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首页> 外文OA文献 >Kinetics of Intrahepatic Hepatitis C Virus (HCV)-Specific CD4+ T Cell Responses in HCV and Schistosoma mansoni Coinfection: Relation to Progression of Liver Fibrosis
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Kinetics of Intrahepatic Hepatitis C Virus (HCV)-Specific CD4+ T Cell Responses in HCV and Schistosoma mansoni Coinfection: Relation to Progression of Liver Fibrosis

机译：丙型肝炎病毒和曼氏血吸虫合并感染中肝内丙型肝炎病毒（HCV）特异性CD4 + T细胞反应的动力学：与肝纤维化进展的关系

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The kinetics of intrahepatic hepatitis C virus (HCV)-specific CD4+ T cell responses and their role in progression of fibrosis have not previously been characterized. Subjects with HCV/Schistosoma mansoni coinfection have a more rapid progression of HCV liver fibrosis than do those with HCV infection alone. The present prospective longitudinal study compared the liver histology, HCV-specific intrahepatic and peripheral CD4+ T cell proliferative responses, and cytokines (enzyme-linked immunospot) in 48 subjects with unresolved acute HCV infection with or without S. mansoni coinfection, at 6-10 months after acute infection and at the end of follow-up ( months), and the findings were correlated 96±8.7 to the rate of progression of fibrosis per year. Coinfected subjects had significant worsening of fibrosis, compared with subjects with HCV infection alone. At baseline, subjects with HCV infection alone had stronger multispecific intrahepatic HCV-specific CD4+ T helper 1 responses than did coinfected subjects, who had either no responses or weak, narrowly focused responses, and, over time, these T cell responses were maintained only in the liver. The rate of progression of fibrosis and virus load inversely correlated with intrahepatic HCV-specific CD4+ T cell response. The present prospective analysis indicates that enhancement of progression of liver fibrosis is associated with failure to develop early, multispecific, HCV-specific CD4+ Th1 responses, suggesting that novel therapeutic approaches inducing strong cellular immune responses might limit subsequent liver damage in individuals with chronic hepatitis C
机译：肝内丙型肝炎病毒（HCV）特异的CD4 + T细胞反应的动力学及其在纤维化进程中的作用尚未得到表征。 HCV /曼氏血吸虫合并感染的受试者比单纯HCV感染的受试者具有更快的HCV肝纤维化进程。本前瞻性纵向研究在6-10岁时比较了48例未解决的急性HCV感染伴或不伴曼氏沙门氏菌感染的48位受试者的肝脏组织学，HCV特异性肝内和外周CD4 + T细胞增殖反应以及细胞因子（酶联免疫斑点）。急性感染后数月和随访结束（数月）时，发现与每年纤维化进展速度相关96±8.7。与单独感染HCV的受试者相比，合并感染的受试者的纤维化严重恶化。在基线时，仅HCV感染的受试者比无感染或弱，狭窄且集中应答的合并感染受试者具有更强的多特异性肝内HCV特异性CD4 + T辅助1反应，并且随着时间的推移，这些T细胞反应仅在肝脏。纤维化的进展速度和病毒载量与肝内HCV特异性CD4 + T细胞反应呈负相关。目前的前瞻性分析表明，肝纤维化进程的增强与未能早期，多特异性，HCV特异性CD4 + Th1反应产生有关，提示诱导强细胞免疫反应的新型治疗方法可能会限制慢性丙型肝炎患者的后续肝损害

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