Relevant bibliographies by topics / Hepatitis G virus Victoria

Academic literature on the topic 'Hepatitis G virus Victoria'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Hepatitis G virus Victoria"

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Reshetnyak, Vasiliy Ivanovich, Tatiana Igorevna Karlovich, and Ljudmila Urievna Ilchenko. "Hepatitis G virus." World Journal of Gastroenterology 14, no. 30 (2008): 4725. http://dx.doi.org/10.3748/wjg.14.4725.

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Patrick, Christian C. "HEPATITIS G VIRUS." Pediatric Infectious Disease Journal 17, no. 11 (November 1998): 1045–46. http://dx.doi.org/10.1097/00006454-199811000-00017.

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Versalovic, James. "Hepatitis G virus." Clinical Microbiology Newsletter 19, no. 21 (November 1997): 161–64. http://dx.doi.org/10.1016/s0196-4399(00)89182-5.

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Fairley, Christopher K., David E. Leslie, Suellen Nicholson, and Ian D. Gust. "Epidemiology and hepatitis C virus in Victoria." Medical Journal of Australia 153, no. 5 (September 1990): 271–73. http://dx.doi.org/10.5694/j.1326-5377.1990.tb136899.x.

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Shadur, B., J. MacLachlan, and B. Cowie. "Hepatitis D virus in Victoria 2000-2009." Internal Medicine Journal 43, no. 10 (October 2013): 1081–87. http://dx.doi.org/10.1111/imj.12247.

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Kew, Michael C., and Chris Kassianides. "HGV: hepatitis G virus or harmless G virus?" Lancet 348 (December 1996): S10. http://dx.doi.org/10.1016/s0140-6736(96)98020-4.

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Karayiannis, P., J. Pickering, M. Chiaramonte, and HC Thomas. "Hepatitis G virus infection." Lancet 349, no. 9056 (March 1997): 954. http://dx.doi.org/10.1016/s0140-6736(05)62732-8.

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Schleicher, Sabine, Andrea Normann, Michael Gregor, Georg Hess, and Bertram Flehmig. "Hepatitis G virus infection." Lancet 349, no. 9056 (March 1997): 954–55. http://dx.doi.org/10.1016/s0140-6736(05)62733-x.

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Robert Halasz, Ola Weiland, Matti S. "GB Virus C/Hepatitis G Virus." Scandinavian Journal of Infectious Diseases 33, no. 8 (January 2001): 572–80. http://dx.doi.org/10.1080/00365540110027123.

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Kiyosawa, Kendo, and Eiji Tanaka. "GB Virus C/Hepatitis G Virus." Intervirology 42, no. 2-3 (1999): 185–95. http://dx.doi.org/10.1159/000024979.

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Dissertations / Theses on the topic "Hepatitis G virus Victoria"

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Halasz, Robert. "Epidemiology and clinical importance of GB virus C/hepatitis G virus /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-3997-7/.

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Cuceanu, Narcisa Manuela. "Structural and genetic analysis of hepatitis G virus/GB virus-C." Thesis, University of Edinburgh, 1999. http://hdl.handle.net/1842/22126.

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This thesis describes the genetic analysis of the heterogeneity of HGV/GBV-C and the characterization of the terminal regions of the viral genome. The sequence diversity across the HGV/GBV-C genome was significantly lower than that observed with HCV isolates. Comparative analysis of twenty-seven complete genome HGV/GBV-C sequences indicated the presence of four phylogenetic groups and this study demonstrated that these groupings could be reproduced by analysis of the 5'-untranslated region (5'-UTR) and of various sub-fragments. At the same time, the analysis of the 5'-UTR variability indicated the existence of group-specific polymorphisms, many of which are covariant and consistent with the proposed secondary structure of this region. An important difference between the polyproteins of HGV/GBV-C and HCV is the absence of a putative HGV/GBC-C core protein which is usually encoded at the 5'-end of the genome of flaviviruses. The buoyant density of HGV/GBV-C particles in human plasma was estimated to be between 1.07-1.12 g/ml, much lower than that of the other members of Flaviviridae family, except HCV. No HGV/GBV-C RNA was detected in fractions with densities higher than 1.17 g/ml which is expected for virus particles in immune complexes or in fractions with densities higher than 1.21 g/ml, the density range of HCV nucleocapsids. These biophysical properties correlate with the absence of a core-like protein in the genome of HGV/GBV-C isolates from different phylogenetic groups. The absence of the HGV/GBV-C nucleocapsid was also revealed by the sequence analysis data since no conserved open reading frame capable of encoding a core-like protein was identified. Generally, the untranslated regions at the 5' and 3' termini of a RNA virus genome contain regulatory elements important for viral RNA replication, transcription, translation and viral packaging. A comprehensive comparison and analysis of the primary sequence and secondary structure of the 3'-UTR of different HGV/GBV-C isolates allowed the construction of a common secondary structure model for this region and the identification of structural elements that may be involved in viral replication.
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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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Berg, Thomas. "Chronische Hepatitis C." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2002. http://dx.doi.org/10.18452/13812.

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Die vorliegende Habilitationsschrift befasst sich schwerpunktmäßig vor allem mit der Klinik und Therapie der Hepatitis C. Evaluiert wurden: 1. verschiedene therapeutische Strategien, 2. die Ursachen der "Non-Response" auf eine anti-virale Therapie sowie 3. die klinische Relevanz der neu entdeckten Hepatitis-assoziierten Viren und 4. ihre Bedeutung bei Patienten mit akuter bzw. chronischer Lebererkrankung unklarer Ätiologie sowie bei Patienten vor und nach Lebertransplantation. Ad 1. Aus dem Vergleich verschiedener Therapie-Konzepte wie der Kurzzeit- Kombinationstherapie, Triple-Therapie, Hochdosis-Interferon?-Therapie und der Anwendung antiviraler Substanzen wie Ribavirin und Amantadin ergaben sich neue Erkenntnisse hinsichtlich relevanter prognostischer Parameter für die Therapieresponse. Ad 2. Analysiert wurden die möglichen molekularen Mechanismen der Therapieresponse bzw. Non-Response sowie der Stellenwert von Interaktionen bestimmter HCV-Proteine (NS5A, E2, sogenannte PKR-eIF2a Phosphorylisations-Homologie-Domäne [PePHD]) mit den Interferon? induzierten Effektorproteinen. Es konnte gezeigt werden, daß die Anzahl der Mutationen innerhalb des NS5A Proteins einen prognostischen Parameter darstellen hinsichtlich der Response auf eine Interferon?-Therapie. Dagegen spielen Mutationen innerhalb der PePHD-Region keine Rolle. Ad 3. Aus den Untersuchungen zur klinischen Relevanz der neu entdeckten Hepatitis-assoziierten Viren GB Virus-C/Hepatitis G Virus (GBV-C/HGV) und TT-Virus (TTV) ergaben sich keine Hinweise bzgl. eines Einflusses von GBV-C/HGV bzw. TTV-Infektionen auf den Verlauf der chronischen Hepatitis C. Die durchgeführten Verlaufsuntersuchungen bei koinfizierten Patienten sprechen dafür, daß es sich um Interferon-sensitive Viren handelt; jedenfalls beeinflussen sie nicht die IFN?-induzierte Response. Ad 4. Untersucht wurden ferner die Prävalenz, Transmission und Relevanz der GBV-C/HGV und TTV-Infektion im Hinblick auf ihre Hepatitis-induzierenden Eigenschaften. Die Ergebnisse belegen, dass beide Viren parenteral übertragen werden, und dass sie eine hohe Prävalenz bei Patienten mit parenteralen Risikofaktoren besitzen. Eine Hepatitis-induzierende Potenz dieser Viren konnten wir nicht beobachten; bei der Mehrzahl aller chronisch infizierter Personen ließen sich keine Zeichen einer chronischen Hepatitis finden.
The major goal of this thesis is the analysis of the clinical outcome of patients with Hepatitis C virus (HCV) infection and the response to therapy. Analysed were 1. different types of therapeutic strategies 2. causes responsible for ineffective antiviral therapy (non-response) 3. clinical relevance of the newly discovered hepatitis-associated viruses and 4. the role of these viruses in patients with acute or chronic hepatitis of unknown causes and in those receiving liver grafts. Ad 1. Compared were different therapeutic concepts such as short-term combination therapy, triple-therapy, high dose IFN?-therapy and the use of antiviral substances such as ribavirin and amantadine. It emerged that relevant prognostic parameters can be deduced with respect to the therapeutic response rate. Ad 2. Analysed were possible molecular mechanisms, which may interfere with response or non-response to antiviral therapy. In this respect, we focussed on the interaction of certain HCV-proteins as NS5A, E2, so-called PKR-eIF2a phosphorylisation-homology-domain (PePHD). with the interferon-?-induced effector proteins. There is evidence, that number of mutations within the NS5A proteins are of prognostic relevance with respect to the response to interferon?-therapy. In contrast, mutations within the PePHD-region do not play any role in this respect. Ad 3. We also studied the clinical relevance of the newly discovered viruses GBV-C/HGV and TTV, and found, that they have no impact concerning the course of chronic hepatitis C. These viruses are interferon-sensitive and do not influence the IFNa-response as it could be documented by following the course of co-infected patients. Ad 4. Our studies also focused on the prevalence, transmission and relevance of GBV-C/HGV and TTV infections with respect to their role as hepatitis-inducing agents. We can show that both virus types are parenterally transmitted. There is a high prevalence for both types in patients confronted with risk factors for parenteral factors. From analysis of many patients being chronically infected with these viruses it became quite clear that they lack any important potency to provoke chronic liver disease.
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Tucker, Timothy Johan Paul. "Epidemiology, molecular characterisation and tropism of the Hepatitis G Virus / GBV-C." Doctoral thesis, University of Cape Town, 1999. http://hdl.handle.net/11427/25669.

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The hepatitis G virus and GBV-C are recently discovered variants of the same virus belonging to the family Flavivirus (HGV/GBV-C). Although initially thought to be a hepatitis virus, it has been shown to have no association with liver disease. No work has been performed on the prevalence or molecular characteristics of HGV/GBV-C in southern Africa. In addition, although it is clear that the liver is not the primary site of replication, there is no data on the sites of HGV/GBV-C replication in normal subjects. Thus, this study aimed to assess the prevalence of HGV/GBV-C carriage in the urban and rural adult Black communities of the Western and Eastern Cape Provinces of South Africa, and compare it to the prevalence of serological markers of the hepatitis viruses A-E. In addition, this study aimed to assess the molecular features of South African HGV/GBV-C isolates and demonstrate the organs where viral replication was present. The mean prevalences of antibodies to hepatitis A lgG, hepatitis B surface antigen and antibodies to hepatitis B surface antigen were 98%, 4.3% and 61.1 % respectively. The mean prevalence of antibodies to hepatitis C was 1.8%. No significant differences in prevalence were shown between the urban and rural regions for these viruses. The mean anti-hepatitis E prevalence varied from 5.8% to 19.1 % in the different regions. Those living in mud houses without access to chlorinated tap water had a significantly higher prevalence of antihepatitis E. No anti-hepatitis D positive samples were isolated. The overall prevalence of HGV/GBV-C was 26.9%, with rural communities having a significantly lower prevalence than urban communities. A significant relationship was observed between HGV/GBV-C infection with the use of illicit drugs, female gender, younger age and past blood transfusions. Phylogenetic analysis demonstrated a novel fourth South African HGV/GBV-C genotype, distinct from the previously described genotypes 1-3. In addition, certain isolates showed a major deletion in the highly conserved 5' non-coding region of HGV/GBV-C. Analysis of 23 tissue biopsies from infected cadavers suggested that the spleen and bone marrow were the primary sites of HGV/GBVC replication.
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ISHIKAWA, TETSUYA. "IMMUNOREGULATION OF HEPATITIS B VIRUS INFECTION : RATIONALE AND CLINICAL APPLICATION." Nagoya University School of Medicine, 2012. http://hdl.handle.net/2237/16732.

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Larios, Paterna Cristina. "Péptidos de fusión del virus de la hepatitis G: definición, síntesis y caracterización biofísica." Doctoral thesis, Universitat de Barcelona, 2006. http://hdl.handle.net/10803/1806.

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Un primer paso para conocer la entrada del virus de la hepatitis G en la célula es conocer dónde se encuentra el péptido de fusión. Por esta razón, éste fue el principal objetivo de la presente tesis. Dentro de la familia "Flaviviridae", los péptidos de fusión
descritos hasta el momento, se encuentran en la zona interna de la proteína estructural.
El virus de la hepatitis G se asemeja estructuralmente al virus de la hepatitis C, por ello,la búsqueda del péptido de fusión se centró en la proteína estructural E2 también presente en el virus de la hepatitis C. Las regiones escogidas dentro de la proteína estructural pertenecen a la región amino terminal, E2(7-26), y la zona interna (E2(279-298).
Estas secuencias fueron sintetizadas mediante metodología en fase sólida y se estudió la
interacción entre los péptidos y modelos de membrana de distinta complejidad (monocapas lipídicas, bicapas lipídicas). Las técnicas utilizadas para conocer la interacción entre ambos fueron las isotermas de Langmuir, la calorimetría diferencial de barrido, la espectroscopia de fluorescencia, la espectroscopia de UV y la microscopía.
Además se estudió la conformación adoptada por los péptidos por las técnicas de dicroísmo circular y espectroscopia de infrarrojos por transformada de Fourier. De todos los resultados obtenidos el péptido que interaccionó en mayor medida con los modelos de membrana, además de desestabilizar y producir fusión fue E2(279-298). Este péptido producía un cambio en su conformación al interaccionar con membranas fosfolipídicas(sobre todo en presencia de cargas negativas) hacia una estructura de tipo alfa-hélice. Este cambio hacia una estructura más ordenada podría proporcionar la conformación activa del péptido responsable de la desestabilización de las membranas.
The hepatitis G virus (GBV-C/HGV) is a enveloped RNA virus belonging to the "Flaviviridae" family. The natural history of the GBV-C/HGV infection is at present not fully understood and its potential to cause hepatitis in humans is questionable.
Elucidation of the mechanism of the fusion of enveloped viruses to target membranes has attracted considerable attention because of its relative simplicity and potential clinical importance. Apart from the functions of viral binding to target membranes and the activation of viral fusion proteins, usually only one viral protein is responsible for the membrane fusion step. However, the nature of the interaction of viral fusion proteins with membranes and the mechanism by which these proteins accelerate the formation of membrane fusion intermediates are poorly understood. In this sense, specialized
hydrophobic conserved domains ("fusion peptides") have been postulated to be absolutely required for the fusogenic activity.
The main objective of the present work was the knowlegment of the fusion peptide of the hepatitis G virus. For this purpose we have performed studies with different synthetic peptides belonging the envelope protein E2 of hepatitis G virus. The selected peptides were from the amino terminal part of the protein (E2(7-26)) and from the internal part (E2(279-298)). We have analysed lipid-peptide interactions depending on the degree of complexity of model membranes: monolayer studies (surface activity,
insertion of peptides into monolayers) and liposomes studies (differential scanning
calorimetry, fluorescence measurements). The peptides were compared for their ability
to interact and perturb membranes. In addition, they were also tested for their ability to
induce both leakage of vesicular contents and vesicle fusion as well as to lyse erythrocytes. Furthermore, we have studied the conformational behaviour of the peptides in water and in different membrane environments by Fourier-transform infrared spectroscopy (FTIR) and circular dichroism (CD). The results obtained showed that the E2(279-298) sequence was able to interact, penetrate and permeabilize vesicles
bilayers in a higher extent than E2(7-26) sequence. Furthermore, the interaction with
membranes induced a change in the internal peptide to an alpha-helical conformation while
the amino terminal sequence did not. This indicate that this internal segment peptide
could be involved in the fusion of hepatitis G virus into cell membrane.
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Alay, Romero Maria Teresa. "Estudis fisicoquímics de diferents seqüències peptídiques del virus de l’Hepatitis G." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/285310.

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El contingut de la tesi radica fonamentalment en l’ús de models de membrana biològica per a l’estudi del comportament fisicoquímic de seqüències peptídiques derivades del GB-virus C (GBV-C). La concomitància d’aquest virus amb el virus causant del SIDA (HIV) ha demostrat disminuir notablement la virulència d’aquets darrer. És per això que és important conèixer el comportament de pèptids que són fragments de les proteïnes del GBV-C per a posteriori poder enfocar l’estudi de la inhibició de la capacitat infectiva del HIV per part del GBV-C. Es tracta d’un estudi bàsic però amb resultats que contribueixen al disseny de noves estructures peptídiques per a ser emprades com una nova estratègia per a enfocar el tractament de la SIDA. Finalment indicar que aquest tema s’engloba dins del camp de la nanotecnologia pel que fa a l’ús de liposomes en els distints estudis presentats. Els resultats obtinguts es presenten en les següents publicacions: 1. Alay, M.; Busquets, M.A., Haro, I.; Rojo, N.; Alsina, M.A.; Prat, J. Merocyanine 540 for spectroscopic analysis of the interaction of a peptide sequence of hepatitis G virus with liposomes. Luminescence, 17: 263-264 (2002). 2. Alay, M.; Prat, J.; Haro, I.; Rojo, N.; Alsina, M.A.; Busquets, M.A. Spectroscopic analysis of the interaction of a peptide sequence of Hepatitis G virus with bilayers. Talanta, 60: 269-277 (2003). 3. Alay, M.; Prat, J.; Alsina, M.A.; Busquets, M.A. Effect of merocyanine 540 on Langmuir-Blodgett films and liposomes of zwitterionic, anionic and cationic lipid composition. Journal de Physique IV. 113: 3 -6 (2004) 4. Alay, M.; Alsina, M.A.; Haro, I.; Prat, J.; Busquets, M.A. Analysis of the effect of a peptide sequence of the E2 protein (HGV/GBV-C) on the physicochemical properties of zwitterionic and negatively charged bilayers. Luminescence 20: 445-450 (2005) 5. Alay, M.; Alsina, M.A.; Haro, I.; Prat, J.; Busquets, M.A. Interaction of E2 (GBV-C/HGV)-derived peptides with liposomes: fluorescence anisotropy and fluorescence resonance energy transfer methods. Luminescence 21: 360 -361 (2006) 6. Alay, M.; Haro, I., Girona, V.; Prat, J.; Busquets, M.A. Interaction of two overlapped synthetic peptides from GB virus C with charged mono and bilayers. Colloids and Surfaces B-Biointerfaces105: 7 -13 (2013)
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Lai, Agnes Suet Wah. "Hepatitis C and G virus infection and non-Hodgkin lymphoma in a case-control study from British Columbia, Canada." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/31732.

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Background & Aims: Both Hepatitis C virus (HCV) and Hepatitis G virus (HGV) are single-stranded positive sense RNA viruses belonging to the Flaviviridae family. Epidemiological evidence has suggested an association between HCV infection and non Hodgkin lymphoma (NHL), but the association has mostly been seen in regions where the prevalence is high. Canadian studies have reported no significant association. The role of HGV infection in NHL has also been suggested, but there is little epidemiologic evidence. We investigated HCV, HGV and risk of NHL in a population-based case-control study in British Columbia, Canada. Methods: Cases were aged 20-79, diagnosed between March 2000 and February 2004, and residents in Greater Vancouver or Victoria. Cases with HIV or a prior transplant were excluded. Controls were chosen from the Provincial Health Insurance Client Registry and were age/sex/region frequency matched to cases. Results: Antibodies for HCV were measured in plasma of 795 cases and 697 control subjects. HCV seropositivity was 2.4% in cases and 0.7% in controls [odds ratio (OR)=3.4, (95%) confidence interval (CI)=1.3-9.1)]. The highest risks were associated with diffuse large B-cell lymphoma (OR=8.3, 95%CI=2.9-23.9), marginal zone lymphoma (OR=4.5, 95%CI=1.1-19.2) and small lymphocytic lymphoma/chronic lymphocytic leukemia (OR=6.9, 95%CI=1.3-36.8). HGV viremia was determined in plasma by the RT-PCR technique in 553 cases and 438 control subjects. The prevalence of HGV viremia was 4.5% in cases and 1.8% in controls (OR=3.2, 95%CI=1.4-7.3). The associations were strongest for cases with diffuse large B-cell lymphoma (OR=5.7, 95%CI=2.3-14.6), marginal zone lymphoma (OR=3.5, 95%CI=1.2-10.4) and other/unknown B-cell lymphoma (OR=4.9, 95%CI=1.3-17.6). Interpretation: Our results provide further evidence that exposure to HCV and HGV contribute to NHL risk. The associations were strongest for cases with diffuse large B-cell lymphoma and marginal zone lymphoma.
Medicine, Faculty of
Graduate
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Pérez, Escoda María Teresa. "Diseño y síntesis de péptidos para el diagnóstico de la infección por el virus de la hepatitis G (GBV-C/HGV)." Doctoral thesis, Universitat de Barcelona, 2007. http://hdl.handle.net/10803/1807.

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El virus de la hepatitis G (GBV-C/HGV) es un virus ARN perteneciente a la familia Flaviviridae. Su prevalencia, basada en la positividad del ARN, oscila entre el 1 y el 4% en la población general. Sin embargo este porcentaje aumenta hasta el 20-30% en los individuos expuestos a sangre o sus derivados, en individuos infectados por el virus de la hepatitis C o por el virus de la inmunodeficiencia humana (HIV), hecho que indica que se transmite principalmente por vía parenteral. Aunque no está claro su potencial patogénico, los estudios más recientes sugieren que la infección por este virus reduce la mortalidad en los pacientes infectados por el HIV, de ahí el interés en disponer de una herramienta que permita el diagnóstico de la infección por GBV-C/HGV de un modo rápido y sencillo.
Desde hace años, los péptidos sintéticos se vienen utilizando en sistemas de diagnóstico para muchas enfermedades, sin embargo, los péptidos lineales que mimetizan epítopos B son débilmente reconocidos por los anticuerpos, y por ello, existe la tendencia de utilizar combinaciones más complejas que permitan mejorar tanto la sensibilidad como la especificidad de los ensayos.

En esta tesis se han diseñado y sintetizado, utilizando la metodología de síntesis en fase sólida, construcciones peptídicas en las que se combinan regiones de proteínas de envoltura y no estructurales. Se han sintetizado tanto péptidos quiméricos, que contienen más de un epítopo (lineales y ramificados), como péptidos cíclicos en los que los epítopos sufren restricción de movilidad.
La capacidad antigénica de las construcciones sintéticas se ha evaluado utilizando principalmente la técnica del enzimoinmunoensayo (ELISA) aunque también se ha investigado la utilidad de la técnica de la resonancia del plasmón de superficie (SPR) para detectar la presencia de anticuerpos anti-GBV-C/HGV en muestras de suero de individuos pertenecientes tanto a los grupos de riesgo como en la población sana. Además, se ha realizado un estudio conformacional con la finalidad de establecer una correlación entre la estructura secundaria adoptada por los péptidos y su capacidad antigénica. Finalmente, se ha estudiado la capacidad inmunogénica de las construcciones peptídicas en animales de experimentación.

Los resultados obtenidos muestran, por un lado, que las construcciones en las que se combinan varios epítopos son las que presentan una mejor precisión diagnóstica, y por otro lado, que la introducción de restricción de movilidad permite incrementar la sensibilidad mostrada por la molécula precursora lineal.
"Design and synthesis of peptides for serodiagnose of the hepatitis G virus (GBV-C/HGV) infection".

The GB virus C, so called hepatitis G virus (GBV-C/HGV), is a single-strand RNA virus belonging to the Flaviviridae family. The prevalence rate of GBV-C/HGV in healthy blood donors is 1-4% in worldwide and about 20-35% in high risk populations, thus indicating that this virus is transmitted via the parenteral route. Although controversial data exit concerning the potential to cause hepatitis in humans recent studies suggest that coinfection with HIV is associated with prolonged survival. For this reason it would be interesting to find an easy tool to diagnose this apparently non-pathogenic virus.
In recent years, synthetic peptides that mimic specific epitopes of infectious agents have been used in diagnostic systems for various diseases. The main drawback of this approach is that peptides representing topographic B-cell epitopes are poorly recognised by antibodies. There is a tendency toward using chimeric to avoid those problems and to improve the sensitivity and specificity of the assays.
In this thesis, new putative epitopes located both in envelope and in nonstructural proteins of GBV-C/HGV were synthesized using solid-phase chemistry. The corresponding synthetic peptides, obtained in linear, multimeric and cyclic forms, were used as antigens in ELISA and in real-time bioespecific interaction measurements (SPR) to detect GBV-C/HGV-specific antibodies in different panels of human sera. Furthermore, CD and FT-IR have been used in conjunction to characterize the conformational changes therein with synthetic constructs that could explain their different antigenicity.
The results obtained showed, on one hand, that the combination of different antigens seems to be necessary to ensure good sensitivity and more specificity and, on the other hand, that cyclic compounds show higher ability to recognize anti-GBV-C/HGV antibodies than its parent peptide. Our results offer a new approach to develop new diagnostic peptide based biosensors for serodiagnosis of GBV-C/HGV infection.
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Book chapters on the topic "Hepatitis G virus Victoria"

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Ehling, A., B. Gierten, and T. Arndt. "Hepatitis G-Virus (HGV/GBV-C)." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1432-1.

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Ehling, A., B. Gierten, and T. Arndt. "Hepatitis G-Virus (HGV/GBV-C)." In Springer Reference Medizin, 1101. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1432.

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Uhle, C., A. Huth-Kühne, R. Seelig, T. Goeser, and R. Zimmermann. "Prävalenz and Virusinaktivierung des Hepatitis-G-Virus." In 28. Hämophilie-Symposion Hamburg 1997, 271–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59915-6_41.

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Bagasra, Omar, Muhammad Sheraz, and Donald Gene Pace. "Hepatitis G Virus or GBV-C: A Natural Anti-HIV Interfering Virus." In Viruses: Essential Agents of Life, 363–88. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4899-6_18.

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Seifried, E., H. Bialleck, H. Weber, E. Waschk, S. Marx, S. Tschauder, and W. K. Roth. "Die Prävalenz des GB-Virus-C/Hepatitis-G-Virus in Blutspenden und seine Übertragung auf Empfänger." In 27. Hämophilie-Symposion Hamburg 1996, 54–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80403-8_9.

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Nübling, M., and J. Löwer. "GB-C/Hepatitis G Virus bei Hämophilen, Dialysepatienten, HIV-Infizierten und sein Nachweis in Blutprodukten." In 27. Hämophilie-Symposion Hamburg 1996, 47–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80403-8_8.

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"Hepatitis G Virus (HGV)." In Lexikon der Infektionskrankheiten des Menschen, 387. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-39026-8_456.

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"Antikörper gegen Hepatitis-G-Virus." In Springer Reference Medizin, 158. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_310247.

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Cramp, Matthew, Ashwin Dhanda, and Nikolai V. Naoumov. "Hepatitis viruses (excluding hepatitis C virus)." In Oxford Textbook of Medicine, edited by Christopher P. Conlon, 889–96. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0096.

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Viral hepatitis is an ancient disease which remains a major health problem worldwide. The group of hepatitis viruses includes five unrelated human viruses (A to E), which differ in their genome organization, biology, and epidemiology, while being united by their hepatotropism. About 10–15% of cases of viral hepatitis are considered as non-A to E hepatitis, whose aetiology is still unknown, but the search for which has led to the identification of several new viruses (e.g. hepatitis G virus or GB virus-C, TT, and SEN viruses) of uncertain pathogenic significance. Thus, the search for new hepatitis agents responsible for the small proportion of cases with cryptogenic hepatitis continues.
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Rizza, Stacey A. "Viral Hepatitis." In Mayo Clinic Infectious Diseases Board Review, 295–300. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199827626.003.0030.

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Many viruses can cause multisystem disease in humans. There are 5 hepatotropic viruses that primarily infect the human liver and cause hepatitis: A, B, C, D, and E. In 1996 a sixth virus, hepatitis G virus, was described, but its role in human disease remains uncertain. According to the Centers for Disease Control and Prevention, approximately 10 cases of viral hepatitis per 100,000 people are reported each year in the United States. The causes, diagnosis, and treatment of each virus are reviewed.
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Conference papers on the topic "Hepatitis G virus Victoria"

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Al-absi, Enas, Nadima Haj Ali, Aisha Khan, Makiyeh Khalili, Tameem Hadwan, Naema Al-mawlawi, Raed Abuodeh, and Gheyath Khalid Nasrallah. "Infection Rates And Phylogenetic Analysis Of Hepatitis G Virus (hgv)/gb Virus C (gbv-c) Among Qatari Blood Donors." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbop0582.

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"SECRETOS DE OFICIO DEL DULCERX." In 23° Congreso de la Sociedad Española de Patología Dual (SEPD) 2021. SEPD, 2021. http://dx.doi.org/10.17579/sepd2021o039.

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A partir del incremento de uso de metanfetamina (denominada localmente como “cristal”) por vía fumada, inyectada, esnifada y/o rectal en la Ciudad de México, y cuyos usuarios se autodenominan coloquialmente como “dulceros”, se presenta el reporte de resultados del programa de Reducción de Riesgos y Daños en Clínica Especializada Condesa. En un primer momento se describe el proceso de elaboración de la guía “Secretos de oficio del dulcerx” que tiene por objetivo captar población de hombres que tienen sexo con hombres que mantienen relaciones sexuales bajo el efecto de metanfetamina, ácido gamma-hidroxibutírico (GHB), ketamina, poppers, estimulantes para la erección, entre otras, la cual está sustentada en una postura enfocada en la reducción de riesgos y daños y ha sido distribuída tanto de manera digital como en sitios de encuentro. En un segundo momento se describe el trabajo colaborativo de pares y organizaciones de la sociedad civil en la difusión e implementación de estrategias descritas en la guía adaptadas para la población mexicana encaminadas a la reducción de riesgos y daños ante el uso de sustancias, así como la reducción de la transmisión de Virus de Inmunodeficiencia Humana (VIH), Virus de Hepatitis B (VHB), Virus de Hepatitis C (VHC), Sífilis y otras Infecciones de Transmisión Sexual (ITS). Por último, se describe el funcionamiento del programa de Reducción de Riesgos y Daños en Clínica Especializada Condesa de la Ciudad de México, en el que se contemplan nueve intervenciones diferentes: a) capacitación para el consumo, b) psicoeducación, c) vacunación, d) pruebas de detección y tratamiento para VIH, VHB, VHC, ITS, e) profilaxis pre y post-exposición, f) deshabituación y sustitución de sustancias, g) recolección segura de parafernalia y, h) entrega de kits de reducción de riesgos y daños, i) intervención psicológica.
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