Institute of Antibody Engineering, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, 510515, China.
School of Life Sciences, Sun Yat-sen University, Guangzhou, 510275, China.
Virol Sin. 2019 Feb;34(1):42-49. doi: 10.1007/s12250-018-0070-x. Epub 2019 Jan 4.
Hepatitis B virus (HBV) is an important human pathogen belonging to the Hepadnaviridae family, Orthohepadnavirus genus. Over 240 million people are infected with HBV worldwide. The reverse transcription during its genome replication leads to low fidelity DNA synthesis, which is the source of variability in the viral proteins. To investigate the variability quantitatively, we retrieved amino acid sequences of 5,167 records of all available HBV genotypes (A-J) from the Genbank database. The amino acid sequences encoded by the open reading frames (ORF) S/C/P/X in the HBV genome were extracted and subjected to alignment. We analyzed the variability of the lengths and the sequences of proteins as well as the frequencies of amino acids. It comprehensively characterized the variability and conservation of HBV proteins at the level of amino acids. Especially for the structural proteins, hepatitis B surface antigens (HBsAg), there are potential sites critical for virus assembly and immune recognition. Interestingly, the preS1 domains in HBsAg were variable at some positions of amino acid residues, which provides a potential mechanism of immune-escape for HBV, while the preS2 and S domains were conserved in the lengths of protein sequences. In the S domain, the cysteine residues and the secondary structures of the alpha-helix and beta-sheet were likely critical for the stable folding of all HBsAg components. Also, the preC domain and C-terminal domain of the core protein are highly conserved. However, the polymerases (HBpol) and the HBx were highly variable at the amino acid level. Our research provides a basis for understanding the conserved and important domains of HBV viral proteins, which could be potential targets for anti-virus therapy.
乙型肝炎病毒 (HBV) 是一种重要的人类病原体,属于嗜肝 DNA 病毒科,正嗜肝 DNA 病毒属。全球有超过 2.4 亿人感染 HBV。其基因组复制过程中的逆转录导致 DNA 合成保真度低,这是病毒蛋白变异性的来源。为了定量研究这种变异性,我们从 Genbank 数据库中检索了所有可用的 HBV 基因型(A-J)的 5167 条记录的氨基酸序列。从 HBV 基因组的开放阅读框 (ORF) S/C/P/X 中提取并对编码的氨基酸序列进行比对。我们分析了蛋白质长度和序列以及氨基酸频率的变异性。它全面描述了 HBV 蛋白在氨基酸水平上的变异性和保守性。特别是对于结构蛋白,乙型肝炎表面抗原 (HBsAg),有一些关键的潜在位点对于病毒组装和免疫识别至关重要。有趣的是,HBsAg 的前 S1 结构域在一些氨基酸残基位置上是可变的,这为 HBV 提供了一种免疫逃避的潜在机制,而前 S2 和 S 结构域在蛋白质序列的长度上是保守的。在 S 结构域中,半胱氨酸残基和α-螺旋和β-折叠的二级结构可能对所有 HBsAg 成分的稳定折叠至关重要。此外,核心蛋白的前 C 结构域和 C 末端结构域高度保守。然而,聚合酶 (HBpol) 和 HBx 在氨基酸水平上高度可变。我们的研究为理解 HBV 病毒蛋白的保守和重要结构域提供了基础,这些结构域可能是抗病毒治疗的潜在靶点。