Division of Gastroenterology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
J Infect Dis. 2020 Nov 27;222(Suppl 9):S802-S813. doi: 10.1093/infdis/jiaa279.
HCV-HIV coinfected patients exhibit rapid progression of liver damage relative to HCV monoinfected patients. The availability of new directly acting antiviral agents has dramatically improved outcomes for coinfected patients as sustained virologic response rates now exceed 95% and fibrosis-related parameters are improved. Nevertheless, coinfected patients still have a higher mortality risk and more severe hepatocellular carcinoma compared to HCV monoinfected patients, implying the existence of pathways unique to people living with HIV that continue to promote accelerated liver disease. In this article, we review the pathobiology of liver disease in HCV-HIV coinfected patients in the directly acting antiviral era and explore the mechanisms through which HIV itself induces liver damage. Since liver disease is one of the leading causes of non-AIDS-related mortality in HIV-positive patients, enhancing our understanding of HIV-associated fibrotic pathways will remain important for new diagnostic and therapeutic strategies to slow or reverse liver disease progression, even after HCV cure.
HCV-HIV 合并感染患者的肝损伤进展速度相对于 HCV 单感染患者更快。新型直接作用抗病毒药物的出现显著改善了合并感染患者的预后，因为持续病毒学应答率现在超过 95%，纤维化相关参数得到改善。然而，与 HCV 单感染患者相比，合并感染患者的死亡率更高，肝细胞癌更严重，这意味着 HIV 感染者存在独特的途径，这些途径仍在继续促进加速肝病的发生。在本文中，我们在直接作用抗病毒时代综述了 HCV-HIV 合并感染患者肝病的病理生理学，并探讨了 HIV 本身导致肝损伤的机制。由于肝病是 HIV 阳性患者非艾滋病相关死亡的主要原因之一，因此，为了减缓或逆转肝病进展，即使在 HCV 治愈后，深入了解 HIV 相关纤维化途径对于新的诊断和治疗策略仍然很重要。
