Hepatitis B virus core antigen (HBc Ag) accumulation in an HBV nonproducer clone of HepG2-transfected cells is associated with cytopathic effect.

Hepatitis B virus core antigen (HBc Ag) accumulation in an HBV nonproducer clone of HepG2-transfected cells is associated with cytopathic effect.
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DOI:
10.1016/0042-6822(90)90280-5
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发表时间:
1990-11
期刊:
影响因子:
3.7
通讯作者:
P. Roingeard;J. Romet‐Lemonne;D. Leturcq;A. Goudeau;M. Essex
P. Roingeard;J. Romet‐Lemonne;D. Leturcq;A. Goudeau;M. Essex
中科院分区:
医学3区
文献类型:
--
作者:
P. Roingeard;J. Romet‐Lemonne;D. Leturcq;A. Goudeau;M. Essex

文献摘要

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本文研究了用完全B病毒脱氧核糖核酸(HBV DNA)转染的肝母细胞瘤HepG 2细胞系的两个克隆。将这两个克隆(其中一个是HBV生产者)中HBV Ag生产的动力学和细胞病变效应与亲本HepG 2细胞系的动力学和细胞病变效应进行比较。用酶联免疫吸附试验(ELISA)检测B型肝炎表面抗原(HBs Ag)和B型肝炎e抗原(HBe Ag)。用单克隆抗-HBc建立了检测B型肝炎核心抗原(HBc Ag)的ELISA方法。在细胞内和细胞外隔室中部分定量了HBs、HBe和HBc Ag的量。HBV生产克隆从生长期开始分泌高水平的HBc、HBe和HBs Ag,并且未观察到细胞病变效应。HBV非生产克隆产生高水平的HBs和HBe Ag,但在上清液中没有检测到HBc Ag;相反,HBc Ag在细胞内室中积累。在该克隆中,在细胞融合后4天观察到显著的细胞死亡,对应于显著的HBc Ag释放到上清液中。这些结果表明在HBV非生产克隆中与HBc Ag积累相关的细胞病变效应,但在HBV生产克隆中无细胞病变效应。这表明,病毒学因素以及宿主的免疫反应可能被认为是在解释肝损伤发生在B型肝炎。
Two clones of the hepatoblastoma HepG2 cell line transfected with complete hepatitis B virus deoxyribonucleic acid (HBV DNA) were studied. The kinetics and cytopathic effect of HBV Ag production in these two clones (one of which was an HBV producer) were compared to those of the parent HepG2 cell line. The presence of hepatitis B surface antigen (HBs Ag) and hepatitis B e antigen (HBe Ag) was determined by commercial enzyme-linked immunosorbent assay (ELISA). A hepatitis B core antigen (HBc Ag)-specific ELISA assay was developed, using monoclonal anti-HBc to detect HBc Ag. Amounts of HBs, HBe, and HBc Ags were partially quantified in both intracellular and extracellular compartments. The HBV producer clone excreted high levels of HBc, HBe, and HBs Ags from the beginning of the growth phase, and no cytopathic effect was observed. The HBV nonproducer clone produced high levels of HBs and HBe Ags, but there was no detectable HBc Ag in the supernatant; instead, HBc Ag accumulated in the intracellular compartment. In this clone, significant cell death was observed 4 days after cell confluency, corresponding with notable HBc Ag release into the supernatant. These results suggest a cytopathic effect associated with HBc Ag accumulation in the HBV nonproducer clone, but no cytopathic effect in the HBV producer clone. This suggests that virological factors as well as the host's immune response may be considered in explaining liver injury occurring in hepatitis B.