HBsAg 下降作为慢性 HBV 感染的治疗终点：HBV 治愈

StephenW

HBsAg 下降作为慢性 HBV 感染的治疗终点：HBV 治愈
玛丽亚姆·莫尼
1和斯科特·冯
2,*
1
渥太华大学医学系，渥太华，ON K1Y 4E9，加拿大
2
多伦多大学医学系，多伦多，ON M5G 2C4，加拿大
*
通讯作者。
学术编辑：Carla S. Coffin
病毒 2022, 14(4), 657; https://doi.org/10.3390/v14040657
收到日期：2022 年 2 月 7 日 / 修订日期：2022 年 3 月 1 日 / 接受日期：2022 年 3 月 10 日 / 发布日期：2022 年 3 月 22 日
（这篇文章属于特刊 B 型肝炎管理和实现 HBV 治愈的最新进展）
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抽象的
尽管在过去的两到三十年中有效的疫苗和抗病毒疗法已经出现，但慢性乙型肝炎病毒 (HBV) 感染仍然是全球主要的健康威胁，是肝硬化和肝癌的主要原因。功能性 HBV 治愈定义为乙型肝炎表面抗原 (HBsAg) 丢失和无法检测到的血清 HBV DNA 与慢性 HBV 感染患者的临床结局改善相关。然而，自发性 HBsAg 消失是罕见的，每年仅发生在所有 HBsAg 阳性个体中的 1%。此外，目前可用的抗病毒疗法的功能性治愈率甚至更低，每年接受治疗的患者不到 1%。尽管如此，HBsAg 消失已成为抗病毒治疗的新靶点或治疗终点。最近，围绕新型抗病毒药物的开发引起了广泛关注，例如小干扰 RNA (siRNA)、核心组装调节剂 (CAM)、核酸聚合物 (NAP) 等，这些药物可与核仁 (t) 联合使用ide 类似物和可能的免疫调节疗法，以在很大比例的慢性乙型肝炎患者中实现功能性治愈。还需要新的检测方法，提高检测极低水平 HBsAg 的灵敏度并确定 HBsAg 产生的来源，以测量HBV治愈的新抗病毒治疗。在这篇叙述性综述中，我们将定义 HBV 治愈，讨论 HBsAg 产生的各种来源，评估当前和未来抗病毒药物的 HBsAg 消失率，回顾与自发性 HBsAg 消失相关的临床因素，并探讨功能性治愈的临床意义。查看全文
关键词：乙型肝炎病毒（HBV）；乙肝治愈；乙型肝炎表面抗原（HBsAg）；抗病毒治疗

StephenW

HBsAg Loss as a Treatment Endpoint for Chronic HBV Infection: HBV Cure
by Maryam Moini
1 and Scott Fung
2,*
1
Department of Medicine, University of Ottawa, Ottawa, ON K1Y 4E9, Canada
2
Department of Medicine, University of Toronto, Toronto, ON M5G 2C4, Canada
*
Author to whom correspondence should be addressed.
Academic Editor: Carla S. Coffin
Viruses 2022, 14(4), 657; https://doi.org/10.3390/v14040657
Received: 7 February 2022 / Revised: 1 March 2022 / Accepted: 10 March 2022 / Published: 22 March 2022
(This article belongs to the Special Issue Recent Advances in Management of Hepatitis B and towards Achieving a HBV Cure)
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Abstract
Despite the availability of effective vaccines and antiviral therapy over the past two to three decades, chronic hepatitis B virus (HBV) infection remains a major global health threat as a leading cause of cirrhosis and liver cancer. Functional HBV cure defined as hepatitis B surface antigen (HBsAg) loss and undetectable serum HBV DNA is associated with improved clinical outcomes in patients with chronic HBV infection. However, spontaneous loss of HBsAg is rare and occurs in only 1% of all HBsAg-positive individuals annually. Furthermore, the rate of functional cure with currently available antiviral therapy is even lower, <1% patients on treatment per year. Nonetheless, HBsAg loss has become the new target or therapeutic endpoint for antiviral treatment. Recently, there has been much excitement surrounding the development of novel antiviral agents such as small interfering RNA (siRNA), core assembly modulators (CAMs), nucleic acid polymers (NAPs) among others, which may be used in combination with nucleos(t)ide analogs and possibly immunomodulatory therapies to achieve functional cure in a significant proportion of patients with chronic hepatitis B. Novel assays with improved sensitivity for detection of very low levels of HBsAg and to determine the source of HBsAg production will also be required to measure efficacy of newer antiviral treatments for HBV cure. In this narrative review, we will define HBV cure, discuss various sources of HBsAg production, evaluate rates of HBsAg loss with current and future antiviral agents, review clinical factors associated with spontaneous HBsAg loss, and explore clinical implications of functional cure. View Full-Text
Keywords: hepatitis B virus (HBV); HBV cure; hepatitis B surface antigen (HBsAg); antiviral therapy

StephenW

https://www.mdpi.com/1999-4915/14/4/657/htm