Impaired Virion Secretion by Hepatitis B Virus Immune Escape Mutants and Its Rescue by Wild-Type Envelope Proteins or a Second-Site Mutation
Impaired Virion Secretion by Hepatitis B Virus Immune Escape Mutants and Its Rescue by Wild-Type Envelope Proteins or a Second-Site Mutation
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DOI：
10.1128/jvi.02701-12
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发表时间：
2013-02-01
影响因子：
5.4
通讯作者：
Tong, Shuping
中科院分区：
文献类型：
--
作者：
Kwei, Karen;Tang, Xiaoli;Tong, Shuping
尽管有免疫预防措施，但乙肝病毒免疫逃逸突变与疫苗失败和移植肝再感染有关，但其生物学特性仍很不清楚。将20个这样的突变体导入人肝癌细胞系中，发现许多病毒颗粒分泌严重受损，通过共表达野生型包膜蛋白或引入新的糖基化位点可以在不同程度上挽救病毒颗粒的分泌。与它们在维持分子内或分子间二硫键方面的作用一致，“a”决定簇中的半胱氨酸残基对病毒粒子的分泌至关重要。
Hepatitis B virus immune escape mutants have been associated with vaccine failure and reinfection of grafted liver despite immune prophylaxis, but their biological properties remain largely unknown. Transfection of 20 such mutants in a human hepatoma cell line identified many with severe impairment in virion secretion, which can be rescued to various extents by coexpression of wild-type envelope proteins or introduction of a novel glycosylation site. Consistent with their role in maintaining intra- or intermolecular disulfide bonds, cysteine residues within the "a" determinant are critical for virion secretion.