中文摘要：

瞄准：为了调查肝炎 B (HBV ) 感染是否激活 DNA 损坏反应和 DNA 修理，余因子禁止 HBV 感染和复制。方法：人的 hepatocyte 房间线 HL7702 被学习。Immunoblotting 被执行测试混乱的表示变异毛细管扩张(ATM )-Rad3-related 蛋白质(ATR ) ， p21 和 Chk1 的磷酸化的水平， p53， H2AX， ATM 在感染 HBV 或 non-infected-cells。特殊短 RNAi oligos 是 transfected 导致在 HL7702 击倒的短暂 ATR。ATR-ATM 化学禁止者咖啡因(CF ) 和茶硷(TP ) ，或 Chk1 禁止者 7-hydroxystaurosporine (UCN01 ) 被学习决定他们是否压制细胞的 DNA 损坏反应， MG132 禁止 proteasome。结果：ATR 检查点小径，在 DNA 对单个海滨的裂缝作出回应，响应 HBV 感染被激活。ATR 击倒的房间减少了 HBV DNA 收益，暗示那 HBV 感染和复制能激活并且利用激活的 DNA 损坏反应。CF/TP 或 UCN01 分别地在 70% 和 80% 减少了 HBV DNA 收益。在 HBV 感染减少了 HBV DNA 收益以前， HBV 废除了由 p21 蛋白质的降级的 p21，和介绍表明小径的 ATR 依赖的 DNA 损坏。与这结果一致，在 MG132 处理以后的 p21 累积严厉地也减少了 HBV DNA 收益。结论：HBV 感染能与由禁止为 HBV 复制要求的细胞的基因指向宿主细胞蛋白质的治疗学的途径被治疗或由恢复，回答由 HBV 废除了，因此提供一条潜在的途径给 HBV 感染的预防和处理。

英文摘要：

AIM： To investigate whether hepatitis B virus （HBV） infection activates DNA damage response and DNA repair cofactors inhibit HBV infection and replication. METHODS： Human hepatocyte cell line HL7702 was studied. Immunoblotting was performed to test the expression of ataxia telangiectasia-mutated （ATM）- Rad3-related protein （ATR）, p21 and the level of phosphorylation of Chkl, p53, H2AX, ATM in HBV-infected or non-infected-cells. Special short RNAi oligos was transfected to induce transient ATR knockdown in HL7702. ATR-ATN chemical inhibitors caffeine （CF） and theophylline （TP）, or Chkl inhibitor 7-hydroxystaurosporine （UCN01） was studied to determine whether they suppress cellular DNA damage response and NG132 inhibits proteasome. RESULTS： The ATR checkpoint pathway, responding to single-strand breaks in DNA, was activated in response to HBV infection. ATR knockdown cells decreased the HBV DNA yields, implying that HBV infection and replication could activate and exploit the activated DNA damage response. CF/TP or UCN01 reduced the HBV DNA yield by 70% and 80%, respectively. HBV abrogated the ATR-dependent DNA damage signaling pathway by degrading p21, and introduction of the p21 protein before HBV infection reduced the HBV DNA yield. Consistent with this result, p21 accumulation after NG132 treatment also sharply decreased the HBV DNA yield. CONCLUSION： HBV infection can be treated with therapeutic approaches targeting host cell proteins by inhibiting a cellular gene required for HBV replication or by restoring a response abrogated by HBV, thus providing a potential approach to the prevention and treatment of HBV infection.