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首页> 外文期刊>International Journal of Molecular Sciences >Molecular Mechanisms of Liver Fibrosis in HIV/HCV Coinfection
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Molecular Mechanisms of Liver Fibrosis in HIV/HCV Coinfection

机译：HIV / HCV合并感染中肝纤维化的分子机制

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摘要

Chronic hepatitis C virus (HCV) infection is an important cause of morbidity and mortality in people coinfected with human immunodeficiency virus (HIV). Several studies have shown that HIV infection promotes accelerated HCV hepatic fibrosis progression, even with HIV replication under full antiretroviral control. The pathogenesis of accelerated hepatic fibrosis among HIV/HCV coinfected individuals is complex and multifactorial. The most relevant mechanisms involved include direct viral effects, immune/cytokine dysregulation, altered levels of matrix metalloproteinases and fibrosis biomarkers, increased oxidative stress and hepatocyte apoptosis, HIV-associated gut depletion of CD4 cells, and microbial translocation. In addition, metabolic alterations, heavy alcohol use, as well drug use, may have a potential role in liver disease progression. Understanding the pathophysiology and regulation of liver fibrosis in HIV/HCV co-infection may lead to the development of therapeutic strategies for the management of all patients with ongoing liver disease. In this review, we therefore discuss the evidence and potential molecular mechanisms involved in the accelerated liver fibrosis seen in patients coinfected with HIV and HCV.
机译：慢性丙型肝炎病毒（HCV）感染是合并感染人类免疫缺陷病毒（HIV）的人们发病和死亡的重要原因。几项研究表明，即使在完全抗逆转录病毒控制下进行HIV复制，HIV感染也会促进HCV肝纤维化的加速发展。在HIV / HCV合并感染的个体中，肝纤维化加速的发病机制是复杂和多因素的。涉及的最相关机制包括直接的病毒作用，免疫/细胞因子失调，基质金属蛋白酶和纤维化生物标记物水平的改变，氧化应激和肝细胞凋亡的增加，与艾滋病相关的CD4细胞的肠道消耗以及微生物易位。另外，代谢改变，大量饮酒以及药物使用可能在肝病的发展中具有潜在作用。了解HIV / HCV合并感染中肝纤维化的病理生理学和调节可能会导致制定治疗策略，以管理所有进行性肝病的患者。因此，在这篇综述中，我们讨论了在合并感染HIV和HCV的患者中看到的与加速肝纤维化有关的证据和潜在分子机制。

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