丁型肝炎病毒 (HDV) 感染与乙型肝炎病毒 (HBV) 感染相关，影响全球约 1200 万至 7200 万人。与单独的乙型肝炎病毒或丙型肝炎病毒相比，丁型肝炎病毒会导致更快速的肝硬化进展和更高的肝细胞癌发生率。丁型肝炎病毒需要乙型肝炎病毒进入肝细胞并组装和分泌新的病毒颗粒。大约 95% 的人在急性 HDV-HBV 合并感染后，两种病毒都会被清除，而 HBV 感染者的 HDV 重复感染会导致 90% 以上的感染患者出现慢性 HDV-HBV 感染。与单独的乙型肝炎相比，慢性丁型肝炎会导致更快进展的肝病。大约 30% 至 70% 的慢性丁型肝炎患者在诊断时患有肝硬化，超过 50% 在诊断后 10 年内死于肝病。然而，最近的研究表明，进展是可变的，超过 50% 的人可能有惰性病程。由于缺乏认识以及对 HDV 抗体和 HDV RNA 的可靠诊断测试的机会有限，只有约 20% 至 50% 的丁型肝炎感染者得到诊断。乙型肝炎疫苗通过预防乙型肝炎病毒感染来预防丁型肝炎病毒感染，但没有疫苗可以保护已确诊乙型肝炎病毒感染的人免受丁型肝炎病毒感染。干扰素α可抑制HDV复制，并降低肝脏相关事件的发生率，例如肝失代偿、肝细胞癌、肝移植或死亡率，从每年8.5%降低至每年3.3%。干扰素α的不良反应如疲劳、抑郁和骨髓抑制很常见。乙肝病毒核苷类似物，如恩替卡韦或替诺福韦，对丁肝病毒无效。 bulevirtide（阻止 HDV 进入肝细胞）和 lonafarnib（干扰 HDV 组装）的 3 期随机临床试验表明，与安慰剂或观察相比，这些疗法在 96 周后在高达 56% 的患者中获得了病毒学和生化反应布勒韦肽单药治疗后的死亡率为 19%，洛那法尼、利托那韦和聚乙二醇干扰素 α 治疗 48 周后的死亡率为 19%。 HDV 感染影响着全世界约 1200 万至 7200 万人，并且与肝硬化和肝衰竭的进展速度更快以及肝细胞癌的发生率高于肝细胞癌相关。单独感染乙型肝炎病毒。布勒韦肽最近在欧洲被批准用于治疗 HDV，而聚乙二醇干扰素 α 是大多数国家唯一可用的治疗方法。

Hepatitis D virus (HDV) infection occurs in association with hepatitis B virus (HBV) infection and affects approximately 12 million to 72 million people worldwide. HDV causes more rapid progression to cirrhosis and higher rates of hepatocellular carcinoma than HBV alone or hepatitis C virus.HDV requires HBV to enter hepatocytes and to assemble and secrete new virions. Acute HDV-HBV coinfection is followed by clearance of both viruses in approximately 95% of people, whereas HDV superinfection in an HBV-infected person results in chronic HDV-HBV infection in more than 90% of infected patients. Chronic hepatitis D causes more rapidly progressive liver disease than HBV alone. Approximately 30% to 70% of patients with chronic hepatitis D have cirrhosis at diagnosis and more than 50% die of liver disease within 10 years of diagnosis. However, recent studies suggested that progression is variable and that more than 50% of people may have an indolent course. Only approximately 20% to 50% of people infected by hepatitis D have been diagnosed due to lack of awareness and limited access to reliable diagnostic tests for the HDV antibody and HDV RNA. The HBV vaccine prevents HDV infection by preventing HBV infection, but no vaccines are available to protect those with established HBV infection against HDV. Interferon alfa inhibits HDV replication and reduces the incidence of liver-related events such as liver decompensation, hepatocellular carcinoma, liver transplant, or mortality from 8.5% per year to 3.3% per year. Adverse effects from interferon alfa such as fatigue, depression, and bone marrow suppression are common. HBV nucleos(t)ide analogues, such as entecavir or tenofovir, are ineffective against HDV. Phase 3 randomized clinical trials of bulevirtide, which blocks entry of HDV into hepatocytes, and lonafarnib, which interferes with HDV assembly, showed that compared with placebo or observation, these therapies attained virological and biochemical response in up to 56% of patients after 96 weeks of bulevirtide monotherapy and 19% after 48 weeks of lonafarnib, ritonavir, and pegylated interferon alfa treatment.HDV infection affects approximately 12 million to 72 million people worldwide and is associated with more rapid progression to cirrhosis and liver failure and higher rates of hepatocellular carcinoma than infection with HBV alone. Bulevirtide was recently approved for HDV in Europe, whereas pegylated interferon alfa is the only treatment available in most countries.