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首页> 外文期刊>Antiviral therapy >Evolution of T-cell responses to hepatitis C virus (HCV) during pegylated interferon plus ribavirin treatment in HCV-monoinfected and in HCV/HIV-coinfected patients.
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Evolution of T-cell responses to hepatitis C virus (HCV) during pegylated interferon plus ribavirin treatment in HCV-monoinfected and in HCV/HIV-coinfected patients.

机译:聚乙二醇化干扰素加利巴韦林治疗期间,HCV单感染和HCV / HIV合并感染患者T细胞对丙型肝炎病毒(HCV)反应的演变。

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BACKGROUND: The role of T-cell immunity in chronic hepatitis C virus (HCV) infection remains controversial. As in HIV infection, virus replication could drive or be contained by T-cell immunity. We have examined the effect of HIV coinfection and of suppression of HCV replication with therapy on HCV-specific T-cell responses. PATIENTS AND METHODS: Thirty-five patients with chronic hepatitis C (17 coinfected with HIV) initiating anti-HCV therapy were analysed. HCV-specific responses were assessed at different time points using intracellular interferon-gamma staining in response to a panel of overlapping peptides comprising E2, NS3, NS5a and NS5b HCV proteins. RESULTS: At baseline, HCV-specific responses were significantly lower in HIV-coinfected patients. At week 12 of therapy, CD8+ T-cell responses against all HCV proteins significantly decreased in HCV-monoinfected patients and this was maintained throughout the follow-up period. Although the same trend occurred in the HIV-coinfected group, differenceswere not significant. CD4+ T-cell responses against NS3 significantly diminished in the HCV-monoinfected group, whereas in coinfected patients CD4+ T-cell responses were low at baseline and did not experience any significant variation. CONCLUSIONS: HCV-specific T-cell responses are lower in HIV-coinfected patients and vanish following complete suppression of HCV replication under successful HCV therapy, suggesting that they are dependent on continuous antiqenic stimulation.
机译:背景:T细胞免疫在慢性丙型肝炎病毒(HCV)感染中的作用仍存在争议。就像在HIV感染中一样,病毒复制可以驱动T细胞免疫或被其抑制。我们已经检查了HIV合并感染和HCV特异性T细胞反应治疗对HCV复制的抑制作用。患者与方法:分析了35例开始抗HCV治疗的慢性丙型肝炎(17例合并感染HIV)患者。使用细胞内干扰素-γ染色在不同时间评估HCV特异性应答,以应对一组包含E2,NS3,NS5a和NS5b HCV蛋白的重叠肽。结果:在基线时,HIV感染患者的HCV特异性应答明显降低。在治疗的第12周,在HCV单感染的患者中,针对所有HCV蛋白的CD8 + T细胞反应显着降低,并且在整个随访期间均保持这种状态。尽管在HIV感染组中发生了相同的趋势,但差异并不显着。在HCV单感染组中,针对NS3的CD4 + T细胞反应显着降低,而在合并感染的患者中,CD4 + T细胞反应在基线时很低,并且没有任何明显的变化。结论:在成功感染HCV的患者中,HCV感染患者的HCV特异性T细胞反应较低,并且在完全抑制HCV复制后消失,这表明它们依赖于持续的抗刺激性。

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