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(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. -
(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. -
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. -
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. -
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. -
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 -
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. -
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. -
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]. -
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. -
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. -
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.