ObjectiveTo evaluate the relationship between hepatitis B virus (HBV) preS1 antigen and the virus replication index human hepatitis B e antigen (HBeAg) and liver function. MethodsA total of 310 cases of serum samples from patients with chronic HBV treated in our hospital between May and July 2012 were examined and studied. HBV preS1 antigen was detected by ELISA; HBeAg was detected by the Architect i2000 system; and alanine transaminase (ALT) was detected by kinetic method. ResultsThe detection rate of HBV preS1 antigen was higher in HBeAg positive group. HBV preS1 antigen was correlated with HBeAg which was an index of virus replication. HBV preS1 antigen was correlated with ALT levels. ConclusionThe levels of HBV preS1 antigen may reflect the replication of HBV and the reactiveness condition of chronic hepatitis.
Objective To study the relationship of hepatitis B virus （HBV） to spontaneous rupture of hepatocellular carcinoma （HCC-SR） and its mechanism. Method The related literatures about theory of HCC-SR were consulted and reviewed. Results The injury of small arteries was usually followed in patients with HCC-SR， which was related to vascular autoimmune injury caused by the HBV infection. The small arteries in which immune complex deposited were readily injured， as a result HCC-SR happened while vascular load increased. Conclusion The HBV infection resulted in vascular autoimmune injury maybe a important factor in the pathogenesis of HCC-SR.
目的 建立一个规范化、标准化的肝炎病毒（HBV）感染患者和对照组标本库。 方法 通过对四川绵阳地区大型流行病调查，收集HBV感染患者捐赠的血液标本（ELISA）检测调查者血样乙肝表面抗原（HBsAg），完整记录其实验报告，临床干预及流行病学调查资料。 结果 重大专项传染病综合防治四川示范区项目启动至今共收集血液组织标本87 478份，其中HBV检出阳性标本60 571份；保留相关阴性对照标本26 907份。 结论 建立HBV 感染患者及对照组血液标本库，可为乙肝的综合防治与研究提供高质量标本及相关流行病调查信息。
目的：建立能表达乙肝病毒（hepatitis B virus,HBV）preS2S抗原蛋白的荷瘤小鼠模型，为研究HBV核酸疫苗的体内CTL应答及免疫治疗作用提供简便易行的研究模型。 方法：以免疫印迹法验证SP2/0-S2S细胞中有HBV preS2S抗原的稳定表达，将SP2/0-S2S细胞种植到BALB/c小鼠胁部皮下（荷瘤），观察能否生长成瘤，以及成瘤的时间、肿瘤大小和荷瘤后小鼠的生存时间；以免疫组织化学法检测小鼠肿瘤组织HBV preS2S抗原的表达。以不表达preS2S抗原蛋白的SP2/0-CMV细胞荷瘤小鼠作为阴性对照。结果：荷瘤后3天～1周，SP2/0-S2S细胞可在小鼠皮下形成实体肿瘤，成瘤率为100%，肿瘤细胞中有preS2S抗原表达，荷瘤后小鼠的平均生存时间为16±1天；与不表达preS2S抗原蛋白的SP2/0-CMV细胞荷瘤小鼠相比，成瘤率、成瘤时间、肿瘤大小及生存时间差异。结论：建立了能表达HBV preS2S抗原蛋白的荷瘤小鼠模型，可用于HBV核酸疫苗的体内CTL应答及免疫治疗作用的实验研究。同时也建立了不表达preS2S抗原蛋白的荷瘤小鼠模型，可用作阴性对照。
The infection of Hepatitis B virus (HBV) can result in severe consequences, including chronic hepatitis, liver fibrosis, cirrhosis, and even liver cancer. Effective antiviral treatment has the potential to slow down the progression of the disease. HBV serum biomarkers play a crucial role in the dynamic management of chronic hepatitis B (CHB) patients. However, the conventional hepatitis B virus markers, such as hepatitis B serologic testing and HBV DNA, are insufficient to meet the clinical requirements. This review provided a comprehensive overview of the current research on the quantification of HBsAg and anti-HBc, HBV RNA and HBV core-associated antigen, which summarized the crucial role these markers play in the administration of antiviral medications, predicting the efficacy of treatment and anticipating the likelihood of virologic rebound following drug cessation, as well as assessing disease progression in CHB patients.
Drugs may induce hepatitis B virus (HBV) reactivation (HBV-R). Here we have reviewed the definition and harm of HBV-R, the risk drugs and their underlying mechanism, the influence factors, as well as the early intervention measures. It is shown that multiple drugs, including chemotherapy drugs, immunotherapy drugs, directly acting antivirals, cell therapy, etc., can induce HBV-R by affecting host immunity or directly activating HBV transcription factors. HBV-R could cause severe liver damage, even interruption of treatment of original diseases, affecting the prognosis of patients. Through precisely identifying risk drugs, monitoring the influence factors, and prescribing preventive anti-HBV regimen if necessary, the incidence of HBV-R can be significantly reduced. It is also suggested that clinical physicians should not only pay attention to the early identification and intervention of HBV-R, but also further study the mechanism of HBV-R in depth, especially the underlying mechanism between host, HBV and risk factors. This will help to promote the discovery of more valuable markers for risk prediction and targets for early intervention, and to further reduce the risk of HBV-R and improve the prognosis of patients.