乙型肝炎病毒adr型C区突变调节人类白细胞抗原-Ⅰ的表达

目的研究HBV adr型C区突变对机体HLA-I表达的调节机制。方法构建HBV C区突变株L97、G87、V60的真核表达载体,转染HepG2细胞,检测转染细胞中HLA-I的表达以及抗原提呈相关基因LMP2、TAP1、tapasin的mRNA表达情况。结果各转染细胞株均能有效表达HBeAg,但表达量不同,野生株高于C区突变株;各转染细胞株均有HLA-I的表达,其中以L97突变株表达量最高;TAP1 mRNA表达上调,LMP2 mRNA及tapasin mRNA均未见明显表达。结论HBV C区突变株可降低HBeAg的表达,且均能维持甚至上调HLA-I的表达,TAP1 mRNA的表达上调可能是HLA-I表达增强的原因之一。

Study on the mechanism of HLA- Ⅰ -expressing regulation caused by the core region mutation of HBV adr subtype

Objective To study the influence and mechanism of HBV core region mutation on HLA- I expression. Methods Euloryotic expression vectors of HBV core region mutations L97, G87 and V60 were constructed and transfected into HepG2 cells. Then the expressions of HLA-I were detected by RT-PCR genes, including LMP2, TAPI and tapasin, were measured nsing RT-PCR. Results Different levels of HBsAg in the supernatants of transfected cells were detected by ELISA. The HBsAg of the mutated groups was markedly higher than that of the wild ones. All the transfected cells expressed HLA-I molecules, especially the L97 group. It was also found that the mRNA of TAPI gene was up-regulated, while the mRNA of LMP and tapasin genes had no changes. Conclusions The core region mutation of HBV can lower the expression of HBsAg; mutated groups and wild ones both can increase the expression of HLA-I molecules. The up-regulation of TAP-I gene expression might be the cause of these changes.