Clark Daniel N, Hu Jianming
Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, United States.
Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, United States.
Antiviral Res. 2015 Nov;123:132-7. doi: 10.1016/j.antiviral.2015.09.011. Epub 2015 Sep 25.
Hepatitis B virus (HBV) infections rely on the proper functioning of the viral polymerase enzyme, a specialized reverse transcriptase (RT) with multiple activities. All currently approved antiviral drugs for the treatment of chronic HBV infection, except for interferon, target the RT and belong to the same chemical class - they are all nucleoside analogs. Viral DNA synthesis is carried out by the RT enzyme in several different steps, each with distinct RT conformational requirements. In principle, each stage may be targeted by distinct antiviral drugs. In particular, the HBV RT has the unique ability to initiate viral DNA synthesis using itself as a protein primer in a novel protein priming reaction. In order to help identify RT inhibitors and study their mechanisms of action, a number of experimental systems have been developed, each varying in its ability to dissect the protein priming stage and subsequent stages of viral DNA synthesis at the molecular level. Two of the most effective drugs to date, entecavir and tenofovir, can inhibit both the protein priming and the subsequent DNA elongation stages of HBV DNA synthesis. Interestingly, clevudine, a thymidine analog, can inhibit both protein priming and DNA elongation in a non-competitive manner and without being incorporated into the viral DNA. Thus, a nucleoside RT inhibitor (NRTI) can functionally mimic a non-NRTI (NNRTI) in its inhibition of the HBV RT. Therefore, novel NRTIs as well as NNRTIs may be developed to inhibit the DNA synthesis activity of the HBV RT. Furthermore, additional activities of the RT that are also essential to HBV replication, including specific recognition of the viral RNA and its packaging into viral nucleocapsids, may be exploited for antiviral development. To achieve a more potent inhibition of viral replication and ultimately cure chronic HBV infection, the next generation of anti-HBV therapies will likely need to include NRTIs, NNRTIs, and other agents that target the viral RT as well as other viral and host factors in various combinations. This article forms part of a symposium in Antiviral Research on "An unfinished story: from the discovery of the Australia antigen to the development of new curative therapies for hepatitis B."
乙型肝炎病毒(HBV)感染依赖于病毒聚合酶的正常功能,这是一种具有多种活性的特殊逆转录酶(RT)。目前所有批准用于治疗慢性HBV感染的抗病毒药物,除干扰素外,均靶向RT,且属于同一化学类别——它们都是核苷类似物。病毒DNA合成由RT酶分几个不同步骤进行,每个步骤都有不同的RT构象要求。原则上,每个阶段都可能被不同的抗病毒药物靶向。特别是,HBV RT具有独特的能力,能够在一种新型的蛋白质引发反应中以自身作为蛋白质引物启动病毒DNA合成。为了帮助鉴定RT抑制剂并研究其作用机制,已经开发了许多实验系统,每个系统在分子水平上剖析蛋白质引发阶段和病毒DNA合成后续阶段的能力各不相同。迄今为止,两种最有效的药物恩替卡韦和替诺福韦,能够抑制HBV DNA合成的蛋白质引发和随后的DNA延伸阶段。有趣的是,胸苷类似物克拉夫定能够以非竞争性方式抑制蛋白质引发和DNA延伸,且不会掺入病毒DNA。因此,核苷逆转录酶抑制剂(NRTI)在抑制HBV RT方面可以在功能上模拟非核苷逆转录酶抑制剂(NNRTI)。因此,可以开发新型NRTI以及NNRTI来抑制HBV RT的DNA合成活性。此外,RT的其他对HBV复制也至关重要的活性,包括对病毒RNA的特异性识别及其包装到病毒核衣壳中,也可用于抗病毒药物开发。为了更有效地抑制病毒复制并最终治愈慢性HBV感染,下一代抗HBV疗法可能需要包括NRTI、NNRTI以及其他靶向病毒RT以及其他病毒和宿主因子的药物,并以各种组合形式使用。本文是《抗病毒研究》中关于“一个未完成的故事:从澳大利亚抗原的发现到乙型肝炎新治愈疗法的开发”研讨会的一部分。