Metagenomic Identification of Diverse Animal Hepaciviruses and Pegiviruses
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Discovery of a Novel Simian Pegivirus in Common Marmosets
bioRxiv preprint doi: https://doi.org/10.1101/2020.05.24.113662; this version posted May 24, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.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 4.0 International license. 1 Discovery of a novel simian pegivirus in 2 common marmosets (Callithrix jacchus) 3 with lymphocytic enteritis 4 5 Heffron AS1, Lauck M1, Somsen ED1, Townsend EC1, Bailey AL2, Eickhoff J3, Newman CM1, 6 Kuhn J4, Mejia A5, Simmons HA5, O'Connor DH1. 7 Affiliations 8 1 Department of Pathology and Laboratory Medicine, School of Medicine and Public Health, 9 University of Wisconsin-Madison, Madison, Wisconsin, United States of America 10 2 Department of Pathology and Immunology, Washington University School of Medicine, St. 11 Louis, Missouri, United States of America 12 3 Department of Biostatistics & Medical Informatics, University of Wisconsin-Madison, Madison, 13 WI, United States of America 14 4 Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious 15 Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland, United States of 16 America 17 5 Wisconsin National Primate Research Center, University of Wisconsin-Madison, Madison, 18 Wisconsin, United States of America 19 Abstract 20 From 2010 to 2015, 73 common marmosets (Callithrix jacchus) housed at the Wisconsin 21 National Primate Research Center (WNPRC) were diagnosed postmortem with lymphocytic 22 enteritis. We used unbiased deep-sequencing to screen the blood of deceased enteritis-positive 23 marmosets for the presence of RNA viruses. -
Origins and Evolution of the Global RNA Virome
bioRxiv preprint doi: https://doi.org/10.1101/451740; this version posted October 24, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Origins and Evolution of the Global RNA Virome 2 Yuri I. Wolfa, Darius Kazlauskasb,c, Jaime Iranzoa, Adriana Lucía-Sanza,d, Jens H. 3 Kuhne, Mart Krupovicc, Valerian V. Doljaf,#, Eugene V. Koonina 4 aNational Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, Maryland, USA 5 b Vilniaus universitetas biotechnologijos institutas, Vilnius, Lithuania 6 c Département de Microbiologie, Institut Pasteur, Paris, France 7 dCentro Nacional de Biotecnología, Madrid, Spain 8 eIntegrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious 9 Diseases, National Institutes of Health, Frederick, Maryland, USA 10 fDepartment of Botany and Plant Pathology, Oregon State University, Corvallis, Oregon, USA 11 12 #Address correspondence to Valerian V. Dolja, [email protected] 13 14 Running title: Global RNA Virome 15 16 KEYWORDS 17 virus evolution, RNA virome, RNA-dependent RNA polymerase, phylogenomics, horizontal 18 virus transfer, virus classification, virus taxonomy 1 bioRxiv preprint doi: https://doi.org/10.1101/451740; this version posted October 24, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 19 ABSTRACT 20 Viruses with RNA genomes dominate the eukaryotic virome, reaching enormous diversity in 21 animals and plants. The recent advances of metaviromics prompted us to perform a detailed 22 phylogenomic reconstruction of the evolution of the dramatically expanded global RNA virome. -
The GB Viruses: a Review and Proposed Classification of GBV-A, GBV-C (HGV), and GBV-D in Genus Pegivirus Within the Family Flaviviridae
Journal of General Virology (2011), 92, 233–246 DOI 10.1099/vir.0.027490-0 Review The GB viruses: a review and proposed classification of GBV-A, GBV-C (HGV), and GBV-D in genus Pegivirus within the family Flaviviridae Jack T. Stapleton,1 Steven Foung,2 A. Scott Muerhoff,3 Jens Bukh4,5 and Peter Simmonds5 Correspondence 1Department of Internal Medicine, Veterans Administration Medical Center and the University Jack T. Stapleton of Iowa, Iowa City, IA, USA [email protected] 2Department of Pathology, Stanford University, Stanford, CA, USA 3Abbott Diagnostics Division, Abbott Laboratories, Abbott Park, IL, USA 4Copenhagen Hepatitis C Program (CO-HEP), Department of Infectious Diseases and Clinical Research Centre, Copenhagen University Hospital, Hvidovre, Denmark, and Department of International Health, Immunology and Microbiology, Faculty of Health Sciences, University of Copenhagen, Denmark 5Centre for Infectious Diseases, University of Edinburgh, Edinburgh, UK In 1967, it was reported that experimental inoculation of serum from a surgeon (G.B.) with acute hepatitis into tamarins resulted in hepatitis. In 1995, two new members of the family Flaviviridae, named GBV-A and GBV-B, were identified in tamarins that developed hepatitis following inoculation with the 11th GB passage. Neither virus infects humans, and a number of GBV-A variants were identified in wild New World monkeys that were captured. Subsequently, a related human virus was identified [named GBV-C or hepatitis G virus (HGV)], and recently a more distantly related virus (named GBV-D) was discovered in bats. Only GBV-B, a second species within the genus Hepacivirus (type species hepatitis C virus), has been shown to cause hepatitis; it causes acute hepatitis in experimentally infected tamarins. -
REVIEW Hepatitis C Virus
DOI:http://dx.doi.org/10.7314/APJCP.2012.13.12.5917 Hepatitis C Virus -Proteins, Diagnosis, Treatment and New Approaches for Vaccine Development REVIEW Hepatitis C Virus - Proteins, Diagnosis, Treatment and New Approaches for Vaccine Development Hossein Keyvani1, Mehdi Fazlalipour2*, Seyed Hamid Reza Monavari1, Hamid Reza Mollaie2 Abstract Background: Hepatitis C virus (HCV) causes acute and chronic human hepatitis infection and as such is an important global health problem. The virus was discovered in the USA in 1989 and it is now known that three to four million people are infected every year, WHO estimating that 3 percent of the 7 billion people worldwide being chronically infected. Humans are the natural hosts of HCV and this virus can eventually lead to permanent liver damage and carcinoma. HCV is a member of the Flaviviridae family and Hepacivirus genus. The diameter of the virus is about 50-60 nm and the virion contains a single-stranded positive RNA approximately 10,000 nucleotides in length and consisting of one ORF which is encapsulated by an external lipid envelope and icosahedral capsid. HCV is a heterogeneous virus, classified into 6 genotypes and more than 50 subtypes. Because of the genome variability, nucleotide sequences of genotypes differ by approximately 31-34%, and by 20-23% among subtypes. Quasi-species of mixed virus populations provide a survival advantage for the virus to create multiple variant genomes and a high rate of generation of variants to allow rapid selection of mutants for new environmental conditions. Direct contact with infected blood and blood products, sexual relationships and availability of injectable drugs have had remarkable effects on HCV epidemiology. -
Arenaviridae Astroviridae Filoviridae Flaviviridae Hantaviridae
Hantaviridae 0.7 Filoviridae 0.6 Picornaviridae 0.3 Wenling red spikefish hantavirus Rhinovirus C Ahab virus * Possum enterovirus * Aronnax virus * * Wenling minipizza batfish hantavirus Wenling filefish filovirus Norway rat hunnivirus * Wenling yellow goosefish hantavirus Starbuck virus * * Porcine teschovirus European mole nova virus Human Marburg marburgvirus Mosavirus Asturias virus * * * Tortoise picornavirus Egyptian fruit bat Marburg marburgvirus Banded bullfrog picornavirus * Spanish mole uluguru virus Human Sudan ebolavirus * Black spectacled toad picornavirus * Kilimanjaro virus * * * Crab-eating macaque reston ebolavirus Equine rhinitis A virus Imjin virus * Foot and mouth disease virus Dode virus * Angolan free-tailed bat bombali ebolavirus * * Human cosavirus E Seoul orthohantavirus Little free-tailed bat bombali ebolavirus * African bat icavirus A Tigray hantavirus Human Zaire ebolavirus * Saffold virus * Human choclo virus *Little collared fruit bat ebolavirus Peleg virus * Eastern red scorpionfish picornavirus * Reed vole hantavirus Human bundibugyo ebolavirus * * Isla vista hantavirus * Seal picornavirus Human Tai forest ebolavirus Chicken orivirus Paramyxoviridae 0.4 * Duck picornavirus Hepadnaviridae 0.4 Bildad virus Ned virus Tiger rockfish hepatitis B virus Western African lungfish picornavirus * Pacific spadenose shark paramyxovirus * European eel hepatitis B virus Bluegill picornavirus Nemo virus * Carp picornavirus * African cichlid hepatitis B virus Triplecross lizardfish paramyxovirus * * Fathead minnow picornavirus -
Hepatitis C Virus Vaccine Research: Time to Put up Or Shut Up
viruses Review Hepatitis C Virus Vaccine Research: Time to Put Up or Shut Up Alex S. Hartlage 1,2 and Amit Kapoor 1,3,* 1 Center for Vaccines and Immunity, Abigail Wexner Research Institute at Nationwide Children’s Hospital, Columbus, OH 43205, USA; [email protected] 2 Medical Scientist Training Program, College of Medicine and Public Health, The Ohio State University, Columbus, OH 43205, USA 3 Department of Pediatrics, College of Medicine and Public Health, The Ohio State University, Columbus, OH 43205, USA * Correspondence: [email protected] Abstract: Unless urgently needed to prevent a pandemic, the development of a viral vaccine should follow a rigorous scientific approach. Each vaccine candidate should be designed considering the in- depth knowledge of protective immunity, followed by preclinical studies to assess immunogenicity and safety, and lastly, the evaluation of selected vaccines in human clinical trials. The recently concluded first phase II clinical trial of a human hepatitis C virus (HCV) vaccine followed this approach. Still, despite promising preclinical results, it failed to protect against chronic infection, raising grave concerns about our understanding of protective immunity. This setback, combined with the lack of HCV animal models and availability of new highly effective antivirals, has fueled ongoing discussions of using a controlled human infection model (CHIM) to test new HCV vaccine candidates. Before taking on such an approach, however, we must carefully weigh all the ethical and health consequences of human infection in the absence of a complete understanding of HCV immunity and pathogenesis. We know that there are significant gaps in our knowledge of adaptive immunity necessary to prevent chronic HCV infection. -
Human Pegivirus Isolates Characterized by Deep Sequencing
Human pegivirus isolates characterized by deep sequencing from hepatitis C virus-RNA and human immunodeficiency virus-RNA–positive blood donations, France François Jordier, Marie-Laurence Deligny, Romain Barré, Catherine Robert, Vital Galicher, Rathviro Uch, Pierre-Edouard Fournier, Didier Raoult, Philippe Biagini To cite this version: François Jordier, Marie-Laurence Deligny, Romain Barré, Catherine Robert, Vital Galicher, et al.. Human pegivirus isolates characterized by deep sequencing from hepatitis C virus-RNA and human immunodeficiency virus-RNA–positive blood donations, France. Journal of Medical Virology, Wiley- Blackwell, 2018, 91 (1), pp.38-44. 10.1002/jmv.25290. hal-01869364 HAL Id: hal-01869364 https://hal.archives-ouvertes.fr/hal-01869364 Submitted on 27 Jul 2021 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Copyright Human pegivirus isolates characterized by deep sequencing from hepatitis C virus‐RNA and human immunodeficiency virus‐RNA–positive blood donations, France François Jordier1 | Marie‐Laurence Deligny1 | Romain Barré1 | Catherine Robert2 | Vital Galicher1 | Rathviro Uch1 | Pierre‐Edouard Fournier3 | Didier Raoult2 | Philippe Biagini1 1Biologie des Groupes Sanguins, ‐ Etablissement Français du Sang Provence Human pegivirus (HPgV, formerly GBV C) is a member of the genus Pegivirus, family Alpes Côte d’Azur Corse, Aix Marseille Flaviviridae. -
Ribavirin Inhibits West Nile Virus Replication and Cytopathic Effect in Neural Cells
1214 CONCISE COMMUNICATION Ribavirin Inhibits West Nile Virus Replication and Cytopathic Effect in Neural Cells Ingo Jordan,1 Thomas Briese,1 Nicole Fischer,1 1Emerging Diseases Laboratory, Departments of Microbiology Johnson Yiu-Nam Lau,2 and W. Ian Lipkin1 and Molecular Genetics, Neurology, and Anatomy and Neurobiology, University of California, Irvine, and 2ICN Pharmaceuticals, Costa Mesa, California West Nile virus (WNV) is an emerging mosquito-borne pathogen that was reported for the ®rst time in the Western hemisphere in August 1999, when an encephalitis outbreak in New York City resulted in 62 clinical cases and 7 deaths. WNV, for which no antiviral therapy has been described, was recently recovered from a pool of mosquitoes collected in New York City. In anticipation of the recurrence of WNV during the summer of 2000, an analysis was made of the ef®cacy of the nucleoside analogue ribavirin, a broad-spectrum antiviral compound with activity against several RNA viruses, for treatment of WNV infection. High doses of ribavirin were found to inhibit WNV replication and cytopathogenicity in human neural cells in vitro. The Flaviviridae, a family of enveloped positive-strand RNA substantial [3]. Genetic analysis of the envelope protein se- viruses, include West Nile virus (WNV), as well as other sig- quence indicated that the viral strain most closely resembled ni®cant human pathogens, such as hepatitis C, yellow fever, an isolate from a goose in Israel in 1998, demonstrating the dengue, Japanese encephalitis, and St. Louis encephalitis vi- wide geographic distribution of this emerging pathogen [4, 5]. ruses [1]. Whereas hepatitis C virus (genus Hepacivirus) may Antiviral therapy for hepatitis C has been described [6]; how- be transmitted by blood products or sexual activity, most mem- ever, no speci®c treatment has been reported for WNV or other bers of the Flavivirus genus, including WNV, are transmitted ¯avivirus infections. -
Dissertation Bats As Reservoir Hosts
DISSERTATION BATS AS RESERVOIR HOSTS: EXPLORING NOVEL VIRUSES IN NEW WORLD BATS Submitted by Ashley Malmlov Department of Microbiology, Immunology, and Pathology In partial fulfillment of the requirements For the Degree of Doctor of Philosophy Colorado State University Fort Collins, Colorado Spring 2018 Doctoral Committee: Advisor: Tony Schountz Richard Bowen Page Dinsmore Kristy Pabilonia Copyright by Ashley Malmlov 2018 All Rights Reserved ABSTRACT BATS AS RESERVOIR HOSTS: EXPLORING NOVEL VIRUSES IN NEW WORLD BATS Order Chiroptera is oft incriminated for their capacity to serve as reservoirs for many high profile human pathogens, including Ebola virus, Marburg virus, severe acute respiratory syndrome coronavirus, Nipah virus and Hendra virus. Additionally, bats are postulated to be the original hosts for such virus families and subfamilies as Paramyxoviridae and Coronavirinae. Given the perceived risk bats may impart upon public health, numerous explorations have been done to delineate if in fact bats do host more viruses than other animal species, such as rodents, and to ascertain what is unique about bats to allow them to maintain commensal relationships with zoonotic pathogens and allow for spillover. Of particular interest is data that demonstrate type I interferons (IFN), a first line defense to invading viruses, may be constitutively expressed in bats. The constant expression of type I IFNs would hamper viral infection as soon as viral invasion occurred, thereby limiting viral spread and disease. Another immunophysiological trait that may facilitate the ability to harbor viruses is a lack of somatic hypermutation and affinity maturation, which would decrease antibody affinity and neutralizing antibody titers, possibly facilitating viral persistence. -
Conventional and Unconventional Mechanisms for Capping Viral Mrna
REVIEWS Conventional and unconventional mechanisms for capping viral mRNA Etienne Decroly1, François Ferron1, Julien Lescar1,2 and Bruno Canard1 Abstract | In the eukaryotic cell, capping of mRNA 5′ ends is an essential structural modification that allows efficient mRNA translation, directs pre-mRNA splicing and mRNA export from the nucleus, limits mRNA degradation by cellular 5′–3′ exonucleases and allows recognition of foreign RNAs (including viral transcripts) as ‘non-self’. However, viruses have evolved mechanisms to protect their RNA 5′ ends with either a covalently attached peptide or a cap moiety (7‑methyl-Gppp, in which p is a phosphate group) that is indistinguishable from cellular mRNA cap structures. Viral RNA caps can be stolen from cellular mRNAs or synthesized using either a host- or virus-encoded capping apparatus, and these capping assemblies exhibit a wide diversity in organization, structure and mechanism. Here, we review the strategies used by viruses of eukaryotic cells to produce functional mRNA 5′-caps and escape innate immunity. Pre-mRNA splicing The cap structure found at the 5′ end of eukaryotic reactions involved in the viral RNA-capping process, A post-transcriptional mRNAs consists of a 7‑methylguanosine (m7G) moi‑ and the specific cellular factors that trigger a response modification of pre-mRNA, in ety linked to the first nucleotide of the transcript via a from the innate immune system. which introns are excised and 5′–5′ triphosphate bridge1 (FIG. 1a). The cap has several exons are joined in order to form a translationally important biological roles, such as protecting mRNA Capping, decapping and turnover of host RNA functional, mature mRNA. -
Discovery of a Novel Human Pegivirus in Blood Associated with Hepatitis C Virus Co-Infection
RESEARCH ARTICLE Discovery of a Novel Human Pegivirus in Blood Associated with Hepatitis C Virus Co- Infection Michael G. Berg1☯, Deanna Lee2,3☯, Kelly Coller1, Matthew Frankel1, Andrew Aronsohn4, Kevin Cheng1, Kenn Forberg1, Marilee Marcinkus1, Samia N. Naccache2,3, George Dawson1, Catherine Brennan1, Donald M. Jensen4, John Hackett, Jr.1, Charles Y. Chiu2,3,5* 1 Abbott Laboratories, Abbott Park, Illinois, United States of America, 2 Department of Laboratory Medicine, University of California, San Francisco, California, United States of America, 3 UCSF-Abbott Viral Diagnostics and Discovery Center, San Francisco, California, United States of America, 4 Center for Liver Diseases, University of Chicago Medical Center, Chicago, Illinois, United States of America, 5 Department of Medicine, Division of Infectious Diseases, University of California, San Francisco, California, United States of America ☯ These authors contributed equally to this work. * [email protected] OPEN ACCESS Citation: Berg MG, Lee D, Coller K, Frankel M, Abstract Aronsohn A, Cheng K, et al. (2015) Discovery of a Novel Human Pegivirus in Blood Associated with Hepatitis C virus (HCV) and human pegivirus (HPgV), formerly GBV-C, are the only known Hepatitis C Virus Co-Infection. PLoS Pathog 11(12): human viruses in the Hepacivirus and Pegivirus genera, respectively, of the family Flaviviri- e1005325. doi:10.1371/journal.ppat.1005325 dae. We present the discovery of a second pegivirus, provisionally designated human pegi- Editor: Christian Drosten, University of Bonn, virus 2 (HPgV-2), by next-generation sequencing of plasma from an HCV-infected patient GERMANY with multiple bloodborne exposures who died from sepsis of unknown etiology. HPgV-2 is Received: September 20, 2015 highly divergent, situated on a deep phylogenetic branch in a clade that includes rodent and Accepted: November 12, 2015 bat pegiviruses, with which it shares <32% amino acid identity. -
Structure Unveils Relationships Between RNA Virus Polymerases
viruses Article Structure Unveils Relationships between RNA Virus Polymerases Heli A. M. Mönttinen † , Janne J. Ravantti * and Minna M. Poranen * Molecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, Viikki Biocenter 1, P.O. Box 56 (Viikinkaari 9), 00014 Helsinki, Finland; heli.monttinen@helsinki.fi * Correspondence: janne.ravantti@helsinki.fi (J.J.R.); minna.poranen@helsinki.fi (M.M.P.); Tel.: +358-2941-59110 (M.M.P.) † Present address: Institute of Biotechnology, Helsinki Institute of Life Sciences (HiLIFE), University of Helsinki, Viikki Biocenter 2, P.O. Box 56 (Viikinkaari 5), 00014 Helsinki, Finland. Abstract: RNA viruses are the fastest evolving known biological entities. Consequently, the sequence similarity between homologous viral proteins disappears quickly, limiting the usability of traditional sequence-based phylogenetic methods in the reconstruction of relationships and evolutionary history among RNA viruses. Protein structures, however, typically evolve more slowly than sequences, and structural similarity can still be evident, when no sequence similarity can be detected. Here, we used an automated structural comparison method, homologous structure finder, for comprehensive comparisons of viral RNA-dependent RNA polymerases (RdRps). We identified a common structural core of 231 residues for all the structurally characterized viral RdRps, covering segmented and non-segmented negative-sense, positive-sense, and double-stranded RNA viruses infecting both prokaryotic and eukaryotic hosts. The grouping and branching of the viral RdRps in the structure- based phylogenetic tree follow their functional differentiation. The RdRps using protein primer, RNA primer, or self-priming mechanisms have evolved independently of each other, and the RdRps cluster into two large branches based on the used transcription mechanism.