检索结果-南通市图书馆

Replication of clinical hepatitis B virus isolate and its application for selecting antiviral agents for chronic hepatitis B patients

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2008年第22期14卷 3490-3496页

作者： Yin-Ping lu Tao Guo Bao-Ju Wang ji-Hua Dong jian-Fang Zhu Zhao Liu meng-ji lu Dong-Liang Yang Department of Virology Union Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 Hubei Province China Division of Clinical Immunology Tongji Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 Hubei Province China Institute of Virology Duisburg-Essen University Essen 45122 Germany

AIM: To establish a cell model harboring replicative clinical hepatitis B virus (HBV) isolates and evaluate its application in individualized selection of anti-HBV agents for chronic hepatitis B (CHB) patients. METHODS: The full-length HBV genomic DNA from 8 CHB patients was amplified by polymerase chain reaction (PCR). All the patients were treated with lamivudine for at least seven months and finally became resistant to lamivudine. The amplified HBV DNA fragments were inserted into pHY106 vectors by Sap Ⅰ?digestion. The recombinant plasmids containing 1.1 copies of HBV genome were transiently transfected into Huh7 cell line, and the levels of HBsAg, HBeAg and intercellular HBV replicative intermediates were determined by ELISA and Southern blot analysis, respectively, with or without lamivudine and adefovir treatment. The antiviral treatment with adefovir was administered to the patients and analyzed in parallel. RESULTS: A total of 25 independent HBV isolateswere obtained from the sera of 8 patients, each patient had at least two isolates. One isolate from each individual was selected and subcloned into pHY106 vector, including 5 isolates with YVDD mutation and 3 isolates with YIDD mutation. All recombinant plasmids harboring HBV isolates were transfected into Huh7 cells. The results indicated that HBV genome carried in HBV replicons of clinical HBV isolates could effectively replicate and express in Huh7 cells. Adefovir, but not lamivudine, inhibited HBV replication both in vitro and in vivo, and in vitro inhibition was dose-dependent. CONCluSION: The novel method described herein enables individualized selection of anti-HBV agents in clinic and is useful in future studies of antiviral therapy for CHB.

关键词： Hepatitis B virus Chronic hepatitis B Hepatitis B virus isolate Antiviral agents

Hepatitis B virus infection:defective surface antigen expression and pathogenesis

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2018年第31期24卷 3488-3499页

作者： Chun-Chen Wu Ying-shan Chen Liang Cao Xin-Wen Chen meng-ji lu State Key Laboratory of Virology Wuhan Institute of VirologyChinese Academy of SciencesWuhan 430071Hubei ProvinceChina Department of Microbiology and Immunology Feinberg School of Medicine Northwestern UniversityChicagoIL 60611United States Institute of Virology University Hospital of EssenEssen 45122Germany

Hepatitis B virus(HBV) infection is a global public health concern. HBV causes chronic infection in patients and can lead to liver cirrhosis, hepatocellular carcinoma, and other severe liver diseases. Thus, understanding HBV-related pathogenesis is of particular importance for prevention and clinical intervention. HBV surface antigens are indispensable for HBV virion formation and are useful viral markers for diagnosis and clinical assessment. During chronic HBV infection, HBV genomes may acquire and accumulate mutations and deletions, leading to the expression of defective HBV surface antigens. These defective HBV surface antigens have been found to play important roles in the progression of HBV-associated liver diseases. In this review, we focus our discussion on the nature of defective HBV surface antigen mutations and their contribution to the pathogenesis of fulminant hepatitis B. The relationship between defective surface antigens and occult HBV infection are also discussed.

关键词： Hepatitis B surface protein Defective surface antigen mutants Endoplasmic reticulum stress Fulminant hepatitis B Occult hepatitis B virus infection Pathogenesis

Construction and Characterization of a Hepatitis B Virus Replicon

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

中国病毒学 2007年第1期22卷 8-13页

作者： Yin-ping lu Bao-ju WANG ji-hua DONG Zhao LIU Shi-he GUAN meng-ji lu Dong-liang YANG Department of Virology Union Hospital of Tongji Medical College Huazhong University of Science and Tech- nology Wuhan 430022 P R. China Division of Clinical Immunology Tongji Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 P. R. China Institute of Virology Duisburg-Essen University Essen 45147 Germany

建立复制细胞肝炎 B 病毒(HBV ) 当模特儿并且在抗病毒的药评估决定它的应用程序，我们构造了表情包含了 HBV 染色体的 1.3 个拷贝，并且在 Huh7 房间在短暂 transfection 以后测量了病毒的复制的水平的 plasmid。我们然后观察了抗病毒... 详细信息

建立复制细胞肝炎 B 病毒(HBV ) 当模特儿并且在抗病毒的药评估决定它的应用程序，我们构造了表情包含了 HBV 染色体的 1.3 个拷贝，并且在 Huh7 房间在短暂 transfection 以后测量了病毒的复制的水平的 plasmid。我们然后观察了抗病毒的药管理的效果。HBV (ayw ) 基因碎片的 1.3 褶层被 PCR 和限制 endonuclease 消化克隆进 pCR2.1。recombinant plasmid 是进 Huh7 房间， HBsAg， HBeAg 和 HBV 的短暂 transfected 在 Huh7 房间的上层清液的 DNA 被 ELISA 和即时 PCR 分别地测量；细胞内部的 HBV replicative 中介和细胞内部的 HBV 抄本被南部的污点和北污点分别地检测。adefovir 的抗病毒的效果，新奇 anti-HBV 核苷酸类似物，在这个细胞的模型系统被评估。结果显示 HBV replicon 的 recombinant plasmid 成功地被构造；在 plasmid pHBV1.3 带的 HBV 染色体能高效地复制并且被表示在哈 7 个房间， adefovir 能在这个细胞的模型，和抑制禁止 HBV 复制是剂量依赖者。结论是 HBV replicon，能在 hepatoma 房间高效地开始病毒的复制，可以是在 HBV 复制和抗病毒的药的学习的一个有用工具。关键词肝炎 B 病毒 - 传染 replicon - 表示向量 CLC 数字 R373 基础条款：国家自然科学基础(No.30271170， No.30170889 ) 。

关键词： Hepatitis B virus Infectious replicon Expression vector

Antiviral Effect of Interferon-Induced Guanylate Binding Protein-1 against Coxsackie Virus and Hepatitis B Virus B3 in Vitro

在线全文

学校读者我要写书评

暂无评论

中国病毒学 2007年第3期22卷 193-198页

作者： Yin-ping lu　 Bao-ju WANG　 ji-hua DONG　 Zhao LIU　 Shi-he GUAN　 meng-ji lu 　 Dong-liang YANG Department of Virology Union Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China Division of Clinical Immunology Tongji Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Institute of Virology Duisburg-Essen University Essen 45147 Germany

Guanylate binding protein-1(GBP-1)is an interferon-induced *** observe its antiviral effect against Hepatitis B virus(HBV)and Coxsackie virus B3(CVB3),we constructed an eukaryotic expression vector of human GBP-1(hGBP-1).Full-length encoding sequence of hGBP-1 was amplified by long chain RT-PCR and inserted into a pCR2.1 vector,then subcloned into a pCDNA3.1(-)*** hGBP-1 plasmids and pHBV1.3 carrying 1.3-fold genome of HBV were contransfected into HepG2 cells,and inhibition effect of hGBP-1 against HBV replication was *** cells transfected with recombinant hGBP-1 plasmids were challenged with CVB3,and viral yield in cultures were *** results indicated that recombinant eukaryotic expression plasmid of hGBP-1 was constructed successfully and the hGBP-1 gene carried in this plasmid could be efficiently expressed in HepG2 cells and Hela ***-1 inhibit CVB3 but not HBV replication in *** results demonstrate that hGBP-1 mediates an antiviral effect against CVB3 but not HBV and perhaps plays an important role in the interferon-mediated antiviral response against CVB3.

关键词：柯萨奇病毒干扰素乙型肝炎病毒抗滤过性病原体鸟苷酸结合蛋白质

Genetic variation of hepatitis B virus and its significance forpathogenesis

在线全文

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2016年第1期22卷 126-144页

作者： Zhen-Hua Zhang Chun-Chen Wu Xin-Wen Chen Xu Li Jun Li meng-ji lu Department of Infectious Diseases the First Affiliated HospitalAnhui Medical UniversityHefei 230022Anhui ProvinceChina School of Pharmacy Anhui Medical UniversityHefei 230022Anhui ProvinceChina State Key Lab of Virology Wuhan Institute of VirologyChinese Academy of SciencesWuhan 430071Hubei ProvinceChina Institute of Virology University Hospital of EssenUniversity of Duisburg-Essen45122 EssenGermany

Hepatitis B virus(HBV)has a worldwide distribution and is endemic in many *** to its unique life cycle which requires an error-prone reverse transcriptase for replication,it constantly evolves,resulting in tremendous genetic variation in the form of genotypes,sub-genotypes,and *** recent years,there has been considerable research on the relationship between HBV genetic variation and HBV-related pathogenesis,which has profound implications in the natural history of HBV infection,viral detection,immune prevention,drug treatment and *** this review,we attempted to provide a brief account of the influence of HBV genotype on the pathogenesis of HBV infection and summarize our current knowledge on the effects of HBV mutations in different regions on HBV-associated pathogenesis,with an emphasis on mutations in the pre S/S proteins in immune evasion,occult HBV infection and hepatocellular carcinoma(HCC),mutations in polymerase in relation to drug resistance,mutations in HBV core and e antigen in immune evasion,chronicalization of infection and hepatitis B-related acute-on-chronic liver failure,and finally mutations in HBV x proteins in HCC.

关键词： Hepatitis B virus Genotype Variation Pathogenesis

Interference of Hepatitis B Virus with Cellular Signaling

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Virologica Sinica 2008年第2期23卷 100-106页

作者： Yang XU Chun-wei SHE Xiao-yong ZHANG Rong-juan PEI meng-ji lu Institut fiir Virologie Universitiitsklinikum Essen Essen 45122 Germany State KeyLab of Virology Wuhan Institute of Virology Chinese Academy of Sciences Wuhan 430071 China GraduateSchool of the Chinese Academy of Sciences Beijing 100072 China

The presence of hepatitis B virus (HBV) proteins leads to changes in the cellular gene expression. As a consequence, the cellular signaling processes are influenced by the actions of HBV proteins. It has been shown that HBV nucleocapsid protein and the amino-terminal part of polymerase termed as terminal protein (TP) could inhibit interferon signaling. Further, the global gene expression profiles differ in hepatoma cells with and without HBV gene expression and replication. The expression of interferon (IFN) stimulated genes (ISGs) was differently regulated in cells with HBV replication and could be modulated by antiviral treatments. The HBV TP has been found to modulate the ISG expression and enhance the HBV replication. The modulation of the cellular signaling processes by HBV may have significant implications for pathogenesis.

关键词： Hepatitis B virus, HBV Cellular signaling

Inhibitory effect of miR-125b on hepatitis C virus core protein-induced TLR2/My D88 signaling in THP-1 cells

在线全文

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2016年第17期22卷 4354-4361页

作者： Cheng Peng Hua Wang Wen-jing Zhang Sheng-Hua jie Qiao-Xia Tong meng-ji lu Dong-Liang Yang Department of Infectious Diseases Union Hospital Tongji Medical College Huazhong University of Science and Technology Institute of Virology University Hospital of Essen University of Duisburg-Essen

AIM: To investigate the role of mi R-125 b in regulating monocyte immune responses induced by hepatitis C virus(HCV) core ***: Monocytic THP-1 cells were treated with various concentrations of recombinant HCV core protein, and cytokines and mi R-125 b expression in these cells were analyzed. The requirement of Tolllike receptor 2(TLR2) or My D88 gene for HCV core protein-induced immune responses was determined by the transfection of THP-1 cells with gene knockdown vectors expressing either TLR2 si RNA or My D88 si RNA. The effect of mi R-125 b overexpression on TLR2/My D88 signaling was examined by transfecting THP-1 cells with mi R-125 b mimic RNA ***: In response to HCV core protein stimulation, cytokine production was up-regulated and mi R-125 b expression was down-regulated in THP-1 cells. The modulatory effect of HCV core protein on cellular events was dose-dependent and required functional TLR2 or My D88 gene. Forced mi R-125 b expression abolished the HCV core protein-induced enhancement of tumor necrosis factor-α, interleukin(IL)-6, and IL-10 expression by 66%, 54%, and 66%, respectively(P luding phosphorylation of NF-k Bp65, ERK, and ***: The inverse correlation between mi R-125 b and cytokine expression after HCV core challenge suggests that mi R-125 b may negatively regulate HCVinduced immune responses by targeting TLR2/My D88 signaling in monocytes.

关键词： mi R-125b Hepatitis virus C Toll like receptor 2 Monocytes Innate immunity

Silencing of UBP43 by shRNA Enhances the Antiviral Activity of Interferon against Hepatitis B Virus

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Virologica Sinica 2008年第5期23卷 339-344页

作者： He-bin FAN Bao-ju WANG Yin-ping lu You-hua HAO Xin-xing YANG meng-ji lu Dong-liang YANG Division of Clinical Immunology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Institute of Virology School of Medicine University of Essen Essen Germany

Previous studies have shown that expression of the interferon-sensitive gene （ISG）15 protease UBP43 is increased in the liver biopsy specimens of patients who do not respond to interferon （IFN）-α therapy. We hypothesized that UBP43 might hinder the ability of IFN to inhibit HBV replication. In this study, we investigated whether vector-based siRNA promoted by HI （psiUBP43） could enhance IFN inhibiting HBV replication in cell culture. UBP43 was specifically silenced using shRNA. In HepG2.2.15 cells, the HBeAg and HBV DNA levels were significantly reduced by IFN after transfection of shRNA, imphicated that vector-based siRNA promoted by H1 （psiUBP43） could enhance IFN inhibiting HBV replication in cell culture. These data suggest that UBP43 modulates the anti-HBV type I IFN response, and is a possible therapeutic target for the treatment of HBV infection.

关键词： UBP43 shRNA Hepatitis B virus Interferon

Effect of Hepatitis C Virus Core Protein on Interferon-Induced Antiviral Genes Expression and Its Mechanisms

在线全文

学校读者我要写书评

暂无评论

中国病毒学 2007年第5期22卷 374-379页

作者： Yan-zi CHANG Yan-chang LEI Wen WU Shan-shan CHEN Han-ju HUANG Dong-liang YANG meng-ji lu Department of Pathogen Biology Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Division of Clinical Immunology Tongji Hospital Huazhong University of Science and Technology Wuhan 430030 China.

Emerging data indicated that HCV subverts the antiviral activity of interferon(IFN);however,whether HCV core protein contributes to the process remains *** the present study,we examined the effect of HCV core protein on interferon-induced antiviral gene expression and whether the effect is involved in the activation and negative regulation of the Jak/STAT signaling *** results showed that,following treatment with IFN-α,the transcription of PKR,MxA and 2'-5'OAS were down-regulated in HepG2 cells expressing the core *** the presence of HCV core protein,ISRE-dependent luciferase activity also *** study indicated that the core protein could inhibit the tyrosine phosphorylation of STAT1,whereas the level of STAT1 expression was ***,SOCS3,the negative regulator of the Jak/STAT pathway,was induced by HCV core *** results suggests that HCV core protein may interfere with the expression of some interferon-induced antiviral genes by inhibiting STAT1 phosphorylation and induction of SOCS3.

关键词：丙型肝炎病毒核心蛋白质 α-干扰素抗病毒基因表达作用机理