我们探究了CCR5基因32碱基缺失(CCR5delta32)(导致无功能受体的表达)与HCV感染临床结局之间的潜在联系。
对1290例慢性感染患者和160例自发清除病毒的患者的CCR5及HCV相关表型进行了分析。
在160例自发清除病毒的患者中,11%存在CCR5delta32等位基因携带,而在1290例慢性感染患者中这一比例为17%(比值比[OR]=0.59,95%置信区间[CI]为0.35 - 0.99,P = 0.047)。与无肝脏炎症的患者(15%,OR = 1.38,95% CI为0.99 - 1.95,P = 0.06)相比,CCR5delta32等位基因携带在有肝脏炎症的患者中出现的频率也更高(19%)。CCR5delta32与持续病毒学应答(P = 0.6)、纤维化分期(P = 0.8)或纤维化进展率(P = 0.4)均无关联。
CCR5delta32等位基因似乎与HCV自发清除率降低有关,但与肝炎进展或对抗病毒治疗的反应无关。