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Hepatitis Virus in Long-Fingered Bats, Myanmar
DISPATCHES Myanmar; the counties are adjacent to Yunnan Province, Hepatitis Virus People’s Republic of China. The bats covered 6 species: Miniopterus fuliginosus (n = 640), Hipposideros armiger in Long-Fingered (n = 8), Rhinolophus ferrumequinum (n = 176), Myotis chi- nensis (n = 11), Megaderma lyra (n = 6), and Hipposideros Bats, Myanmar fulvus (n = 12). All bat tissue samples were subjected to vi- Biao He,1 Quanshui Fan,1 Fanli Yang, ral metagenomic analysis (unpublished data). The sampling Tingsong Hu, Wei Qiu, Ye Feng, Zuosheng Li, of bats for this study was approved by the Administrative Yingying Li, Fuqiang Zhang, Huancheng Guo, Committee on Animal Welfare of the Institute of Military Xiaohuan Zou, and Changchun Tu Veterinary, Academy of Military Medical Sciences, China. We used PCR to further study the prevalence of or- During an analysis of the virome of bats from Myanmar, thohepadnavirus in the 6 bat species; the condition of the a large number of reads were annotated to orthohepadnavi- samples made serologic assay and pathology impracticable. ruses. We present the full genome sequence and a morpho- Viral DNA was extracted from liver tissue of each of the logical analysis of an orthohepadnavirus circulating in bats. 853 bats by using the QIAamp DNA Mini Kit (QIAGEN, This virus is substantially different from currently known Hilden, Germany). To detect virus in the samples, we con- members of the genus Orthohepadnavirus and represents ducted PCR by using the TaKaRa PCR Kit (TaKaRa, Da- a new species. lian, China) with a pair of degenerate pan-orthohepadnavi- rus primers (sequences available upon request). The PCR he family Hepadnaviridae comprises 2 genera (Ortho- reaction was as follows: 45 cycles of denaturation at 94°C Thepadnavirus and Avihepadnavirus), and viruses clas- for 30 s, annealing at 54°C for 30 s, extension at 72°C for sified within these genera have a narrow host range. -
Inhibition of Hepadnaviral Replication by Polyethylenimine-Based Intravenous Delivery of Antisense Phosphodiester Oligodeoxynucleotides to the Liver
Gene Therapy (2001) 8, 874–881 2001 Nature Publishing Group All rights reserved 0969-7128/01 $15.00 www.nature.com/gt RESEARCH ARTICLE Inhibition of hepadnaviral replication by polyethylenimine-based intravenous delivery of antisense phosphodiester oligodeoxynucleotides to the liver M Robaczewska1,2, S Guerret3, J-S Remy4, I Chemin1, W-B Offensperger5, M Chevallier6, J-P Behr4, AJ Podhajska2, HE Blum5, C Trepo1 and L Cova1 1INSERM U271, Lyon, France; 2Faculty of Biotechnology, University of Gdansk and Medical University of Gdansk, Gdansk, Poland; 3Biomaterials Laboratory, Faculty of Pharmacy, Lyon; 4Faculty of Pharmacy, Illkirch, France; 5Department of Medicine, University of Freiburg, Germany; and 6Laboratoires Marcel Me´rieux, Lyon, France Antisense oligodeoxynucleotides (ODNs) appear as attract- fold as compared with the O-ODN-AS2. Following 9-day ive anti-hepatitis B virus (HBV) agents. We investigated in therapy the intrahepatic levels of both DHBV DNA and RNA vivo, in the duck HBV (DHBV) infection model, whether lin- were significantly decreased in the lPEI/O-ODN-AS2-treated ear polyethylenimine (lPEI)-based intravenous delivery of group as compared with the O-ODN-AS2-treated, control the natural antisense phosphodiester ODNs (O-ODNs) can lPEI/O-ODN-treated, and untreated controls. In addition, prevent their degradation and allow viral replication inhibition inhibition of intrahepatic viral replication by lPEI/O-ODN-AS2 in the liver. DHBV-infected Pekin ducklings were injected was not associated with toxicity and was comparable with with antisense O-ODNs covering the initiation codon of the that induced by the phosphorothioate S-ODN-AS2 at a five- DHBV large envelope protein, either in free form (O-ODN- fold higher dose. -
And Giant Guitarfish (Rhynchobatus Djiddensis)
VIRAL DISCOVERY IN BLUEGILL SUNFISH (LEPOMIS MACROCHIRUS) AND GIANT GUITARFISH (RHYNCHOBATUS DJIDDENSIS) BY HISTOPATHOLOGY EVALUATION, METAGENOMIC ANALYSIS AND NEXT GENERATION SEQUENCING by JENNIFER ANNE DILL (Under the Direction of Alvin Camus) ABSTRACT The rapid growth of aquaculture production and international trade in live fish has led to the emergence of many new diseases. The introduction of novel disease agents can result in significant economic losses, as well as threats to vulnerable wild fish populations. Losses are often exacerbated by a lack of agent identification, delay in the development of diagnostic tools and poor knowledge of host range and susceptibility. Examples in bluegill sunfish (Lepomis macrochirus) and the giant guitarfish (Rhynchobatus djiddensis) will be discussed here. Bluegill are popular freshwater game fish, native to eastern North America, living in shallow lakes, ponds, and slow moving waterways. Bluegill experiencing epizootics of proliferative lip and skin lesions, characterized by epidermal hyperplasia, papillomas, and rarely squamous cell carcinoma, were investigated in two isolated poopulations. Next generation genomic sequencing revealed partial DNA sequences of an endogenous retrovirus and the entire circular genome of a novel hepadnavirus. Giant Guitarfish, a rajiform elasmobranch listed as ‘vulnerable’ on the IUCN Red List, are found in the tropical Western Indian Ocean. Proliferative skin lesions were observed on the ventrum and caudal fin of a juvenile male quarantined at a public aquarium following international shipment. Histologically, lesions consisted of papillomatous epidermal hyperplasia with myriad large, amphophilic, intranuclear inclusions. Deep sequencing and metagenomic analysis produced the complete genomes of two novel DNA viruses, a typical polyomavirus and a second unclassified virus with a 20 kb genome tentatively named Colossomavirus. -
HBV Cccdna: Viral Persistence Reservoir and Key Obstacle for a Cure of Chronic Hepatitis B Michael Nassal
Downloaded from http://gut.bmj.com/ on June 8, 2015 - Published by group.bmj.com Gut Online First, published on June 5, 2015 as 10.1136/gutjnl-2015-309809 Recent advances in basic science HBV cccDNA: viral persistence reservoir and key obstacle for a cure of chronic hepatitis B Michael Nassal Correspondence to ABSTRACT frequent viral rebound upon therapy withdrawal Dr Michael Nassal, Department At least 250 million people worldwide are chronically indicates a need for lifelong treatment.6 of Internal Medicine II/ Molecular Biology, University infected with HBV, a small hepatotropic DNA virus that Reactivation can even occur, upon immunosuppres- Hospital Freiburg, Hugstetter replicates through reverse transcription. Chronic infection sion, in patients who resolved an acute HBV infec- Str. 55, Freiburg D-79106, greatly increases the risk for terminal liver disease. tion decades ago,7 indicating that the virus can be Germany; Current therapies rarely achieve a cure due to the immunologically controlled but is not eliminated. [email protected] refractory nature of an intracellular viral replication The virological key to this persistence is an intra- Received 17 April 2015 intermediate termed covalently closed circular (ccc) DNA. cellular HBV replication intermediate, called cova- Revised 12 May 2015 Upon infection, cccDNA is generated as a plasmid-like lently closed circular (ccc) DNA, which resides in Accepted 13 May 2015 episome in the host cell nucleus from the protein-linked the nucleus of infected cells as an episomal (ie, relaxed circular (RC) DNA genome in incoming virions. non-integrated) plasmid-like molecule that gives Its fundamental role is that as template for all viral rise to progeny virus. -
In Vitro Selection and Characterization of Single Stranded DNA Aptamers Inhibiting the Hepatitis B Virus Capsid-Envelope Interaction
Aus dem Veterinärwissenschaftlichen Department der Tierärztlichen Fakultät der Ludwig-Maximilians-Universität München Arbeit angefertigt unter der Leitung von: Univ.-Prof. Dr. Gerd Sutter Angefertigt im Institut für Virologie des Helmholtz Zentrum München (apl.-Prof. Dr. Volker Bruss) In vitro Selection and Characterization of single stranded DNA Aptamers Inhibiting the Hepatitis B Virus Capsid-Envelope Interaction Inaugural-Dissertation zur Erlangung der tiermedizinischen Doktorwürde der Tierärztlichen Fakultät der Ludwig-Maximilians-Universität München von Ahmed El-Sayed Abd El-Halem Orabi aus Sharkia/Ägypten München 2013 Gedruckt mit der Genehmigung der Tierärztlichen Fakultät der Ludwig-Maximilians-Universität München Dekan: Univ.-Prof. Dr. Joachim Braun Berichterstatter: Univ.-Prof. Dr. Gerd Sutter Korreferent: Univ.-Prof. Dr. Bernd Kaspers Tag der Promotion: 20. Juli 2013 My Family Contents Contents 1 INTRODUCTION ................................................................................................... 1 2 REVIEW OF THE LITERATURE ....................................................................... 2 2.1 HEPATITIS B VIRUS (HBV) .............................................................................................. 2 2.1.1 HISTORY AND TAXONOMY .......................................................................................................... 2 2.1.2 EPIDEMIOLOGY AND PATHOGENESIS .......................................................................................... 3 2.1.3 VIRION STRUCTURE .................................................................................................................... -
Interferon Gene Transfer by a Hepatitis B Virus Vector Efficiently Suppresses Wild-Type Virus Infection
Proc. Natl. Acad. Sci. USA Vol. 96, pp. 10818–10823, September 1999 Medical Sciences Interferon gene transfer by a hepatitis B virus vector efficiently suppresses wild-type virus infection ULRIKE PROTZER*, MICHAEL NASSAL*†,PEI-WEN CHIANG*‡,MICHAEL KIRSCHFINK§, AND HEINZ SCHALLER*¶ *Zentrum fu¨r Molekulare Biologie Heidelberg and §Department of Immunology, University of Heidelberg, Im Neuenheimer Feld, D-69120 Heidelberg, Germany; and †University Hospital, Department of Internal Medicine II͞Molecular Biology, University of Freiburg, Hugstetter Strasse 55, D-79106 Freiburg, Germany Communicated by Peter H. Duesberg, University of California, Berkeley, CA, July 13, 1999 (received for review February 25, 1999) ABSTRACT Hepatitis B viruses specifically target the concepts include gene therapy and the use of defective or liver, where they efficiently infect quiescent hepatocytes. Here attenuated viruses to block wild-type viral infection (3). Im- we show that human and avian hepatitis B viruses can be munomodulatory cytokines such as IL-12, IFN-␥ or tumor converted into vectors for liver-directed gene transfer. These necrosis factor-␣ potently suppress hepatitis B virus (HBV) vectors allow hepatocyte-specific expression of a green fluo- replication in an HBV transgenic mouse model (10, 11), rescent protein in vitro and in vivo. Moreover, when used to whereas IL-12 and the Th1 cytokines IFN-␥ and IL-2 seem to transduce a type I interferon gene, expression of interferon play an important role for viral clearance in chronically efficiently suppresses wild-type virus replication in the duck infected patients (12). However, systemic application of cyto- model of hepatitis B virus infection. These data suggest local kines is limited by severe side effects (7, 9). -
Mechanism of Hepatitis B Virus Cccdna Formation
viruses Review Mechanism of Hepatitis B Virus cccDNA Formation Lei Wei and Alexander Ploss * 110 Lewis Thomas Laboratory, Department of Molecular Biology, Princeton University, Washington Road, Princeton, NJ 08544, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-609-258-7128 Abstract: Hepatitis B virus (HBV) remains a major medical problem affecting at least 257 million chronically infected patients who are at risk of developing serious, frequently fatal liver diseases. HBV is a small, partially double-stranded DNA virus that goes through an intricate replication cycle in its native cellular environment: human hepatocytes. A critical step in the viral life-cycle is the conversion of relaxed circular DNA (rcDNA) into covalently closed circular DNA (cccDNA), the latter being the major template for HBV gene transcription. For this conversion, HBV relies on multiple host factors, as enzymes capable of catalyzing the relevant reactions are not encoded in the viral genome. Combinations of genetic and biochemical approaches have produced findings that provide a more holistic picture of the complex mechanism of HBV cccDNA formation. Here, we review some of these studies that have helped to provide a comprehensive picture of rcDNA to cccDNA conversion. Mechanistic insights into this critical step for HBV persistence hold the key for devising new therapies that will lead not only to viral suppression but to a cure. Keywords: hepatitis B virus; HBV; viral replication; cccDNA biogenesis; rcDNA; DNA repair Citation: Wei, L.; Ploss, A. 1. Overview of HBV Life Cycle and cccDNA Biogenesis Mechanism of Hepatitis B Virus cccDNA Formation. Viruses 2021, 13, The hepatotropic HBV belongs to the Hepadnaviridae family and is a blood-borne 1463. -
New Avian Hepadnavirus in Palaeognathous Bird, Germany
RESEARCH LETTERS New Avian Hepadnavirus includes emus (Dromaius novaehollandiae) and ostrich- es (Struthio spp.). in Palaeognathous Bird, In 2015, a deceased adult elegant-crested tinamou Germany kept at Wuppertal Zoo (Wuppertal, Germany) underwent necropsy at the University of Veterinary Medicine Han- 1 1 nover, Foundation (Hannover, Germany). Initial histologic Wendy K. Jo, Vanessa M. Pfankuche, examination revealed moderate, necrotizing hepatitis and Henning Petersen, Samuel Frei, Maya Kummrow, inclusion body–like structures within the hepatocytes. To Stephan Lorenzen, Martin Ludlow, Julia Metzger, identify a putative causative agent, we isolated nucleic ac- Wolfgang Baumgärtner, Albert Osterhaus, ids from the liver and prepared them for sequencing on an Erhard van der Vries Illumina MiSeq system (Illumina, San Diego, CA, USA) Author affiliations: University of Veterinary Medicine Hannover, (online Technical Appendix, https://wwwnc.cdc.gov/EID/ Foundation, Hannover, Germany (W.K. Jo, V.M. Pfankuche, article/23/12/16-1634-Techapp1.pdf). We compared ob- H. Petersen, M. Ludlow, J. Metzger, W. Baumgärtner, tained reads with sequences in GenBank using an in-house A. Osterhaus, E. van der Vries); Center for Systems metagenomics pipeline. Approximately 78% of the reads Neuroscience, Hannover (W.K. Jo, V.M. Pfankuche, aligned to existing avihepadnavirus sequences. A full ge- W. Baumgärtner, A. Osterhaus); Wuppertal Zoo, Wuppertal, nome (3,024 bp) of the putative elegant-crested tinamou Germany (S. Frei, M. Kummrow); Bernhard Nocht Institute for HBV (ETHBV) was subsequently constructed by de novo Tropical Medicine, Hamburg (S. Lorenzen); Artemis One Health, assembly mapping >2 million reads (88.6%) to the virus Utrecht, the Netherlands (A. Osterhaus) genome (GenBank accession no. -
Complete Genome Sequence of a Divergent Strain of Tibetan Frog Hepatitis B Virus Associated to Concave-Eared Torrent Frog
bioRxiv preprint doi: https://doi.org/10.1101/506550; this version posted December 26, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Title: Complete genome sequence of a divergent strain of Tibetan frog hepatitis B virus 2 associated to concave-eared torrent frog Odorrana tormota 3 4 Humberto J. Debat 1*, Terry Fei Fan Ng2 5 6 1Instituto de Patología Vegetal, Centro de Investigaciones Agropecuarias, Instituto Nacional de 7 Tecnología Agropecuaria (IPAVE-CIAP-INTA), X5020ICA, Córdoba, Argentina. 8 2College of Veterinary Medicine, University of Georgia, Athens, Georgia, USA 30602. 9 10 Running title: Tibetan frog hepatitis B virus in Odorrana tormota 11 12 *Address correspondence to: 13 Humberto J. Debat [email protected] 14 15 ORCID ID: 16 HJD 0000-0003-3056-3739, TFFN 0000-0002-4815-8697 17 18 Keywords: dsDNA virus, Hepadnavirus, amphibian virology, frog virus, Odorrana tormota, virus 19 discovery. 20 21 Abstract 22 The family Hepadnaviridae is characterized by partially dsDNA circular viruses of approximately 3.2 kb, 23 which are reverse transcribed from RNA intermediates. Hepadnaviruses (HBVs) have a broad host range 24 which includes humans (Hepatitis B virus), other mammals (genus Orthohepadnavirus), and birds 25 (Avihepadnavirus). HBVs host specificity has been expanded by reports of new viruses infecting fish, 26 amphibians, and reptiles. The tibetan frog hepatitis B virus (TFHBV) was recently discovered in 27 Nanorana parkeri (Family Dicroglossidae) from Tibet. -
Reverse Transcriptase Activity of Hepatitis B Virus Polymerase in Eukaryotic Cell Extracts in Vitro
Reverse Transcriptase Activity of Hepatitis B Virus Polymerase in Eukaryotic Cell Extracts In Vitro Daniel Favre Helpatitis, Lausanne, Switzerland Summary Zusammenfassung: In vitro reverse Transkriptase Aktivität der In hepadnaviruses, reverse transcription is primed by the viral Hepatitis B Virus Polymerase in eukariotischen Zellextrakten reverse transcriptase (RT) and requires the specific interaction In Hepadnaviren wird die reverse Transkription von der viralen between the RT and the viral RNA encapsidation signal termed reversen Transkriptase (RT) ausgeführt. Hier findet eine spezifi- ε. To study the activity of the RT in vitro, the current procedure sche Interaktion zwischen der RT und dem viralen Verpackungs- uses in vitro translated duck hepatitis B virus polymerase, but signal ε statt. Um die Aktivität der RT in vitro zu untersuchen, not the hepatitis B virus polymerase itself, in the rabbit reticulo- wird im aktuellen Protokoll in vitro translatierte Entenhepatitis cyte lysate expression system. B Virus Polymerase, aber nicht die Hepatitis B Virus Polyme- Here, the hepatitis B virus (HBV) polymerase has been suc- rase selbst, in einem Kaninchen Retikulozytenlysat Expressions- cessfully expressed in a translational extract that was obtained system eingesetzt. from monolayer human hepatocyte cells HuH-7. The translated In dieser Arbeit wurde die Hepatitis B Virus (HBV) Polymerase polypeptide retained the RNA-directed polymerase (reverse erfolgreich in einem translationalen Extrakt aus einer einlagigen transcriptase) activity on the viral RNA template containing the Kultur der humanen Hepatozytenzellen HuH-7 exprimiert. Das ε signal. We suggest that the reverse transcription event of the translatierte Polypeptid behielt die RNA-gerichtete Polymerase viral RNA coding for the polymerase and containing an ε struc- (reverse Transkriptase) Aktivität auf dem viralen RNA Template ture is concomitant to the translation of the viral polymerase to mit einem ε Signal. -
Bats Carry Pathogenic Hepadnaviruses Antigenically Related to Hepatitis B Virus and Capable of Infecting Human Hepatocytes
Bats carry pathogenic hepadnaviruses antigenically related to hepatitis B virus and capable of infecting human hepatocytes Jan Felix Drexlera,1, Andreas Geipelb,1, Alexander Königb, Victor M. Cormana, Debby van Rielc, Lonneke M. Leijtenc, Corinna M. Bremerb, Andrea Raschea, Veronika M. Cottontaild,e, Gael D. Magangaf, Mathias Schlegelg, Marcel A. Müllera, Alexander Adamh, Stefan M. Klosed, Aroldo José Borges Carneiroi, Andreas Stöckerj, Carlos Roberto Frankei, Florian Gloza-Rauscha,k, Joachim Geyerl, Augustina Annanm, Yaw Adu-Sarkodien, Samuel Oppongn, Tabea Bingera, Peter Vallod,o, Marco Tschapkad,e, Rainer G. Ulrichg, Wolfram H. Gerlichb, Eric Leroyf,p, Thijs Kuikenc, Dieter Glebeb,1,2, and Christian Drostena,1,2 aInstitute of Virology, University of Bonn Medical Centre, 53127 Bonn, Germany; bInstitute of Medical Virology, Justus Liebig University, 35392 Giessen, Germany; cDepartment of Viroscience, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands; dInstitute of Experimental Ecology, University of Ulm, 89069 Ulm, Germany; eSmithsonian Tropical Research Institute, Balboa Ancón, Republic of Panamá; fCentre International de Recherches Médicales de Franceville, BP 769 Franceville, Gabon; gFriedrich-Loeffler-Institut, Institute for Novel and Emerging Infectious Diseases, 17493 Greifswald-Insel Riems, Germany; hInstitute of Pathology, University of Cologne Medical Centre, 50937 Cologne, Germany; iSchool of Veterinary Medicine, Federal University of Bahia, 40.170-110, Salvador, Brazil; jInfectious Diseases Research Laboratory, University -
Duck Hepatitis B Virus Genesig Advanced
Primerdesign TM Ltd Duck Hepatitis B Virus Pre-core/core protein gene (C protein gene) genesig® Advanced Kit 150 tests For general laboratory and research use only Quantification of Duck Hepatitis B Virus genomes. 1 genesig Advanced kit handbook HB10.03.11 Published Date: 09/11/2018 Introduction to Duck Hepatitis B Virus Duck Hepatitis B virus( DHBV) is responsible for causing Duck Hepatitis. The virus is widely distributed in domestic ducks as well as several species of migratory wild ducks. It is a member of the genus Avihepadnavirus which belongs to the family hepadnaviridae. These are small enveloped viruses with a diameter of 40-45nm. The viral envelope is made up from host cell lipid with viral surface antigens (DHBsAg). This surrounds an icosahedral nucleocapsid composed of virus core antigen (DHBcAg), that itself contains the double stranded DNA genome and viral polymerase. The viral genome is of circular confirmation and is about 3 kb long, containing three overlapping open reading frames (ORFs). The C-ORF encodes the core antigen and pre-core protein which are processed and secreted as DHBcAg, the S-ORF encodes the surface antigen DHBsAg and the P-ORF encodes the viral polymerase. Duck hepatitis B virus is part of a group of viruses that are related but not identical to HBV. Unlike other mammalian hepadna viruses, DHBV has not been associated with significant lesions but causes chronic hepatitis and cirrhosis of the liver. Transmission is predominantly vertical, with the virus being passed from mother to embryo via the yolk sac of the egg. Viral replication in the embryos is observed approximately 6 days after incubation which coincides with embryonic liver formation.