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| 1 | Viral and cellular determinants involved in hepadnaviral entry显示文摘Hepadnaviridae is a family of hepatotropic DNA viruses that is divided into the genera orthohepadnavirus of mammals and avihepadnavirus of birds.All members of this family can cause acute and chronic hepatic infec-tion,which in the case of human hepatitis B virus(HBV) constitutes a major global health problem.Although our knowledge about the molecular biology of these highly liver-specific viruses has profoundly increased in the last two decades,the mechanisms of attachment and productive entrance into the differentiated host hepa-tocytes are still enigmatic.The difficulties in studying hepadnaviral entry were primarily caused by the lack of easily accessible in vitro infection systems.Thus,for more than twenty years,differentiated primary hepato-cytes from the respective species were the only in vitro models for both orthohepadnaviruses(e.g.HBV) and avihepadnaviruses(e.g.duck hepatitis B virus [DHBV]).Two important discoveries have been made recently re-garding HBV:(1) primary hepatocytes from tree-shrews;i.e.,Tupaia belangeri,can be substituted for primary hu-man hepatocytes,and(2) a human hepatoma cell line(HepaRG) was established that gains susceptibility for HBV infection upon induction of differentiation in vitro.A number of potential HBV receptor candidates have been described in the past,but none of them have been confirmed to function as a receptor.For DHBV and prob-ably all other avian hepadnaviruses,carboxypeptidase D(CPD) has been shown to be indispensable for infection,although the exact role of this molecule is still under debate.While still restricted to the use of primary duck hepatocytes(PDH),investigations performed with DHBV provided important general concepts on the first steps of hepadnaviral infection.However,with emerging dataobtained from the new HBV infection systems,the hope that DHBV utilizes the same mechanism as HBV only partially held true.Nevertheless,both HBV and DHBV in vitro infection systems will help to:(1) functionally dis-sect the hepadnaviral entry pathways,(2) perform re-verse genetics(e.g.test the fitness of escape mutants),(3) titrate and map neutralizing antibodies,(4) improve current vaccines to combat acute and chronic infections of hepatitis B,and(5) develop entry inhibitors for future clinical applications. | Dieter Glebe Stephan Urban | 2007 | World Journal of Gastroenterology2007，13，1： | 35 |
| 2 | Recent advances in hepatitis B virus research:A German point of view显示文摘More than 30 years after the discovery of human hepatitis B virus (HBV) this virus remains to be one of the major global health problems. In infected adolescents or adults, 5%-10% will lead to a chronic carrier state, whereas in infected neonates up to 90% develop chronicity. It is estimated that about 370 million people are chronic carriers of HBV worldwide. In many regions of the world, chronic HBV infection is still the major cause of liver cirrhosis and hepatocellular carcinoma. During the last 30 years, many steps of the viral life cycle have been unravelled, mainly due to cloning, sequencing and expression of the genomic DNA extracted from HBV virions. This has lead to the development of a safe and efficient vaccine and sensitive tests for HBV surface protein (HBsAg) allowing reliable diagnosis and screening of blood products. More recently, a growing number of reverse transcriptase inhibitors have been developed. However, together with these improvements new deficiencies in prevention and cure of HBV infections are becoming apparent. Although HBV is a DNA virus, it is highly variable under immunity or drug induced selection pressure, resulting in vaccine-related escape mutants and drug resistance. To overcome these challenging problems new antivirals and optimised vaccines have to be developed. | Dieter Glebe | 2007 | World Journal of Gastroenterology2007，13，1： | 25 |
| 3 | Hepatitis B virus subgenotype F3 reactivation with vaccine escape mutations:A case report and review of the literature显示文摘Hepatitis B represents a global health threat because its chronic course and sequelae contribute to a high morbidity and mortality. Hepatitis B virus(HBV) infection can be controlled by vaccines, antiviral treatment, and by interrupting transmission. Rare vaccine escape mutants are serious because they eliminate vaccine protection. Here, we present a 74-year-old vaccinated patient with HBV reactivation 11 years after kidney transplantation. The patient was HBV-positive but HBs Ag-negative prior to vaccination 6 years before transplantation. The reactivated virus was HBV genotype F3 with vaccine escape mutations G145 R, P120 Q, and Q129 P. The patient was successfully treated with entecavir. The epidemiological reasons for this subgenotype, which is extremely rare in Western Europe, were unclear. This case illustrates that second-generation vaccines are not always effective in a specific group of patients. | Stefan Schlabe Kathrin van Bremen Souhaib Aldabbagh Dieter Glebe Corinna M Bremer Tobias Marsen Walter Mellin Veronica Di Cristanziano Anna M Eis-Hübinger Ulrich Spengler | 2018 | World Journal of Hepatology2018，10，7： | 2 |
| 4 | Genotype-dependent activation or repression of HBV enhancer Ⅱ by transcription factor COUP-TF1显示文摘AIM: To study the expression of HBV enhancer Ⅱ by transcription factor COUP-TF1. METHODS: In order to study the regulation of HBV variants in the vicinity of the NRRE we cloned luciferase constructs containing the HBV enhancer Ⅱ from variants and from HBV genotypes A and D and cotransfected them together with expression vectors for COUP-TF1 into HepG2 cells. RESULTS: Our fi ndings show that enhancer Ⅱ of HBV genotype A is also repressed by COUP-TF1. In contrast, two different enhancer Ⅱ constructs of HBV genotype D were activated by COUP-TF1. The activation was independent of the NRRE because a natural variant with a deletion of nt 1763-1770 was still activated by COUP- TF1. CONCLUSION: Regulation of transcription of the HBV genome seems to differ among HBV genomes derived from different genotypes. These differences in transcriptional control among HBV genotypes may be the molecular basis for differences in the clinical course among HBV genotypes. | Silke F Fischer Katja Schmidt Nicola Fiedler Dieter Glebe Christian Schüttler Jianguang Sun Wolfram H Gerlich Reinald Repp Stephan Schaefer | 2006 | World Journal of Gastroenterology2006，12，37： | 2 |
| 5 | QTL for body weight and condition factor in Atlantic salmon (Salmo salar): com- parative analysis with rainbow trout (Oncorhynchus mykiss) and Arctic eharr (Salvelinus alpinus) 显示文摘 | Reid D P Szanto A Glebe B | 2004 | Heredity2004，94，2： | 1 |
| 6 | Hepatitis B virus rtI233V mutation and resistance to adefovir显示文摘 | Geipel A Glebe D Gerlich WH | 2014 | N Engl J Med2014，370，17： | 1 |
| 7 | Role of glycosaminogly-cans for binding and infection of hepatitis B virus显示文摘 | Leistner CM Gruen-Bernhard S Glebe D | | 0，，1： | 1 |
| 8 | Pre-S1 antigen-dependent infec- tion of Tupaia hepatoeyte cultures with human hepatitis B virus 显示文摘 | Glebe D Aliakbafi M Krass P | 2003 | J Virol2003，77，17： | 1 |
| 9 | Role of glycosaminoglycans for binding and infection of hepatitis B virus显示文摘 | LEISTNER C M GRUEN-BERNHARD S GLEBE D | 2008 | Cell Microbio12008，10，1： | 1 |
| 10 | QTL for body weight and condition factor in Atlantic salmon(Salmo salar): comparative analysis with rainbow trout(Oncorhynchus mykiss) and Arctic charr(Salvelinus alpinus)显示文摘 | Reid D P Santo A Glebe B | 2005 | Heredity2005，94，： | 1 |
| 11 | Pre-S1 antigen-dependent infection of Tupaia hepatocyte cultures with human hepatitis B virus 显示文摘 | Glebe D Aliakbari M Krass P | 2003 | J Virol2003，77，17： | 1 |
| 12 | Pre-sl antigen-dependent infection of Tupaia hepatocyte cultures with human hepatitis B virus 显示文摘 | Glebe D Aliakbari M Krass P | 2003 | J Virol2003，77，17： | 1 |
| 13 | Role of glyeosamin- oglycans for binding and infection of hepatitis B virus显示文摘 | Leistner CM Gruen-Bemhard S Glebe D | 2008 | Cell Mi~ crobiol2008，10，1： | 1 |
| 14 | Correlation of Virus and Host Response Markers with Circulating Immune Complexes during Acute and Chronic Woodchuck Hepatitis Virus Infection 显示文摘 | Glebe D Lorenz H Gerlich WH | 2009 | J Virol2009，83，4： | 1 |
| 15 | QTL for body weight and condition factor in Atlantic almon(Salmosalar):comparative analysis with rainbow trout(Oncorhynchus mykiss)and Arctic Charr(Salvelinus alpinus)显示文摘 | Reid D P Szanto A Glebe B | 2005 | Heredi2005，94，2： | 1 |
| 16 | Molecular approaches to validate disinfectants against human hepatitis B virus显示文摘 | C. Jursch W. Gerlich D. Glebe S. Schaefer O. Marie O. Thraenhart | 2002 | Medical Microbiology and Immunology2002，，4： | 1 |
| 17 | Attachment sites and neutralising epitopes of hepatitis B virus 显示文摘 | Glebe D | 2006 | Minerva Gastroenterol Dietol2006，52，1： | 1 |
| 18 | Molecular virology of hepatitis B virus and targets for antiviral intervention显示文摘 | Glebe D K(o)nig A | 2014 | Intervirology2014，57，34： | 1 |
| 19 | Alternative methods for validation of cell culture infection with duck hepatitis B virus显示文摘 | A. Sauerbrei M. Schacke U. Schultz R. Egerer I. Merkle D. Glebe W. Gerlich P. Wutzler | 2005 | Journal of Virological Methods2005，，2： | 1 |
| 20 | , Transcription of hepatitis B virus in peripheral blood mononuclear cells from persistently infected patients显示文摘 | Stoll-Becker S Repp R Glebe D | 1997 | J Virol1997，71，： | 1 |
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