Centre for Applied Molecular Biology, University of the Punjab, Lahore, Pakistan.
Department of Rehabilitation Science, The University of Lahore, Lahore, Pakistan.
Antivir Ther. 2023 Aug;28(4):13596535231189643. doi: 10.1177/13596535231189643.
In endemic areas, hepatitis C virus (HCV)/hepatitis B virus (HBV) coinfection is common, and patients with coinfection have a higher risk of developing liver disease such as hepatocellular carcinoma, liver fibrosis and cirrhosis. In such cases, HCV predominates, and HBV replication is suppressed by HCV. HCV core proteins and interferons that are activated by HCV are responsible for the suppression of HBV. Immunosuppression is also seen in patients with HCV and HBV coinfections. A decrease in HCV-neutralizing antibody response and circulation of Th1-like Tfh cells is observed in patients with HCV and HBV coinfection. Both viruses interacted in the liver, and treatment of HCV/HBV coinfection is genotype-based and complex due to the interaction of both viruses. In HCV-dominant cases, direct-acting antiviral drugs and peg interferon plus ribavirin are used for the treatment, with continuous monitoring of AST and ALT. HBV-dominant cases are less common and are treated with peg interferon and nucleoside nucleotide analogues with monitoring of AST and ALT. The SVR rate in HCV-HBV coinfection is higher than that in monoinfection when treated with direct-acting antiviral drugs. But there is a risk of reactivation of HBV during and after therapy. The rate of reactivation is lower in patients treated with direct-acting antiviral drugs as compared to those treated with peg interferon plus ribavirin. Biomarkers of HBV such as HBcrAg, HBV DNA and HBVpg RNA are not effective in the prediction of HBV reactivation; only the hepatitis B surface antigen titre can be used as a biomarker for HBV reactivation. HCV can also be reactive, but this is found in very rare cases in which HBV is present and is treated first.
在流行地区，丙型肝炎病毒（HCV）/乙型肝炎病毒（HBV）合并感染很常见，合并感染者发生肝癌、肝纤维化和肝硬化等肝病的风险更高。在这种情况下，HCV 占主导地位，HBV 复制受到 HCV 的抑制。HCV 核心蛋白和由 HCV 激活的干扰素负责抑制 HBV。HCV 和 HBV 合并感染者也会出现免疫抑制。HCV 和 HBV 合并感染者观察到 HCV 中和抗体反应和 Th1 样滤泡辅助性 T 细胞（Tfh）的循环减少。两种病毒在肝脏中相互作用，由于两种病毒的相互作用，HCV/HBV 合并感染的治疗基于基因型且较为复杂。在 HCV 占主导的情况下，使用直接作用抗病毒药物和聚乙二醇干扰素加利巴韦林进行治疗，持续监测 AST 和 ALT。HBV 占主导的情况较少见，使用聚乙二醇干扰素和核苷酸类似物治疗，并监测 AST 和 ALT。与单感染相比，直接作用抗病毒药物治疗 HCV-HBV 合并感染的 SVR 率更高。但在治疗过程中和治疗后有 HBV 再激活的风险。与使用聚乙二醇干扰素加利巴韦林治疗的患者相比，使用直接作用抗病毒药物治疗的患者再激活的风险较低。HBV 的生物标志物如 HBcrAg、HBV DNA 和 HBVpg RNA 不能有效预测 HBV 再激活；只有乙型肝炎表面抗原滴度可作为 HBV 再激活的生物标志物。HCV 也可能有反应，但在 HBV 存在并首先治疗的情况下，这种情况非常罕见。
