Dissertations / Theses: 'Hepatitis B virus'

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Kandpal, Manish. "Role of defective hepatitis B virus in wild-type hepatitis B virus replication." Thesis, IIT Delhi, 2017. http://localhost:8080/xmlui/handle/12345678/7247.

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駱淑芳 and Suk-fong Anna Lok. "Replication of hepatitis B virus in Chinese patients with chronic hepatitis B virus infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1990. http://hub.hku.hk/bib/B31981392.

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Kidd-Ljunggren, Karin. "Genetic variability in hepatitis B virus." Lund : Depts. of Infectious Diseases and Medical Microbiology, University of Lund, 1995. http://books.google.com/books?id=KDZsAAAAMAAJ.

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Umeda, Makoto. "Hepatitis B virus infection in lymphatic tissues in inactive hepatitis B carriers." Kyoto University, 2007. http://hdl.handle.net/2433/135682.

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Arauz-Ruiz, Patricia. "Molecular epidemiology of hepatitis A and hepatitis B virus in central America /." Stockholm : Repro Print, 2002. http://diss.kib.ki.se/2002/91-7349-208-6/.

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Williams, David James. "Hepatitis B virus core gene deletions." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363171.

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7

Williams, Stephen John. "Chronic hepatitis B virus infection : prevention and treatment." Thesis, The University of Sydney, 1989. https://hdl.handle.net/2123/26390.

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Hepatitis B virus (HBV) infection is an increasing public health problem in Australia particularly in certain 'high-risk' subgroups of the population. In order to establish cost-effective screening and vaccination programs directed towards the control and possible eradication of HBV infection, accurate information is needed about the modes of spread and the numbers of "at risk" individuals in particular community subgroups. In addition, treatment strategies must be developed for established HBV carriers since at least 35% of such individuals will die directly related to complications of the disease. This Thesis is the compilation of a series of investigations into familial transmission of chronic HBV infection, the efficacy of alpha interferon treatment of chronic active hepatitis (CAH) B and the effects of such treatment on hepatic drug metabolism. The results have important implications for prevention of HBV infection by screening and vaccination programs, for the selection of patients for inclusion in treatment trials and for the methods by which such treatments can be monitored for responses, and they provide new information about clinically-relevant effects of interferon treatment on the metabolism of other drugs. An overview of the virology of hepatitis B virus (HBV), the biology of HBV infection and the resultant disease states is presented in Chapter 1. In Chapter 2, a prospective study examining the incidence of and factors determining intrafamily HBV transmission in a mixed Caucasian and Asian population is presented. Household contacts of both Asian and Caucasian HBV carriers were clearly demonstrated as being at high-risk for HBV infection. Several factors were identified to be associated with a higher rate of transmission of HBV infection within families; namely, if the index case was Asian rather than Caucasian, had an HBsAg-positive mother rather than an HBsAg-positive father, was HBeAg-positive rather than HBeAg-negative , and had chronic rather than acute HBV infection. In Chapter 3, the first Australian study of alpha interferon (rIFN-aA) in the treatment of CAH-B is reported. While rlFN-aA was demonstrated to have inhibitory effects on HBV replication, the overall response rate was disappointing and not significantly different from the spontaneous seroconversion rate observed in the control group. A major goal of the present study was to establish whether serological changes of HBV infection, that could be induced by interferon, were associated with changes in hepatic function or affected the natural history of this otherwise progressive chronic liver disease. The results provide an important contribution to new knowledge in that although sustained HBV serological improvement was obtained in only 35% of treated patients, this change in the biological state of the virus-host interaction provided a beneficial change in the natural history of chronic liver disease as assessed clinically, biochemically and by direct morphologic examination. In addition, the results presented in Chapter 4 have a novel bearing on whether changes in chronic hepatitis B disease activity improve hepatic metabolic function. Sequential determinations of a simplified 2 point antipyrine clearance (CLAP) test indicated that HBeAg seroconversion was associated consistently with a quantitatively important increase in CLAp while reactivation led to a deterioration in hepatic metabolic function as indicated by the CLAp test. In addition, the CLAp test was a more sensitive and specific indicator of hepatic metabolic function compared to more conventional tests of liver function (serum albumin and bilirubin concentrations, and prothrombin time). Part C describes studies in which the effects of interferon on hepatic drug metabolism have been examined. In human studies in vivo, antipyrine and theophylline were employed as substrates for the cytochrome P-450dependent mixed function oxidase system. The study described in Chapter 6 provides the first direct evidence that interferon inhibits hepatic drug metabolism in humans; a significant reduction in antipyrine clearance was demonstrated following a single intramuscular injection of interferon. In Chapter 7 the clinical relevance of the observed effect of interferon on antipyrine metabolism was confirmed by the demonstration that interferon also impairs theophylline elimination. This demonstrated one of the most profound therapy-induced inhibitions of drug metabolism yet observed in man. In addition, the effect of interferon on hepatic drug metabolism appears to be relatively selective for some cytochrome P-450 isozymes, specifically that concerned with N-demethylation of theophylline. The mechanism for the interferon-mediated impairment of hepatic oxidative drug metabolism observed in the human in vivo studies was then explored by experiments in animals. The isolated perfused rat liver model was utilized to study effects on the intact liver, while hepatic microsomal androstenedione hydroxylation pathways were measured as a probe to assess interferon effects on individual cytochrome P-450 isozymes. The results demonstrated that the effect of IFN on drug metabolism is, at least in rats, species specific. Moreover, the reduction in total hepatic P-450 content produced by lFN appeared to result from a generalized lowering of P-450 isozymes rather than being specific for individual forms. The apparent discrepancy between these findings and the observation in humans that human rlFN-ocA depressed the P-450 isozyme(s) responsible for the Ndemethylation pathway of theophylline metabolism to a greater degree than the 8-hydroxylation pathway may be due to species differences or to the specific types of interferon studied. In any event it is likely that the clearance of many other xenobiotics as well as endogenous substances metabolized by P-450 may be impaired by interferon and future studies should be directed towards examining the effects of interferons on other such clinically-relevant compounds. Moreover, the results of the present study indicate that lFN-treated rats should be a good model with which to obtain clearance data for such compounds.

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Lau, Chi Chiu. "Hepatitis B virus and single nucleotide polymorphisms." HKBU Institutional Repository, 2007. http://repository.hkbu.edu.hk/etd_ra/810.

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Taş, Tekin Kaya Selçuk. "Salt anti Hepatit B Virus Core antikoru pozitif kan donörlerinde Hepatit B Virus DNA tespiti /." Isparta : SDÜ Tıp Fakültesi, 2009. http://tez.sdu.edu.tr/Tezler/TT00398.pdf.

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Luo, Ying. "Hepatitis B virus specific immune response after liver transplantation for chronic hepatitis B /." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B3697724X.

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Luo, Ying, and 羅英. "Hepatitis B virus: specific immune response after liver transplantation for chronic hepatitis B." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B3697724X.

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Chen, Augustine, and n/a. "Translational control mechanisms used by the human Hepatitis B virus : an upstream open reading frame modulates expression of the pregenomic RNA." University of Otago. Department of Biochemistry, 2007. http://adt.otago.ac.nz./public/adt-NZDU20080130.123000.

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The human hepatitis B virus (HBV) is a small hepatotropic virus, which affects approximately 350 million chronic sufferers worldwide. It has a compact 3.2 kbp dsDNA genome encoding four major overlapping genes namely core, polymerase, surface and X required for its replication. The virus synthesises a pregenomic RNA (pgRNA) which functions both as an RNA intermediate for reverse transcription into the DNA genome and as the mRNA for the translation of the core (C) and polymerase (P) proteins. The core overlaps the polymerase gene and is translated at a 10 to 1 ratio. The polymerase gene translated from the P AUG codon is preceded by at least 4 upstream AUG codons (uAUGs), namely C AUG, C1 AUG, J AUG and C2 AUG. Various mechanisms have been implicated in the synthesis of the polymerase protein. This led to the currently accepted model which involves leaky scanning and a reinitiation mechanism in polymerase synthesis. However, multiple sequence alignment of the pgRNA revealed a short upstream open reading frame (uORF) highly conserved at the nucleotide level in all HBV subtypes and mammalian hepadnaviruses. This previously unreported uORF, designated as C0 ORF in this study is also conserved in its position and length. Past studies have either omitted this uORF in their test constructs or ignored its potential role. The C0 ORF has a conserved weak initiation context and is located within the epsilon structure within the 5' leader of the pgRNA, required for viral encapsidation. Importantly, the C0 ORF precedes and overlaps the core ORF, which may suggest an alternative model in which the core and polymerase may be translated and coordinately regulated. Fusion of the C0 ORF to luciferase showed for the first time that this uORF is translated through the detection of reporter activity (~20% of C) and also visualisation of the fusion protein via western analysis using anti-C0 and anti-luciferase antibodies. Subsequent removal of the C0 ORF implicated a role in repressing downstream core fusion protein synthesis in HepG2 cells. A similar repression was observed on J expression. To study the effect of C0 on downstream polymerase translation, a pgRNA-like DNA construct was made and subsequent mutations introduced. Mutation of the C0 AUG led to an increase in initiation at the downstream P AUG. Alteration of the existing weak initiation context to an optimal context which favours stronger initiation consistently showed a potential role for C0 ORF in facilitating reinitiation at certain downstream initiation codons including P AUG. Mutations of other uAUGs preceding the P AUG were also done to better understand their roles in regulating polymerase synthesis. The removal of the C AUG markedly increased expression from the P AUG. This study revealed other internal uAUGs in-frame to the C AUG, namely the C1 and C2 AUGs are also effectively translated, further reducing availability of translating ribosomes to downstream P AUG. Indeed the removal of the C1 and C2 AUGs led to a corresponding increase in initiation from the P AUG. Initiation at the internal J AUG was also reported and its removal showed a significant decrease in expression from the P AUG, consistent with the previous model implicating reinitiation at the P initiation site after translation of the short J ORF. The inhibitory role of the 5 uAUGs prior to the P AUG were confirmed when all were removed, giving rise to translation almost equal to that at C AUG. Taken together, these results suggest a new model in which the HBV C0 ORF plays a key role in controlling core and polymerase synthesis by repressing core translation and making available more ribosomes to downstream AUGs possibly facilitating translation reinitiation. In addition, the translation of the C0 ORF across the [epsilon] region may also preclude encapsidation, potentially acting as a switch discriminating the pgRNA template between encapsidation and translation. Therefore, the highly conserved [epsilon] region and C0 ORF present an excellent target for molecular based antiviral drugs (antisense oligonucleotides, aptamers, ribozymes) potentially providing new anti HBV drugs.

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Malinga, Lesibana Anthony. "Molecular characterization of the hepatitis B virus X gene." Thesis, University of Limpopo ( Medunsa Campus ), 2010. http://hdl.handle.net/10386/417.

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Thesis ( M Med (Virological Pathology))--University of Limpopo, 2010.
Introduction: Hepatitis B virus (HBV) is a serious problem worldwide causing various liver diseases such as chronic hepatitis and hepatocellular carcinoma (HCC). The pathogenesis of HBV related HCC is not well established. Hepatitis B X protein (HBx) plays an important role in the pathogenesis of HCC. HBx coded by HBV X gene enhances several cellular pathways in hepatocytes which may lead to HCC. The genetic variability of other HBV genomic regions plays a significant role in diagnosis, vaccine development and drug resistance. However, the genetic variability of HBV X gene is not well understood. In addition the dual basal core promoter mutations found within the X gene have been implicated in the inhibition of hepatitis B e antigen (HBeAg) expression. Studies focusing on HBV X gene are scarce in South Africa. Consequently HBV X gene variability may reveal interesting mutations and substitutions that are important in chronic liver diseases or HCC. This study aimed at characterising HBV X gene at a molecular level isolated from patients with different serological profiles. Methods: This was an exploratory study which used 20 stored sera (-70°C) collected from adult patients at Dr George Mukhari hospital, Pretoria. The samples were already tested for HBsAg, anti-HBs, anti-HBc and HBeAg serological markers (Elecsys, Roche Diagnostics, Penzburg, Germany). HBV DNA extraction was performed from serum using High Pure Viral Nucleic Acid Assay (Roche Diagnostics, Penzburg, Germany). Nested PCR assay was used for the amplification of 465 nucleotide HBV X gene. Sequencing of PCR positive samples was done using spectruMedix SCE2410 genetic analysis system. Six samples selected, were cloned into the pGEM®-T Easy vector system (Promega, Madison, USA). Three clones of each sample were selected and their plasmids purified using Pure Yield™ Plasmid Miniprep System (Promega, Madison, USA). The plasmid DNA was recovered using optimised nested PCR assay and sequenced. A total of 38 sequences were generated from the study and compared with reference strains retrieved from GenBank. Phylogenetic analysis based on HBV X gene sequences was done using MEGA 4 software to determine different genotype clusters. vi Results: HBV X gene was successfully detected and amplified in 20 study samples. The sequenced HBV X gene products revealed mutations and insertions. Particularly a six nucleotide insertion, GCATGG between nucleotides 1611 and 1618 which was detected in five samples. In addition, the six cloned samples confirmed the six nucleotide insertion and other mutations associated with inhibition of hepatitis B e antigen (HBeAg) detected in the study. The substitutions within HBx were detected in the N (1-50 amino acids) and C (51-154) terminals by comparing our sequences with archival sequences from GenBank. Important substitutions found within the N and C terminals were S31A, P38S, A42P, F73L, H94Y, P101S, K118T, D119N, I127T/N, K130M and V131I. These substitutions are associated with various biological functions and pathogenesis. Other substitutions with unknown functions detected in the study include A2G, A3G, A4G, C6W, P42S and V116L. Further mutations of T1753M, A1762T and G1764A associated with inhibition of HBeAg expression were detected in most samples and only one sample had C1766T mutation. Phylogenetic analysis resulted in A, C and D HBV genotypes. Five samples and 11 clones clustered with genotype D, two samples and four clones clustered with genotype C and finally 13 samples and 3 clones clustered with genotype A. Conclusion: HBV X gene was successfully characterised using various molecular methods. HBx substitutions detected are involved in various pathogenic effects and may present a risk of HCC for patients infected with HBV. Genotype D samples displayed most mutations/substitutions and this can be regarded as an important genotype with high risk of HCC. The detection of a six nucleotide insertion (GCATGG) in 5 samples may emerge as a new variant of genotype D. Furthermore triple mutations of T1753M/A1762T/G1764A within basal core promoter region were detected mostly in HBeAg negative samples. However further analysis of HBV X gene variability is needed.

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Lu, Lei. "Effects of antiviral therapies on hepatitis B virus relicaptive intermediates in chronic hepatitis B." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42182359.

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Cheung, Ka-yee Cindy. "Occult hepatitis B virus reinfection in liver transplant recipient." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290562.

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16

Smith, Richard. "Targeting hammerhead ribozymes against hepatitis B virus." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264148.

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Lu, Lei, and 呂雷. "Effects of antiviral therapies on hepatitis B virus relicaptive intermediates in chronic hepatitis B." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42182359.

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Wong, Ka-ho Danny, and 王嘉豪. "Quantitation of hepatitis B virus covalently closed circular DNA in chronic hepatitis B patients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29938855.

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Lo, Kin-hang Ken. "Relationship of serological markers, basic core promoter and precore mutations to genotypes of Hepatitis B virus." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43781287.

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Seto, Wai-kay Walter, and 司徒偉基. "Virologic and serologic kinetics in the natural history and treatment of chronic hepatitis B." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48671071.

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This thesis investigated how virologic and serologic kinetics of the hepatitis B virus (HBV) could influence the natural history and treatment of chronic hepatitis B (CHB). Virologic kinetics were described in the first five studies, with serologic kinetics being described in the next five. The first study delineated the HBV DNA profiles of 1,400 treatment-naive Asian CHB patients. Increasing viremia was noted with increasing age, highlighting the large therapeutic demand in Asian patients with hepatitis B e antigen (HBeAg)-negative CHB. The second study analyzed the association between viral load and liver histology in 319 patients, showing HBV DNA levels to have strong association with HBeAg-negative disease severity. The next three studies investigated the efficacy of baseline and on-treatment HBV DNA levels in predicting clinical outcomes in 117, 165 and 222 patients on telbivudine, lamivudine plus adefovir and entecavir respectively. Absolute on-treatment HBV DNA levels at week 12 or 24 predicted favorable outcome with telbivudine and lamivudine / adefovir therapy, while excellent viremic suppression with very low rate of resistance development was shown in the entecavir study. The following three studies examined the role of serum HBsAg measurements in different disease phases of CHB. First, histology specimens of 140 HBeAg-positive patients were analyzed together with HBsAg levels. High HBsAg titers (>25,000 IU/mL) were found to be predictive of insignificant fibrosis. In the next study involving 300 treatment-naive HBeAg-negative patients stratified by their viral loads, combination of low HBsAg and HBV DNA levels predicted significant HBsAg decline. This is followed by a study comparing HBsAg levels of 203 CHB patients achieving HBsAg seroclearance with 203 age- and sex-matched controls over a 3-year period. Serum HBsAg <200 IU/mL and a significant annual HBsAg reduction were found to be predictive of HBsAg seroclearance. The penultimate study investigated the usage of two novel HBV serologic markers, linearized HBsAg and hepatitis B core-related antigen, in 329 CHB patients achieving HBsAg seroclearance with a conventional HBsAg assay. More than 40% of patients had seropositivity to one or both serologic tests. Finally, the last study of this thesis investigated and compared the changes in serum HBsAg, intrahepatic HBV DNA and covalently closed circular DNA (cccDNA) after 1 year of nucleoside analogue therapy. Minimal changes in both serum HBsAg and intrahepatic cccDNA were noted after 1 year of therapy, but in patients with a significant decline in serum HBsAg levels, there was a corresponding significant reduction in cccDNA. This series of studies illustrated how the monitoring of serum HBV DNA and HBsAg levels could assist in optimizing management strategies for CHB.
published_or_final_version
Medicine
Master
Doctor of Medicine

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Machiya, Tichaona. "Knowledge, attitudes and practices of healthcare workers at the Princess Marina Hospital in Botswana, regarding hepatitis B prevention and control." Thesis, University of Limpopo (Medunsa Campus), 2011. http://hdl.handle.net/10386/457.

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Thesis (MPH))University of Limpopo (Medunsa Campus), 2011.
Introduction: Hepatitis B virus (HBV) is a highly infectious virus responsible for considerable morbidity and mortality world wide. Chronic HBV carriers can transmit HBV parenterally in a hospital setting putting healthcare workers (HCWs) and their patients at risk of infection. Aim and objectives: This study aimed to investigate knowledge, attitudes and practices towards prevention and control of HBV amongst nurses, doctors and laboratory personnel. Objectives were to determine: (a) the knowledge; (b) the attitudes; (c) the practices of nurses, doctors and laboratory personnel; (d) if there are any associations between (1) knowledge and practice, and (2) attitudes and practice; (e) the predictors of HBV vaccination uptake. Materials and Methods: This was a cross-sectional descriptive study. Self-administered questionnaires were distributed to doctors, laboratory staff and nurses at Princess Marina Hospital. Results: Two hundred questionnaires were distributed and a total of 117 were returned, giving an overall response rate of 58.5%. More doctors had good knowledge (38.9% [7/18]), followed by 20% (4/20) of laboratory staff and 11.4% (9/79) of nurses. Most staff (100% [20/20] of laboratory staff; 97.5% [77/79] of nurses; 94.4% [17/18] of doctors) had positive attitudes. More laboratory staff (100 [20/20]) displayed good practices, followed by nurses (94.9% [75/79]); and lastly doctors (88.9% [16/18]). There were no significant associations between knowledge or attitudes and practices. Vaccination was inadequate, with 50.9% (59/116) of HCWs having received at least one dose, and of these only 61% (36/59) receiving all 3 doses. Needle stick injuries occurred in 31.6% (37/117), while 33.9% (39/115) reported blood or body fluid splashes. None of the HCWs accessed PEP after exposure. Being a laboratory worker (OR: 148.4) or doctor (OR: 125.7) were the only predictors of vaccination uptake. Conclusion: There is need to increase knowledge of HCWs, vaccination availability, vaccination uptake, PEP, and reduce the exposures of HCWs.

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Sangfelt, Per. "Prevention and treatment of hepatitis B virus infection /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-301-9/.

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Yuen, Man-fung. "Role of hepatitis B virus genotypes B and C on chronic liver disease in the Chinese." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B33710089.

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Otto, Verena Theresia [Verfasser]. "Monoklonalität Hepatitis B surface Antigen-positiver Leberzellareale bei chronischer Hepatitis-B-Virus-Infektion / Verena Otto." Bonn : Universitäts- und Landesbibliothek Bonn, 2017. http://d-nb.info/1139118781/34.

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Marusawa, Hiroyuki. "Latent hepatitis B virus infection in healthy individuals with antibodies to hepatitis B core antigen." Kyoto University, 2000. http://hdl.handle.net/2433/180879.

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Otto, Verena [Verfasser]. "Monoklonalität Hepatitis B surface Antigen-positiver Leberzellareale bei chronischer Hepatitis-B-Virus-Infektion / Verena Otto." Bonn : Universitäts- und Landesbibliothek Bonn, 2017. http://d-nb.info/1139118781/34.

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Cheung, Ka-yee Cindy, and 張家怡. "Occult hepatitis B virus reinfection in liver transplant recipient." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290562.

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Lupberger, Joachim. "Cultivation of Hepatitis B virus producing cell line HepG2.2.15 on microcarrier and functional characterization of the Hepatitis B virus polymerase." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2007. http://dx.doi.org/10.18452/15668.

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Hepatitis B Virus (HBV) Infektionen verursachen entzündliche Erkrankungen der Leber. Insbesondere die frühen Phasen des HBV Lebenszyklus sind noch nicht geklärt, so ist z.B. der Rezeptorkomplex an den HBV bindet unbekannt. Mittlerweile stehen neue Infektionsmodelle zur Verfügung um den HBV Lebenszyklus zu untersuchen. Dies erfordert eine effiziente Zellkultur basierende Methode um große Mengen infektiöser Partikel zu generieren. Ein Ziel der Arbeit war durch Kultivierung auf Mikrocarrier die HBV Produktion der Zelllinie HepG2.2.15 zu steigern. Die Analyse von Protein und HBV Sekretion, Infektiösität und MAP Signalübertragung ergab eine 18x höhere HBV Produktion bei einer reduzierten Sekretion von subviralen Partikeln durch HepG2.2.15 die auf Mikrocarrier kultiviert wurden. Der Anstieg der Virusproduktion korreliert mit einer verstärkten Aktivierung der MAP Kinase ERK-2, die mit HBV Replikation in Verbindung steht. Ein weiterer wenig verstandener Teil des HBV Lebenszyklus ist der Kernimport des HBV Genoms. Spuren der viralen Polymerase finden sich im Zellkern von HBV infizierten Zellen. Ziel der Arbeit war, Motive in der HBV Polymerase zu finden, die in der Lage sind Zelllokalisation zu beeinflussen. Durch Sequenzvergleich wurde eine konservierte zweiseitige Kernlokalisationssequenz im Terminalen Protein der HBV Polymerase identifiziert, die eine Proteinkinase CKII Erkennungsstelle enthält. Inhibition der CKII Aktivität in HBV infizierten primären Hepatozyten sowie die Zerstörung der CKII Erkennungsstelle im Terminalen Protein inhibieren die HBV Replikation. Die Funktionalität der Kernlokalisationssequenz wurde durch Fusion an GFP bestätigt und war Abhängig von CKII Aktivität in der Zelle. Dies wurde in vitro durch Bindung des Adapterproteins Karyopherin-alpha an CKII-phosphoryliertes Terminales Protein bestätigt. Die HBV Polymerase enthält eine konservierte zweiseitige Kernlokalisationssequenz deren Funktionalität durch CKII Phosphorilierung vermittelt wird.
Hepatitis B virus (HBV) infection causes acute and chronic liver inflammation. Especially the early phase of the HBV life cycle is not clearly understood. For example the receptor complex that mediates viral entry is not known. Novel infection models to study the HBV lifecycle are described that demand for a large amount of cell culture generated infectious HBV particles. One aim was to enhance HBV production of the cell line HepG2.2.15 by cultivation on microcarrier substrate. Analysis of protein and viral particle secretion, infectivity, and cellular MAP kinase signaling revealed an up to 18x increased HBV production and a decreased subviral particle secretion by HepG2.2.15 when cultivated on microcarrier. The observed effect was due to an enhanced phospho-activation of MAP kinase ERK-2 that is tightly associated with HBV replication. Another poorly understood part of the HBV lifecycle is the mechanism that delivers the HBV genome into the nucleus. Traces of HBV polymerase can be found in HBV infected cells. The second objective was to identify motifs on the HBV polymerase that determine its subcellular localization. By sequence alignment a conserved bipartite nuclear localization signal was found in the terminal protein of the HBV polymerase encompassing a protein kinase CKII recognition site. Inhibition of CKII kinase in infected primary hepatocytes and destruction of the identified CKII recognition site in the viral polymerase impaired virus production. The functionality of the putative nuclear localization signal was confirmed by fusion to GFP. Moreover, its functionality was depended on CKII activity that was verified by in vitro binding experiments of terminal protein to the import adaptor karyopherin-alpha. This data identified a nuclear localization signal in the HBV polymerase, which functionality is mediated by CKII phosphorylation.

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杜鈺輝 and Yuk-fai To. "Mannose binding lectin in hepatitis B virus infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31225214.

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To, Yuk-fai. "Mannose binding lectin in hepatitis B virus infection /." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk:8888/cgi-bin/hkuto%5Ftoc%5Fpdf?B23435987.

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31

Payne, Karen Louise. "Hepatitis B virus in silvery gibbons (Hylobates moloch)." Thesis, Payne, Karen Louise (2004) Hepatitis B virus in silvery gibbons (Hylobates moloch). Masters by Research thesis, Murdoch University, 2004. https://researchrepository.murdoch.edu.au/id/eprint/248/.

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This research investigated a number of issues regarding hepatitis B virus (HBV) in the silvery gibbon (Hylobates moloch). Due to the relatively recent discovery of the virus in nonhuman primate populations, specific knowledge of the biological behaviour of the virus is presently lacking, with current information largely extrapolated from the behaviour of HBV in human infections. In order to manage the captive and wild populations of this critically endangered species, information regarding the behaviour of the virus in gibbons and the likely impact of the viral infection is essential. The research was performed at Perth Zoo, with the study population consisting of the current and historical members of the zoo's silvery gibbon colony. Because this gibbon species is critically endangered, the study was conducted with minimal intervention to the population with samples collected largely on an opportunistic basis from a small study population. Review of the history of the virus within the Perth Zoo colony provided epidemiological evidence to indicate vertical transmission in three gibbons (Hecla, Uban and Jury). It would appear that vertical transmission is the primary mode of transmission leading to dispersal of the virus through the captive population of silvery gibbons. Elevated concentrations of the liver enzymes alanine aminotransferase and aspartate aminotransferase were found in three gibbons (Perth 2, Uban and Jury), and may suggest a pathogenic role of the virus in this species. Histological examination of the livers of Uban and Perth 2 failed to demonstrate definitive evidence of cirrhosis, however mild fibrosis was seen in both cases and may represent an early stage of liver pathology associated with chronic hepatitis B infection. The vaccination protocol developed at Perth Zoo was successful in preventing neonatal transmission of the virus from a high infectivity carrier mother in at least two individuals, and was also successful in producing a protective level of immunity against the virus in all three of the individuals tested. Sequencing of the complete hepatitis B genome from one gibbon (Hecla) revealed that she was infected with GiHV (Gibbon hepatitis B virus), an indigenous strain of HBV previously identified in a number of gibbon species, but not previously confirmed in the silvery gibbon. Hecla's strain of HBV was shown to be more closely related to other nonhuman primate strains of HBV than to any of the human strains of HBV. 100% nucleotide similarity to two of Hecla's siblings indicates that infection in all three animals was the result of vertical transmission from their mother. Partial sequencing of the virus from a second gibbon (Uban) identified another strain of GiHBV which supports the results of the epidemiological study. Neither gibbon showed a high sequence similarity to the virus sequenced from Ivan, the father of the third carrier gibbon (Jury), although only limited sequence data was available from Ivan. Consequently it is likely that at least three different strains of GiHBV are present within the silvery gibbon population. The information contained in this thesis will assist in the understanding and management of hepatitis B infection in silvery gibbons, as well as the numerous other species of nonhuman primates now shown to be susceptible to this virus.

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Payne, Karen Louise. "Hepatitis B virus in silvery gibbons (Hylobates moloch)." Payne, Karen Louise (2004) Hepatitis B virus in silvery gibbons (Hylobates moloch). Masters by Research thesis, Murdoch University, 2004. http://researchrepository.murdoch.edu.au/248/.

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This research investigated a number of issues regarding hepatitis B virus (HBV) in the silvery gibbon (Hylobates moloch). Due to the relatively recent discovery of the virus in nonhuman primate populations, specific knowledge of the biological behaviour of the virus is presently lacking, with current information largely extrapolated from the behaviour of HBV in human infections. In order to manage the captive and wild populations of this critically endangered species, information regarding the behaviour of the virus in gibbons and the likely impact of the viral infection is essential. The research was performed at Perth Zoo, with the study population consisting of the current and historical members of the zoo's silvery gibbon colony. Because this gibbon species is critically endangered, the study was conducted with minimal intervention to the population with samples collected largely on an opportunistic basis from a small study population. Review of the history of the virus within the Perth Zoo colony provided epidemiological evidence to indicate vertical transmission in three gibbons (Hecla, Uban and Jury). It would appear that vertical transmission is the primary mode of transmission leading to dispersal of the virus through the captive population of silvery gibbons. Elevated concentrations of the liver enzymes alanine aminotransferase and aspartate aminotransferase were found in three gibbons (Perth 2, Uban and Jury), and may suggest a pathogenic role of the virus in this species. Histological examination of the livers of Uban and Perth 2 failed to demonstrate definitive evidence of cirrhosis, however mild fibrosis was seen in both cases and may represent an early stage of liver pathology associated with chronic hepatitis B infection. The vaccination protocol developed at Perth Zoo was successful in preventing neonatal transmission of the virus from a high infectivity carrier mother in at least two individuals, and was also successful in producing a protective level of immunity against the virus in all three of the individuals tested. Sequencing of the complete hepatitis B genome from one gibbon (Hecla) revealed that she was infected with GiHV (Gibbon hepatitis B virus), an indigenous strain of HBV previously identified in a number of gibbon species, but not previously confirmed in the silvery gibbon. Hecla's strain of HBV was shown to be more closely related to other nonhuman primate strains of HBV than to any of the human strains of HBV. 100% nucleotide similarity to two of Hecla's siblings indicates that infection in all three animals was the result of vertical transmission from their mother. Partial sequencing of the virus from a second gibbon (Uban) identified another strain of GiHBV which supports the results of the epidemiological study. Neither gibbon showed a high sequence similarity to the virus sequenced from Ivan, the father of the third carrier gibbon (Jury), although only limited sequence data was available from Ivan. Consequently it is likely that at least three different strains of GiHBV are present within the silvery gibbon population. The information contained in this thesis will assist in the understanding and management of hepatitis B infection in silvery gibbons, as well as the numerous other species of nonhuman primates now shown to be susceptible to this virus.

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au, karen payne@perthzoo wa gov, and Karen Louise Payne. "Hepatitis B Virus in Silvery Gibbons (Hylobates moloch)." Murdoch University, 2004. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20050204.154840.

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This research investigated a number of issues regarding hepatitis B virus (HBV) in the silvery gibbon (Hylobates moloch). Due to the relatively recent discovery of the virus in nonhuman primate populations, specific knowledge of the biological behaviour of the virus is presently lacking, with current information largely extrapolated from the behaviour of HBV in human infections. In order to manage the captive and wild populations of this critically endangered species, information regarding the behaviour of the virus in gibbons and the likely impact of the viral infection is essential. The research was performed at Perth Zoo, with the study population consisting of the current and historical members of the zoos silvery gibbon colony. Because this gibbon species is critically endangered, the study was conducted with minimal intervention to the population with samples collected largely on an opportunistic basis from a small study population. Review of the history of the virus within the Perth Zoo colony provided epidemiological evidence to indicate vertical transmission in three gibbons (Hecla, Uban and Jury). It would appear that vertical transmission is the primary mode of transmission leading to dispersal of the virus through the captive population of silvery gibbons. Elevated concentrations of the liver enzymes alanine aminotransferase and aspartate aminotransferase were found in three gibbons (Perth 2, Uban and Jury), and may suggest a pathogenic role of the virus in this species. Histological examination of the livers of Uban and Perth 2 failed to demonstrate definitive evidence of cirrhosis, however mild fibrosis was seen in both cases and may represent an early stage of liver pathology associated with chronic hepatitis B infection. The vaccination protocol developed at Perth Zoo was successful in preventing neonatal transmission of the virus from a high infectivity carrier mother in at least two individuals, and was also successful in producing a protective level of immunity against the virus in all three of the individuals tested. Sequencing of the complete hepatitis B genome from one gibbon (Hecla) revealed that she was infected with GiHV (Gibbon hepatitis B virus), an indigenous strain of HBV previously identified in a number of gibbon species, but not previously confirmed in the silvery gibbon. Hecla's strain of HBV was shown to be more closely related to other nonhuman primate strains of HBV than to any of the human strains of HBV. 100% nucleotide similarity to two of Heclas siblings indicates that infection in all three animals was the result of vertical transmission from their mother. Partial sequencing of the virus from a second gibbon (Uban) identified another strain of GiHBV which supports the results of the epidemiological study. Neither gibbon showed a high sequence similarity to the virus sequenced from Ivan, the father of the third carrier gibbon (Jury), although only limited sequence data was available from Ivan. Consequently it is likely that at least three different strains of GiHBV are present within the silvery gibbon population. The information contained in this thesis will assist in the understanding and management of hepatitis B infection in silvery gibbons, as well as the numerous other species of nonhuman primates now shown to be susceptible to this virus.

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Ngui, Siew Lin. "Molecular analysis of hepatitis B virus transmission events." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299915.

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Frampton, Nicholas Ross. "Impact of hypoxia on hepatitis B virus replication." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8467/.

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Hepatitis B virus (HBV) is one of the world’s unconquered diseases, with 370 million chronically infected globally. HBV replicates in hepatocytes within the liver that exist under a range of oxygen tensions from 11% in the peri-portal area to 3% in the peri-central lobules. HBV transgenic mice show a zonal pattern of' viral antigen with expression in the peri-central areas supporting a hypothesis that low oxygen regulates HBV replication. We investigated this hypothesis using a recently developed in vitro model system that supports HBV replication. We demonstrate that low oxygen significantly increases covalently closed circular viral DNA (cccDNA), viral promoter activity and pre-genomic RNA (pgRNA) level, consistent with low oxygen boosting viral transcription. Hypoxia inducible factors (HIFs) regulate cellular responses to low oxygen and we investigated a role for HIF-1\(\alpha\) or HIF-2\(\alpha\) on viral transcription. A combination of HIF inhibitors and silencing of HIF-l\(\alpha\) and HIF-2\(\alpha\) ablated the effect of low oxygen on cccDNA and pgRNA, suggesting a role in regulating HBV transcription. This study highlights a new role for hepatic oxygen levels to regulate multiple steps in the HBV life cycle and this may impact on future treatments for viral associated pathologies.

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Bernstein, Peter Philipp. "Funktionelle Charakterisierung der Interaktion des Hepatitis-C-Virus-Core-Proteins mit der Hepatitis-B-Virus-Replikation." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975965786.

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Majlessi, Atash. "Sequenzanalysen von Hepatitis B Virus-Varianten in Patienten mit fibrosierender cholestatischer Hepatitis /." Hamburg, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000254747.

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Dahlström, Elin, and Viberg Ellinor Funegård. "Knowledge about hepatitis B virus infection and attitudes towards hepatitis B virus vaccination among Vietnamese university students in Ho Chi Minh City : – A quantitative study." Thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-200430.

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Introduktion: Hepatit B är ett virus med hög smittsamhet som är orsak till den vanligaste leversjukdomen globalt. I Vietnam är prevalensen av hepatit B hög.Syfte: Att undersöka vietnamesiska universitetsstudenters kunskap om hepatit B och attityder till hepatit B vaccination, samt att undersöka om det fanns någon skillnad mellan könen.Metod: En kvantitativ tvärsnittsstudie med hjälp av en enkät. Studien genomfördes på University of Medicine and Pharmacy i Ho Chi Minh City. Förstaårsstudenter på sjuksköterske- och medicinsk teknikprogrammet valdes ut och 233 studenter fyllde i enkäten korrekt och inkluderades i studien.Resultat: Majoriteten av studenterna (95,3%) hade hört om hepatit B viruset (HBV) innan studien ägde rum. Fler än hälften av studenterna (55,4%) visste att HBV inte sprids genom att dela mat med en infekterad person, och 58,4% visste att HBV kan orsaka levercancer. Endast 47,6% visste att HBV är sexuellt överförbart och 39,5% visste att HBV kan smitta från mor till barn perinatalt. Fler manliga studenter än kvinnliga visste att HBV kan överföras genom att dela tandborste med en infekterad person (p= 0,026). Majoriteten av studenterna (93,1%) trodde att de skulle vaccineras mot HBV i framtiden.Slutsats: Studenterna visade att de hade kunskap i ämnet, men studien visar också på en viss brist på kunskap, som är allvarlig. Förbättrad utbildning om HBV är nödvändigt för att vietnamesiska universitetsstudenter ska utöka sin kunskap om HBV.
Introduction: The hepatitis B virus is highly contagious and causes the world’s most common liver infection. Vietnam is a country where the endemicity of hepatitis B is high.Aim: To investigate Vietnamese university students’ knowledge about hepatitis B infection and attitudes towards hepatitis B virus vaccination and to examine if there is a difference between genders.Method: A cross-sectional study with quantitative method using a questionnaire. The study was carried out at the University of Medicine and Pharmacy in Ho Chi Minh City. First year students from the nursing and medical technician programme were selected and 233 students completed the questionnaire and were included in the study.Result: The majority of the university students (95.3%) had heard about hepatitis B virus (HBV). More than half (55.4%) knew correctly that HBV can not be transmitted by sharing food with an infected person, and 58.4% knew that HBV can cause liver cancer. Only 47.6% knew that HBV can be sexually transmitted and 39.5% knew that HBV can be transmitted from mother to child at birth. More male than female students answered correctly that HBV can be transmitted by sharing a toothbrush with an infected person (p= 0.026). Almost all students (93.1%) thought that they would receive HBV vaccination.Conclusion: The students showed insight into the subject, but the result also showed some gaps of knowledge among the university students considered as serious. Improved education about HBV is necessary for university students to increase their knowledge about HBV.

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Ho, Ka-nung Stephen. "Assay for hepatitis B virus (HBV) DNA in serum : recent advances in methodology and its clinical relevance in renal allograft recipients with HBV infection /." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21161276.

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Polis, Suzanne Public Health &amp Community Medicine Faculty of Medicine UNSW. "Hepatitis B and hepatitis C virus in an antenatal population : an epidemiological study." Awarded by:University of New South Wales. School of Public Health and Community Medicine, 2005. http://handle.unsw.edu.au/1959.4/22035.

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Although Australian epidemiology of HBV and HCV has been well described for populations groups at higher risk, but the information available for groups generally considered to be lower risk is much more limited. An understanding of the prevalence of these infections and their risk factors in antenatal women is important to guide testing policy and practice. A study was therefore conducted of the epidemiology of hepatitis B and hepatitis C infection in women. In addition, women were asked about their experience with antenatal testing. A total of 516 women participated in the survey, of these 479 (95%) women had been tested for HCV antibodies .The prevalence of HCV antibodies was 4% overall, and 2% among women who were unaware of their HCV status prior to their antenatal test. A history of injecting drug use and residing with a HCV positive person were significantly associated with HCV infection in multivariate analyses. HBV testing was conducted in 468 (99.6%) of women, and the overall prevalence was 2%. Risk factors identified were birthplace in countries of South East Asia. Women were asked about their perception of antenatal testing and pre-test information. Nearly a third (143, 30.5%) of women who had been tested for HCV infection either said that they did not know whether they had been tested, or said that they had declined testing. The corresponding proportion for HBV infection was 28.8% (135). Over 65% and 66% of women said that had not received any information about testing for HCV and HBV respectively. The finding that virtually all antenatal women were being tested for HCV was in contrast to government and non-government organisation policies of ???selective??? screening in place during the study period. Of concern was the substantial proportion of women who were tested despite reporting that they had declined their clinician???s offer to test for HCV and HBV, and the large number of women who reported an absence of pre-test information. Women who said they had received information reported the delivery and quality of information varied according to the antenatal clinician group, but perceived the overall quality as poor.

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Lo, Kin-hang Ken, and 盧建恆. "Relationship of serological markers, basic core promoter and precore mutations to genotypes of Hepatitis B virus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43781287.

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Kesbiç, Hasan Kaya Selçuk. "Kan donörlerinde Hepatit B virus core antikorlarının saptanması /." Isparta : SDÜ Tıp Fakültesi, 2007. http://tez.sdu.edu.tr/Tezler/TT00328.pdf.

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Gowans, E. J. "Studies on markers of hepatitis B virus replication in man /." Title page, contents and summary only, 1986. http://web4.library.adelaide.edu.au/theses/09PH/09phg722.pdf.

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Nguyen, Thi Thai An [Verfasser], and Michael [Akademischer Betreuer] Nassal. "Recombinant fluorescent myristoylated PreS-containing Hepatitis B virus capsid- like particles = Rekombinante fluoreszierende und myristoylierte PreS-tragende Hepatitis B Virus Kapsidähnliche Partikel." Freiburg : Universität, 2012. http://d-nb.info/1123472548/34.

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Sentjens, Roel Emiel Johannus Henricus. "New developments in hepatitis B, C and G virus." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/87188.

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Nunura, Reyes Juan Manuel. "Factores de riesgo para la infección por el virus de la hepatitis B en el Centro Médico Naval "CMST"." Bachelor's thesis, Universidad Nacional Mayor de San Marcos, 2005. https://hdl.handle.net/20.500.12672/1908.

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Objetivo : Determinar los factores de riesgo asociados a la transmisión del virus de la Hepatitis B (VHB) en el Centro Médico Naval durante el período de estudio. Material y métodos : Estudio de casos y controles. Se evaluaron los pacientes hospitalizados en la Sala de Enfermedades Transmisibles con el diagnóstico de Síndrome ictérico mas hipertransaminasemia ( TGO y/o TGP > 500 u/l ). Los factores de riesgo reportados entre los sujetos infectados con el VHB (B+); fueron comparados con los sujetos no infectados (B-), mediante el análisis bivariado y multivariado. Resultados : Un total de 74 sujetos fueron evaluados serológicamente para VHB, de los cuales 37 fueron positivos ( 35 infección aguda y 2 infección no aguda ). Los sujetos B+ fueron en su mayoría de sexo masculino y tuvieron como factor de riesgo mas significativo una hospitalización previa ( OR:13.33 ). Además se describen los cuadros clínicos y exámenes de laboratorio encontrados en ambos grupos. Conclusión : La fuerte asociación encontrada entre hepatitis B y hospitalización previa, sugiere que la transmisión horizontal nosocomial tiene un rol protagónico en la transmisión del VHB en el Centro Médico Naval.
Tesis de segunda especialidad

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47

Brandenburg, Boerries. "Cell permeable nucleocapsids as a novel tool for efficient gene tran." [S.l.] : [s.n.], 2005. http://www.diss.fu-berlin.de/2005/148/index.html.

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Brandenburg, Boerries. "Cell permeable nucleocapsids as a novel tool for efficient gene transfer & HBV biology." [S.l. : s.n.], 2005. http://www.diss.fu-berlin.de/2005/148/index.html.

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Yuen, Man-fung, and 袁孟峰. "Chronic hepatitis B virus infection in the Chinese: natural history, sequelae, treatment and prevention." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B2333177X.

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Lin, Shing-cho, and 連承祖. "Hepatitis B virus covalently closed circular DNA is associated with methylated histones H3 and H4 and heterochromatin complex proteins : implication of their roles in viral replication." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/194622.

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Hepatitis B virus covalently closed circular DNA (HBV cccDNA) forms a mini-chromosome structure inside infected hepatocyte nuclei and plays an important role in chronic hepatitis B infection. Methylation of cccDNA-bound histone and the associations of heterochromatin HP1 complex related proteins with cccDNA were investigated in this thesis using transient transfection study system and chromatin immunoprecipitation assay. Di- and tri-methylation of histone H3 lysine 4 residue (H3K4), which plays an activating role in eukaryotic transcription, were found to associate with cccDNA in a way in parallel to the level of HBV replication in our system. On the other hand, tri-methylation of H3K9, which plays an inhibitory role in eukaryotic transcription, was found to associate with cccDNA during decline of HBV replication. During the decline of HBV replication, cccDNA was associated with histone methyltransferases SUV39H1 and SUV420H1 and histone demethylase PLU1. The dynamic of the association of heterochromatin protein 1 (HP1) to cccDNA was similar to that of SUV39H1. The association of cccDNA with five HP1 complex-related proteins (three DNA methyltransferases Dnmt3a, Dnmt3b and Dnmt1 and two methylated DNA binding proteins MBD1 and MeCP2) was studied, and their associations could be roughly divided into two stages. From 72 hours to 96 hours post-transfection, there was an increased association of cccDNA with Dnmt3a, Dnmt3b and MBD1, which was in parallel to the increased association of HP1 and SUV39H1with -cccDNA. From 96 hours to 120 hours after transfection, an increased association of Dnmt1 and MeCP2 with cccDNA was detected, which was correlated to that of SUV420H1. At the time when HBV replication was declining at 120 hours post-transfection, a highest association of SUV39H1, SUV420H1, HP1 and all 5 HP1 complex-related proteins with cccDNA was found. In conclusion, methylation of cccDNA-bound histone was associated with HBV replication. Activating H3K4 methylation was found to correlate with increase in HBV replication, while inhibitory H3K9 methylation correlated with decrease in HBV replication. The association of HP1 was in parallel to that of SUV39H1, indicating that HP1-SUV39H1 complex might be involved, and thereby recruiting other proteins for transcription suppression. Recruitment of DNA methyltransferases and methylated DNA binding proteins to cccDNA provided further evidence that methylation of cccDNA plays a role in transcription suppression. This study identified the associations of methylated histone and other related proteins with cccDNA and their correlations with viral replication. These results enhance our knowledge in HBV replication cycles and transcription regulation. It may show a novel area in development of antiviral drugs such as histone methyltransferase modulators.
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Medicine
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