DOCSLIB.ORG

Influence of N-Glycosylation on Expression and Function Of

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Influence of N-Glycosylation on Expression and Function Of pathogens Article Article InfluenceInfluence of N-glycosylation of N-glycosylation on Expression on Expression and andFunction Function of of PseudorabiesPseudorabies Virus Virus Glycoprotein Glycoprotein gB gB Melina Vallbracht,Melina Vallbracht Barbara G., Barbara Klupp and G. Klupp Thomas and C. Thomas Mettenleiter C. Mettenleiter * * Institute ofInstitute Molecular of MolecularVirology and Virology Cell Biology, and Cell Friedrich-Loeffler-Institut, Biology, Friedrich-Loeffler-Institut, 17493 Greifswald-Insel 17493 Greifswald-Insel Riems, Riems, Germany; [email protected]; Melina.Vallbracht@fli.de (M.V.); [email protected] (M.V.); barbara.klupp@fli.de (B.G.K.) (B.G.K.) * Correspondence:* Correspondence: [email protected]; thomas.mettenleiter@fli.de; Tel.: +49-383-517-1250 Tel.: +49-383-517-1250 Abstract: Abstract:Envelope Envelopeglycoprotein glycoprotein (g)B is conserved (g)B is conserved throughout throughout the Herpesviridae the Herpesviridae and mediatesand mediatesfusion fusion of the viralof envelope the viral with envelope cellular with membranes cellular membranes for infectious for infectious entry and entry spread. and Like spread. all viral Like envelope all viral envelope fusion proteins,fusion proteins,gB is modified gB is modifiedby asparagine by asparagine (N)-linked (N)-linked glycosylation. glycosylation. Glycans can Glycans contribute can contribute to to protein function,protein function,intracellular intracellular transport, transport, trafficking, trafficking, structure structure and immune and immune evasion. evasion. gB of the gB ofal- the alpha- phaherpesvirusherpesvirus pseudorabies pseudorabies virus virus(PrV) (PrV)contains contains six consensus six consensus sites for sites N-linked for N-linked glycosylation, glycosylation, but but their functionaltheir functional relevance relevance is unknown. is unknown. Here, Here, we investigated we investigated the occupancy the occupancy and andfunctional functional rel- relevance evance ofof N-glycosylation N-glycosylation sites sites in inPrV PrV gB. gB. To To this this end, end, all all predicted predicted N-glycosylation N-glycosylation sites sites were were in- inactivated activated either singly or in combination by the introduction of conservative mutations (N Q). The resulting resulting proteins were tested for expression,expression, fusionfusion activityactivity inin cell–cellcell–cell fusionfusion assaysassays andand complementationcomple- mentationof of a a gB-deficient gB-deficient PrV PrV mutant. mutant. Our Our results results indicate indicate that that all all six six sites sites are are indeed indeed modified. modified. However, However,while while glycosylation glycosylation at at most most sites sites was was dispensable dispensable for for gB gB expression expression and and fusogenicity, fusogenicity, inactivation inactivationof N154of N154 and and N700 N700 affected affected gB processinggB processing by furinby furin cleavage cleavage and and surface surface localization. localization. Although all Althoughsingle all single mutants mutants were were functional functional in cell–cell in cell– fusioncell fusion and and viral viral entry, entry, simultaneous simultaneous inactivation inacti- of all six vation of N-glycosylationall six N-glycosylation sites severely sites severely impaired impaired fusion fusion activity activity and viral and entry, viral suggestingentry, suggesting a critical role of a critical roleN-glycans of N-glycans for maintaining for maintaining gB structure gB structure and function. and function. Citation: Vallbracht, M.; Klupp, Keywords:Keywords: herpesvirus;herpesvirus; pseudorabies pseudorabies virus; glycoprotein virus; glycoprotein B; membrane B; membrane fusion; N-linked fusion; N-linked glycosyl- glycosyla- Citation: Vallbracht, M.; Klupp, B.G.; B.G.; Mettenleiter, T.C. Influence of Mettenleiter, T.C. Influence of ation; virustion; entry virus entry N-glycosylation on Expression and N-glycosylation on Expression and Function of Pseudorabies Virus Function of Pseudorabies Virus Glycoprotein gB. Pathogens 2021, 10, Glycoprotein gB. Pathogens 2021, 10, x. https://doi.org/10.3390/xxxxx 61. https://doi.org/10.3390/ 1. Introduction1. Introduction pathogens10010061 Received: 14 December 2020 HerpesvirusesHerpesviruses are large-enveloped are large-enveloped double-stranded double-stranded DNA viruses DNA that viruses include that many include many Accepted: 7 January 2021 importantimportant human and human animal and pathogens. animal pathogens. Members Members of the Alphaherpesvirinae of the Alphaherpesvirinae subfamilysubfamily Received: 14 December 2020 Published: 12 January 2021 have thehave broadest the broadest host range, host are range, neurotropic are neurotropic and can and persist can persist in the ininfected the infected hosts hostsfor life for life [1]. Accepted: 7 January 2021 [1]. In additionIn addition to the to thehuman human herpes herpes simplex simplex viruses viruses 1 and 1 and 2 (HSV-1, 2 (HSV-1, -2) -2) and and Varicella Varicella zoster Published: 12 January 2021 Publisher’s Note: MDPI stays zoster virusvirus (VZV), (VZV), this this subfamily containscontains manymany economically economically important important veterinary veterinary pathogens neutral with regard to jurisdictional such as the Varicellovirus Pseudorabies virus (PrV, Suid alphaherpesvirus 1). PrV is the Publisher’s Note: MDPI stayspathogens neu- such as the Varicellovirus Pseudorabies virus (PrV, Suid alphaherpesvirus 1). PrV claims in published maps and causative agent of Aujeszky’s disease in swine and is capable of causing lethal disease in a tral with regard to jurisdictionalis clai-the causative agent of Aujeszky’s disease in swine and is capable of causing lethal dis- institutional affiliations. variety of other mammalian species [2,3]. ms in published maps and institutio-ease in a variety of other mammalian species [2,3]. Infectious entry and spread of herpesviruses require the fusion of the viral envelope nal affiliations. Infectious entry and spread of herpesviruses require the fusion of the viral envelope with thewith host cell the membrane. host cell membrane. Whereas many Whereas enveloped many viruses enveloped encode viruses a single encode but mul- a single but multifunctional glycoprotein (g) for host–cell receptor-binding and membrane fusion [4], Copyright: © 2021 by the authors. tifunctional glycoprotein (g) for host–cell receptor-binding and membrane fusion [4], her- pesvirusesherpesviruses utilize a multiprotein utilize a multiprotein machinery machinery to mediate to these mediate processes. these processes. The so-called The so-called Submitted forCopyright: possible open© 2021 access by the authors. Li- “core-fusion“core-fusion machinery” machinery” which is which conserved is conserved in all herpesviruses in all herpesviruses is formed is by formed gB, the by gB, the publication undercensee the MDPI, terms Basel,and Switzerland. bona fide fusion protein, and the heterodimeric complex of the membrane-bound gH and bona fide fusion protein, and the heterodimeric complex of the membrane-bound gH and conditions ofThis the articleCreative is anCommons open access article anchorless gL (gH/gL) [5]. In addition to the core-fusion machinery, herpesviruses require Attribution (CC BY) license anchorless gL (gH/gL) [5]. In addition to the core-fusion machinery, herpesviruses require distributed under the terms and con- the assistance of nonconserved subgroup-specific receptor-binding proteins such as gD of (http://creativecommons.org/licenses the assistance of nonconserved subgroup-specific receptor-binding proteins such as gD of ditions of the Creative Commons At- the Alphaherpesvirinae for entry [6–8]. /by/4.0/). the Alphaherpesvirinae for entry [6–8]. tribution (CC BY) license (https:// Herpesvirus-mediated membrane fusion is a highly regulated process whose molec- creativecommons.org/licenses/by/ ular details remain incompletely understood. The current model for alphaherpesvirus 4.0/). Pathogens 2021, 10, x. https://doi.org/10.3390/xxxxx www.mdpi.com/journal/pathogens Pathogens 2021, 10, 61. https://doi.org/10.3390/pathogens10010061 https://www.mdpi.com/journal/pathogens Pathogens 2021, 10, 61 2 of 15 entry proposes that gD, gH/gL and gB drive membrane fusion in a cascade-like, pH- independent fashion [9–11]. Binding of gD to an appropriate host cell receptor, such as nectin-1 or herpesvirus entry mediator (HVEM), serves as the initial fusion trigger [12,13]. A conformational change in receptor-bound gD is proposed to allow its crosstalk with gH/gL, possibly by direct interaction between their ectodomains [14]. The gH/gL com- plex is believed to function as a fusion regulator and, upon triggering, is thought to activate gB, the sole fusion executor [5,9,11,15]. Although the exact molecular mechanism of gB fusion activation by gH/gL is unclear, direct interactions between the respective ectodomains and/or cytoplasmic domains have been reported to be essential for fusion activation [16,17]. Activated gB is proposed to facilitate fusion by refolding from a trimeric metastable high-energy pre-fusion conformation to a stable post-fusion state. During the fusogenic conformational change, gB exposes two internal fusion loops that interact with the target membrane [18]. The subsequent fold-back process into the energetically more favorable post-fusion conformation juxtaposes the viral and cellular membranes, ultimately leading to their fusion [5]. gB is the most highly conserved
Load more

Recommended publications
  • (12) United States Patent (10) Patent No.: US 8,993,581 B2 Perrine Et Al
    US00899.3581B2 (12) United States Patent (10) Patent No.: US 8,993,581 B2 Perrine et al. (45) Date of Patent: Mar. 31, 2015 (54) METHODS FOR TREATINGVIRAL (58) Field of Classification Search DSORDERS CPC ... A61K 31/00; A61K 31/166; A61K 31/185: A61K 31/233; A61K 31/522: A61K 38/12: (71) Applicant: Trustees of Boston University, Boston, A61K 38/15: A61K 45/06 MA (US) USPC ........... 514/263.38, 21.1, 557, 565, 575, 617; 424/2011 (72) Inventors: Susan Perrine, Weston, MA (US); Douglas Faller, Weston, MA (US) See application file for complete search history. (73) Assignee: Trustees of Boston University, Boston, (56) References Cited MA (US) U.S. PATENT DOCUMENTS (*) Notice: Subject to any disclaimer, the term of this 3,471,513 A 10, 1969 Chinn et al. patent is extended or adjusted under 35 3,904,612 A 9/1975 Nagasawa et al. U.S.C. 154(b) by 0 days. (Continued) (21) Appl. No.: 13/915,092 FOREIGN PATENT DOCUMENTS (22) Filed: Jun. 11, 2013 CA 1209037 A 8, 1986 CA 2303268 A1 4f1995 (65) Prior Publication Data (Continued) US 2014/OO45774 A1 Feb. 13, 2014 OTHER PUBLICATIONS Related U.S. Application Data (63) Continuation of application No. 12/890,042, filed on PCT/US 10/59584 Search Report and Written Opinion mailed Feb. Sep. 24, 2010, now abandoned. 11, 2011. (Continued) (60) Provisional application No. 61/245,529, filed on Sep. 24, 2009, provisional application No. 61/295,663, filed on Jan. 15, 2010. Primary Examiner — Savitha Rao (74) Attorney, Agent, or Firm — Nixon Peabody LLP (51) Int.
    [Show full text]
  • (Epstein- Barr Virus) No Líquido Cefalorraquidiano De Crianças Com Suspeita De Meningoencefalite No Estado De Minas
    1 Universidade Federal de Minas Gerais Programa de Pós-Graduação em Microbiologia Detecção de human gammaherpesvirus 4 (Epstein- Barr virus) no líquido cefalorraquidiano de crianças com suspeita de meningoencefalite no estado de Minas Gerais Belo Horizonte 2020 2 NATHALIA MARTINS QUINTÃO Detecção de human gammaherpesvirus 4 (Epstein- Barr virus - EBV) no líquido cefalorraquidiano de crianças com suspeita de meningoencefalite no estado de Minas Gerais Dissertação de mestrado apresentada ao Programa de Pós-Graduação em Microbiologia do Instituto de Ciências Biológicas da Universidade Federal de Minas Gerais, como requisito à obtenção do título de Mestre em Microbiologia. Orientadora: Prof.ª. Dr.ª Erna Gessien Kroon Belo Horizonte 2020 3 4 5 RESUMO Epstein-Barr virus pertence à subfamília Gammaherpesvirinae da família Herpesviridae e é o agente etiológico da mononucleose infecciosa. A transmissão de EBV geralmente é pela saliva, sendo o quadro clássico de infecção primária a mononucleose apenas 5% dos casos evoluem para quadros de meningoencefalites. Os grupos de risco são principalmente crianças na primeira infância e pacientes imunocomprometidos. No Brasil, nos últimos 10 anos foram registrados aproximadamente 22 mil casos de meningites e encefalites virais, sendo 52% dos casos em crianças com até 14 anos de idade. O ensaio de PCR em tempo real (qPCR) revoluciona o diagnóstico de neuroinfecções virais. O objetivo deste trabalho foi detectar a presença de DNA genômico e de mRNA de EBV por qPCR para casos de meningoencefalites em pacientes de Minas Gerais e construir, com base na análise de prontuário dos pacientes e dados disponíveis no DATASUS, um breve panorama dos casos de meningoencefalites por EBV.
    [Show full text]
  • Guide for Common Viral Diseases of Animals in Louisiana
    Sampling and Testing Guide for Common Viral Diseases of Animals in Louisiana Please click on the species of interest: Cattle Deer and Small Ruminants The Louisiana Animal Swine Disease Diagnostic Horses Laboratory Dogs A service unit of the LSU School of Veterinary Medicine Adapted from Murphy, F.A., et al, Veterinary Virology, 3rd ed. Cats Academic Press, 1999. Compiled by Rob Poston Multi-species: Rabiesvirus DCN LADDL Guide for Common Viral Diseases v. B2 1 Cattle Please click on the principle system involvement Generalized viral diseases Respiratory viral diseases Enteric viral diseases Reproductive/neonatal viral diseases Viral infections affecting the skin Back to the Beginning DCN LADDL Guide for Common Viral Diseases v. B2 2 Deer and Small Ruminants Please click on the principle system involvement Generalized viral disease Respiratory viral disease Enteric viral diseases Reproductive/neonatal viral diseases Viral infections affecting the skin Back to the Beginning DCN LADDL Guide for Common Viral Diseases v. B2 3 Swine Please click on the principle system involvement Generalized viral diseases Respiratory viral diseases Enteric viral diseases Reproductive/neonatal viral diseases Viral infections affecting the skin Back to the Beginning DCN LADDL Guide for Common Viral Diseases v. B2 4 Horses Please click on the principle system involvement Generalized viral diseases Neurological viral diseases Respiratory viral diseases Enteric viral diseases Abortifacient/neonatal viral diseases Viral infections affecting the skin Back to the Beginning DCN LADDL Guide for Common Viral Diseases v. B2 5 Dogs Please click on the principle system involvement Generalized viral diseases Respiratory viral diseases Enteric viral diseases Reproductive/neonatal viral diseases Back to the Beginning DCN LADDL Guide for Common Viral Diseases v.
    [Show full text]
  • Aujeszky's Disease
    Aujeszky’s Disease Pseudorabies What is Aujeszky’s disease How does Aujeszky’s Can I get Aujeszky’s and what causes it? disease affect my animal? disease? Aujeszky’s disease, or pseudorabies, Disease may vary depending No. Signs of disease have not be is a contagious viral disease that on the age and species of animal reported in humans. primarily affects pigs. The virus causes affected; younger animals are the reproductive and severe neurological most severely affected. Piglets Who should I contact disease in affected animals; death is usually have a fever, stop eating, and if I suspect Aujeszky’s common. The disease occurs in parts show neurological signs (seizures, disease? of Europe, Southeast Asia, Central and paralysis), and often die within 24-36 Contact your veterinarian South America, and Mexico. It was hours. Older pigs may show similar immediately. Aujeszky’s disease is not once prevalent in the United States, symptoms, but often have respiratory currently found in domestic animals in but has been eradicated in commercial signs (coughing, sneezing, difficulty the United States; suspicion of disease operations; the virus is still found in breathing) and vomiting, are less likely requires immediate attention. feral (wild) swine populations. to die and generally recover in 5-10 days. Pregnant sows can abort or How can I protect my animal What animals get give birth to weak, trembling piglets. from Aujeszky’s disease? Aujeszky’s disease? Feral pigs do not usually show any Aujeszky’s disease is usually Pigs are the most frequently signs of disease. introduced into a herd from an affected animals, however nearly all Other animals usually die within a infected animal.
    [Show full text]
  • Virus Entry: What Has Ph Got to Do with It?
    TURNING POINTS Virus entry: What has pH got to do with it? Ari Helenius After several years of working on membrane For almost two years, the virus entry path- Over the following months, we validated proteins using the Semliki Forest virus (SFV) as way and mechanism of host penetration con- all the predictions of our pH hypothesis. For a model, I decided in 1976 to focus my research tinued to elude us. However, in the spring example, we could demonstrate a membrane on the mechanisms by which animal viruses of 1978, I had the chance to participate in a fusion reaction in vitro by simply mixing such as SFV enter and infect their host cells. Dahlem Conference in Berlin called ‘Transport liposomes and SFV, and briefly dropping the pH I had just moved from Finland with the lab of of Macromolecules in Cellular Systems’. It was to 6 or below. Moreover, when we added acidic Kai Simons to the newly founded European an opportune time for a meeting on this topic: medium to cells, we could ‘fool’ surface-bound Molecular Biology Laboratory (EMBL) in pathways of vesicle transport were being dis- viruses into fusing with the plasma membrane; Heidelberg, Germany. I was eager to tackle a covered, receptor-mediated trafficking pro- the entry block caused by weak bases was challenging problem — and one that did not cesses were beginning to be described, and the bypassed and the cells became infected. require work with detergents. important role of clathrin-coated vesicles was Joined by Judy White, Mark Marsh and Relying almost exclusively on electron finally properly appreciated.
    [Show full text]
  • Formation of Influenza Virus Particles Lacking Hemagglutinin on the Viral Envelope Asit K
    University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Papers in Veterinary and Biomedical Science Veterinary and Biomedical Sciences, Department of 1986 Formation of Influenza Virus Particles Lacking Hemagglutinin on the Viral Envelope Asit K. Pattnaik University of Nebraska-Lincoln, [email protected] Donald J. Brown University of California at Los Angeles Debi P. Nayak University of California at Los Angeles Follow this and additional works at: http://digitalcommons.unl.edu/vetscipapers Part of the Biochemistry, Biophysics, and Structural Biology Commons, Cell and Developmental Biology Commons, Immunology and Infectious Disease Commons, Medical Sciences Commons, Veterinary Microbiology and Immunobiology Commons, and the Veterinary Pathology and Pathobiology Commons Pattnaik, Asit K.; Brown, Donald J.; and Nayak, Debi P., "Formation of Influenza Virus Particles Lacking Hemagglutinin on the Viral Envelope" (1986). Papers in Veterinary and Biomedical Science. 198. http://digitalcommons.unl.edu/vetscipapers/198 This Article is brought to you for free and open access by the Veterinary and Biomedical Sciences, Department of at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Papers in Veterinary and Biomedical Science by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. JOURNAL OF VIROLOGY, Dec. 1986, p. 994-1001 Vol. 60, No.3 0022-S38X1861120994-08 $02.00/0 Copyright © 1986, American Society for Microbiology Formation of Influenza Virus Particles
    [Show full text]
  • Shared Ancestry of Herpes Simplex Virus 1 Strain Patton with Recent Clinical Isolates from Asia and with Strain KOS63
    HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Virology Manuscript Author . Author manuscript; Manuscript Author available in PMC 2018 December 01. Published in final edited form as: Virology. 2017 December ; 512: 124–131. doi:10.1016/j.virol.2017.09.016. Shared ancestry of herpes simplex virus 1 strain Patton with recent clinical isolates from Asia and with strain KOS63 Aldo Pourcheta, Richard Copinb, Matthew C. Mulveyc, Bo Shopsina,b, Ian Mohra, and Angus C. Wilsona,# aDepartment of Microbiology, New York University School of Medicine, New York, New York, USA bDepartment of Medicine, New York University School of Medicine, New York, New York, USA cBeneVir Biopharm, Inc., Gaithersburg, Maryland, USA Abstract Herpes simplex virus 1 (HSV-1) is a widespread pathogen that persists for life, replicating in surface tissues and establishing latency in peripheral ganglia. Increasingly, molecular studies of latency use cultured neuron models developed using recombinant viruses such as HSV-1 GFP- US11, a derivative of strain Patton expressing green fluorescent protein (GFP) fused to the viral US11 protein. Visible fluorescence follows viral DNA replication, providing a real time indicator of productive infection and reactivation. Patton was isolated in Houston, Texas, prior to 1973, and distributed to many laboratories. Although used extensively, the genomic structure and phylogenetic relationship to other strains is poorly known. We report that wild type Patton and the GFP-US11 recombinant contain the full complement of HSV-1 genes and differ within the unique regions at only eight nucleotides, changing only two amino acids. Although isolated in North America, Patton is most closely related to Asian viruses, including KOS63.
    [Show full text]
  • Monitoring of Pseudorabies in Wild Boar of Germany—A Spatiotemporal Analysis
    pathogens Article Monitoring of Pseudorabies in Wild Boar of Germany—A Spatiotemporal Analysis Nicolai Denzin 1, Franz J. Conraths 1 , Thomas C. Mettenleiter 2 , Conrad M. Freuling 3 and Thomas Müller 3,* 1 Friedrich-Loeffler-Institut, Institute of Epidemiology, 17493 Greifswald-Insel Riems, Germany; Nicolai.Denzin@fli.de (N.D.); Franz.Conraths@fli.de (F.J.C.) 2 Friedrich-Loeffler-Institut, 17493 Greifswald-Insel Riems, Germany; Thomas.Mettenleiter@fli.de 3 Friedrich-Loeffler-Institut, Institute of Molecular Virology and Cell Biology, 17493 Greifswald-Insel Riems, Germany; Conrad.Freuling@fli.de * Correspondence: Thomas.Mueller@fli.de; Tel.: +49-38351-71659 Received: 16 March 2020; Accepted: 8 April 2020; Published: 10 April 2020 Abstract: To evaluate recent developments regarding the epidemiological situation of pseudorabies virus (PRV) infections in wild boar populations in Germany, nationwide serological monitoring was conducted between 2010 and 2015. During this period, a total of 108,748 sera from wild boars were tested for the presence of PRV-specific antibodies using commercial enzyme-linked immunosorbent assays. The overall PRV seroprevalence was estimated at 12.09% for Germany. A significant increase in seroprevalence was observed in recent years indicating both a further spatial spread and strong disease dynamics. For spatiotemporal analysis, data from 1985 to 2009 from previous studies were incorporated. The analysis revealed that PRV infections in wild boar were endemic in all German federal states; the affected area covers at least 48.5% of the German territory. There were marked differences in seroprevalence at district levels as well as in the relative risk (RR) of infection of wild boar throughout Germany.
    [Show full text]
  • How Influenza Virus Uses Host Cell Pathways During Uncoating
    cells Review How Influenza Virus Uses Host Cell Pathways during Uncoating Etori Aguiar Moreira 1 , Yohei Yamauchi 2 and Patrick Matthias 1,3,* 1 Friedrich Miescher Institute for Biomedical Research, 4058 Basel, Switzerland; [email protected] 2 Faculty of Life Sciences, School of Cellular and Molecular Medicine, University of Bristol, Bristol BS8 1TD, UK; [email protected] 3 Faculty of Sciences, University of Basel, 4031 Basel, Switzerland * Correspondence: [email protected] Abstract: Influenza is a zoonotic respiratory disease of major public health interest due to its pan- demic potential, and a threat to animals and the human population. The influenza A virus genome consists of eight single-stranded RNA segments sequestered within a protein capsid and a lipid bilayer envelope. During host cell entry, cellular cues contribute to viral conformational changes that promote critical events such as fusion with late endosomes, capsid uncoating and viral genome release into the cytosol. In this focused review, we concisely describe the virus infection cycle and highlight the recent findings of host cell pathways and cytosolic proteins that assist influenza uncoating during host cell entry. Keywords: influenza; capsid uncoating; HDAC6; ubiquitin; EPS8; TNPO1; pandemic; M1; virus– host interaction Citation: Moreira, E.A.; Yamauchi, Y.; Matthias, P. How Influenza Virus Uses Host Cell Pathways during 1. Introduction Uncoating. Cells 2021, 10, 1722. Viruses are microscopic parasites that, unable to self-replicate, subvert a host cell https://doi.org/10.3390/ for their replication and propagation. Despite their apparent simplicity, they can cause cells10071722 severe diseases and even pose pandemic threats [1–3].
    [Show full text]
  • Viral Envelope Are Controlled by the Helper Virus Used to Activate The
    DETERMINING FACTOR IN THE CAPACITY OF ROUS SARCOMA VIRUS TO INDUCE TUMORS IN MAMMALS* By HIDESABURO HANAFUSA AND TERUKO HANAFUSA COLLMGE DE FRANCE, LABORATOIRE DE MIDECINE EXPARIMENTALE, PARIS Communidated by Ahdre Lwoff, January 24, 1966 Since Zilber and Kriukoval and Svet-Moldavsky' demonstrated that some strains of Rous sarcoma virus (RSV) are capable of inducing hemorrhagic cysts or sarcomas in newborn rats, numerous attempts have been made to induce tumors by RSVin various species of mammals.3-9 One of the remarkable aspects revealed by these investigations is the strain differences in RSV for this capacity.6-9 Certain strains, such as the Schmidt-Ruppin strain, are active, while others, such as the Bryan strain, are generally inactive in mammals. The cause of such strain differ- ences has not been elucidated. Our previous studies have shown that the Bryan high-titer strain of RSV is a defective virus which cannot reproduce without the help of any one of the avian leukosis viruses.'0 The defectiveness derives from the inability of this strain of RSV to induce the synthesis of its own viral envelope."I An essential role played by the helper virus is to provide the envelope to the RSV genome, whose replica- tion occurs in the infected cells without the aid of helper virus. Thus, several properties of RSV which presumably depend in some way on the character of the viral envelope are controlled by the helper virus used to activate the RSV.11-13 These properties include the antigenicity, the sensitivity to the interference induced by the helper virus, and the host range among genetically different chick embryos.
    [Show full text]
  • Phylogenetic and Recombination Analysis of the Herpesvirus Genus Varicellovirus Aaron W
    Kolb et al. BMC Genomics (2017) 18:887 DOI 10.1186/s12864-017-4283-4 RESEARCH ARTICLE Open Access Phylogenetic and recombination analysis of the herpesvirus genus varicellovirus Aaron W. Kolb1, Andrew C. Lewin2, Ralph Moeller Trane1, Gillian J. McLellan1,2,3 and Curtis R. Brandt1,3,4* Abstract Background: The varicelloviruses comprise a genus within the alphaherpesvirus subfamily, and infect both humans and other mammals. Recently, next-generation sequencing has been used to generate genomic sequences of several members of the Varicellovirus genus. Here, currently available varicellovirus genomic sequences were used for phylogenetic, recombination, and genetic distance analysis. Results: A phylogenetic network including genomic sequences of individual species, was generated and suggested a potential restriction between the ungulate and non-ungulate viruses. Intraspecies genetic distances were higher in the ungulate viruses (pseudorabies virus (SuHV-1) 1.65%, bovine herpes virus type 1 (BHV-1) 0.81%, equine herpes virus type 1 (EHV-1) 0.79%, equine herpes virus type 4 (EHV-4) 0.16%) than non-ungulate viruses (feline herpes virus type 1 (FHV-1) 0. 0089%, canine herpes virus type 1 (CHV-1) 0.005%, varicella-zoster virus (VZV) 0.136%). The G + C content of the ungulate viruses was also higher (SuHV-1 73.6%, BHV-1 72.6%, EHV-1 56.6%, EHV-4 50.5%) compared to the non-ungulate viruses (FHV-1 45.8%, CHV-1 31.6%, VZV 45.8%), which suggests a possible link between G + C content and intraspecies genetic diversity. Varicellovirus clade nomenclature is variable across different species, and we propose a standardization based on genomic genetic distance.
    [Show full text]
  • Supplementary Material
    SUPPLEMENTARY MATERIAL Appendix; Search strategy MEDLINE 1. Herpes Labialis/ 2. Stomatitis, Herpetic/ 3. ((herpe* adj3 (labial* or stomatiti* or gingivostomatiti*)) or cold-sore* or fever-blister*).tw,kf. 4. 1 or 2 or 3 5. Herpes Simplex/ 6. Simplexvirus/ or herpesvirus 1, human/ or herpesvirus 2, human/ 7. (hsv-1 or hsv1 or hsv-2 or hsv2 or simplexvirus or simplex-virus or herpes-simplex or herpe*).tw,kf. 8. exp Mouth/ 9. (lip*1 or mouth or labial* or orolabial* or oro-labial* or perioral or peri-oral or extraoral or extra-oral or intraoral or intra-oral or gingiva* or gingivo*).tw,kf. 10. (5 or 6 or 7) and (8 or 9) 11. 4 or 10 12. Secondary Prevention/ 13. exp Recurrence/ 14. (prevention or recurren* or prophyla*).tw,kf. 15. pc.fs. 16. 12 or 13 or 14 or 15 17. 11 and 16 18. exp animals/ not human*.sh. 19. 17 not 18 EMBASE 1. herpes labialis/ 2. herpetic stomatitis/ 3. ((herpe* adj3 (labial* or stomatiti* or gingivostomatiti*)) or cold-sore* or fever-blister*).tw,kw,dq. 4. 1 or 2 or 3 5. herpes simplex/ 6. simplexvirus/ or exp human alphaherpesvirus 1/ or exp herpes simplex virus 2/ 7. (hsv-1 or hsv1 or hsv-2 or hsv2 or simplexvirus or simplex-virus or herpes-simplex or herpe*).tw,kw,dq. 8. mouth/ or exp cheek/ or exp lip/ or exp mouth cavity/ or exp mouth floor/ or exp mouth mucosa/ or exp palate/ or oral blister/ 9. (lip*1 or mouth or labial* or orolabial* or oro-labial* or perioral or peri-oral or extraoral or extra-oral or intraoral or intra-oral or gingiva* or gingivo*).tw,kw,dq.
    [Show full text]