Global Burden of Norovirus and Prospects for Vaccine Development
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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. -
Encephalomyocarditis Virus Viroporin 2B Activates NLRP3 Inflammasome
Encephalomyocarditis Virus Viroporin 2B Activates NLRP3 Inflammasome Minako Ito, Yusuke Yanagi, Takeshi Ichinohe* Department of Virology, Faculty of Medicine, Kyushu University, Maidashi, Higashi-ku, Fukuoka, Japan Abstract Nod-like receptors (NLRs) comprise a large family of intracellular pattern- recognition receptors. Members of the NLR family assemble into large multiprotein complexes, termed the inflammasomes. The NLR family, pyrin domain-containing 3 (NLRP3) is triggered by a diverse set of molecules and signals, and forms the NLRP3 inflammasome. Recent studies have indicated that both DNA and RNA viruses stimulate the NLRP3 inflammasome, leading to the secretion of interleukin 1 beta (IL-1b) and IL-18 following the activation of caspase-1. We previously demonstrated that the proton-selective ion channel M2 protein of influenza virus activates the NLRP3 inflammasome. However, the precise mechanism by which NLRP3 recognizes viral infections remains to be defined. Here, we demonstrate that encephalomyocarditis virus (EMCV), a positive strand RNA virus of the family Picornaviridae, activates the NLRP3 inflammasome in mouse dendritic cells and macrophages. Although transfection with RNA from EMCV virions or EMCV-infected cells induced robust expression of type I interferons in macrophages, it failed to stimulate secretion of IL-1b. Instead, the EMCV viroporin 2B was sufficient to cause inflammasome activation in lipopolysaccharide-primed macrophages. While cells untransfected or transfected with the gene encoding the EMCV non-structural protein 2A or 2C expressed NLRP3 uniformly throughout the cytoplasm, NLRP3 was redistributed to the perinuclear space in cells transfected with the gene encoding the EMCV 2B or influenza virus M2 protein. 2B proteins of other picornaviruses, poliovirus and enterovirus 71, also caused the NLRP3 redistribution. -
Metagenomic Analysis of the Turkey Gut RNA Virus Community J Michael Day1*, Linda L Ballard2, Mary V Duke2, Brian E Scheffler2, Laszlo Zsak1
Day et al. Virology Journal 2010, 7:313 http://www.virologyj.com/content/7/1/313 RESEARCH Open Access Metagenomic analysis of the turkey gut RNA virus community J Michael Day1*, Linda L Ballard2, Mary V Duke2, Brian E Scheffler2, Laszlo Zsak1 Abstract Viral enteric disease is an ongoing economic burden to poultry producers worldwide, and despite considerable research, no single virus has emerged as a likely causative agent and target for prevention and control efforts. Historically, electron microscopy has been used to identify suspect viruses, with many small, round viruses eluding classification based solely on morphology. National and regional surveys using molecular diagnostics have revealed that suspect viruses continuously circulate in United States poultry, with many viruses appearing concomitantly and in healthy birds. High-throughput nucleic acid pyrosequencing is a powerful diagnostic technology capable of determining the full genomic repertoire present in a complex environmental sample. We utilized the Roche/454 Life Sciences GS-FLX platform to compile an RNA virus metagenome from turkey flocks experiencing enteric dis- ease. This approach yielded numerous sequences homologous to viruses in the BLAST nr protein database, many of which have not been described in turkeys. Our analysis of this turkey gut RNA metagenome focuses in particular on the turkey-origin members of the Picornavirales, the Caliciviridae, and the turkey Picobirnaviruses. Introduction remains elusive, and many enteric viruses can be Enteric disease syndromes such as Poult Enteritis Com- detected in otherwise healthy turkey and chicken flocks plex (PEC) in young turkeys and Runting-Stunting Syn- [3,4]. Regional and national enteric virus surveys have drome (RSS) in chickens are a continual economic revealed the ongoing presence of avian reoviruses, rota- burden for poultry producers. -
African Meningitis Belt
WHO/EMC/BAC/98.3 Control of epidemic meningococcal disease. WHO practical guidelines. 2nd edition World Health Organization Emerging and other Communicable Diseases, Surveillance and Control This document has been downloaded from the WHO/EMC Web site. The original cover pages and lists of participants are not included. See http://www.who.int/emc for more information. © World Health Organization This document is not a formal publication of the World Health Organization (WHO), and all rights are reserved by the Organization. The document may, however, be freely reviewed, abstracted, reproduced and translated, in part or in whole, but not for sale nor for use in conjunction with commercial purposes. The views expressed in documents by named authors are solely the responsibility of those authors. The mention of specific companies or specific manufacturers' products does no imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. CONTENTS CONTENTS ................................................................................... i PREFACE ..................................................................................... vii INTRODUCTION ......................................................................... 1 1. MAGNITUDE OF THE PROBLEM ........................................................3 1.1 REVIEW OF EPIDEMICS SINCE THE 1970S .......................................................................................... 3 Geographical distribution -
Virus-Host Interaction: the Multifaceted Roles of Ifitms And
Virus-Host Interaction: The Multifaceted Roles of IFITMs and LY6E in HIV Infection DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Jingyou Yu Graduate Program in Comparative and Veterinary Medicine The Ohio State University 2018 Dissertation Committee: Shan-Lu Liu, MD, PhD, Advisor Patrick L. Green, PhD Jianrong Li, DVM., PhD Jesse J. Kwiek, PhD Copyrighted by Jingyou Yu 2018 Abstract With over 1.8 million newly infected people each year, the worldwide HIV-1 epidemic remains an imperative challenge for public health. Recent work has demonstrated that type I interferons (IFNs) efficiently suppress HIV infection through induction of hundreds of interferon stimulated genes (ISGs). These ISGs target distinct infection stages of invading pathogens and shape innate immunity. Among these, interferon induced transmembrane proteins (IFITMs) and lymphocyte antigen 6 complex, locus E (LY6E) have been shown to differentially modulate viral infections. However, their effects on HIV are not fully understood. In my thesis work, I provided evidence in Chapter 2 showing that IFITM proteins, particularly IFITM2 and IFITM3, specifically antagonize the HIV-1 envelope glycoprotein (Env), thereby inhibiting viral infection. IFITM proteins interacted with HIV-1 Env in viral producer cells, leading to impaired Env processing and virion incorporation. Notably, the level of IFITM incorporation into HIV-1 virions did not strictly correlate with the extent of inhibition. Prolonged passage of HIV-1 in IFITM-expressing T lymphocytes led to emergence of Env mutants that overcome IFITM restriction. The ability of IFITMs to inhibit cell-to-cell infection can be extended to HIV-1 primary isolates, HIV-2 and SIVs; however, the extent of inhibition appeared to be virus- strain dependent. -
Novel Risk Factors for Coronavirus Disease-Associated Mucormycosis (CAM): a Case Control Study During the Outbreak in India
medRxiv preprint doi: https://doi.org/10.1101/2021.07.24.21261040; this version posted July 26, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . Novel risk factors for Coronavirus disease-associated mucormycosis (CAM): a case control study during the outbreak in India Umang Arora1, Megha Priyadarshi1, Varidh Katiyar2, Manish Soneja1, Prerna Garg1, Ishan Gupta1,- Vishwesh Bharadiya1, Parul Berry1, Tamoghna Ghosh1, Lajjaben Patel1 , Radhika Sarda1, Shreya Garg3, Shubham Agarwal1, Veronica Arora4, Aishwarya Ramprasad1, Amit Kumar1, Rohit Kumar Garg1, Parul Kodan1, Neeraj Nischal1, Gagandeep Singh5, Pankaj Jorwal1, Arvind Kumar1, Upendra Baitha1, Ved Prakash Meena1, Animesh Ray1, Prayas Sethi1, , Immaculata Xess5, Naval Vikram1, Sanjeev Sinha1, Ashutosh Biswas1,Alok Thakar3, Sushma Bhatnagar6, Anjan Trikha7, Naveet Wig1 1Department of Medicine, AIIMS, Delhi, India 2Department of Neurosurgery, AIIMS, Delhi, India 3Department of Otolaryngology & Head-Neck Surgery, AIIMS, Delhi, India 4Department of Medical Genetics, Sir Ganga Ram Hospital, Delhi, India 5Department of Microbiology, AIIMS, Delhi, India 6Department of Onco-anaesthesia and Palliative Medicine, AIIMS, Delhi, India 7Department of Anaesthesiology, Pain Medicine and Critical Care, AIIMS, Delhi, India 1. Umang Arora, MD (Medicine), Junior Resident, Department of Medicine, AIIMS, Delhi, India. E-mail ID: [email protected] 2. Megha Priyadarshi, DM (Infectious disease), Junior Resident, Department of Medicine, AIIMS, Delhi, India. E-mail ID: [email protected] 3. Varidh Katiyar, MCh (Neurosurgery), Chief Resident, Department of Neurosurgery AIIMS, Delhi, India. E-mail ID: [email protected] 4. -
Virus World As an Evolutionary Network of Viruses and Capsidless Selfish Elements
Virus World as an Evolutionary Network of Viruses and Capsidless Selfish Elements Koonin, E. V., & Dolja, V. V. (2014). Virus World as an Evolutionary Network of Viruses and Capsidless Selfish Elements. Microbiology and Molecular Biology Reviews, 78(2), 278-303. doi:10.1128/MMBR.00049-13 10.1128/MMBR.00049-13 American Society for Microbiology Version of Record http://cdss.library.oregonstate.edu/sa-termsofuse Virus World as an Evolutionary Network of Viruses and Capsidless Selfish Elements Eugene V. Koonin,a Valerian V. Doljab National Center for Biotechnology Information, National Library of Medicine, Bethesda, Maryland, USAa; Department of Botany and Plant Pathology and Center for Genome Research and Biocomputing, Oregon State University, Corvallis, Oregon, USAb Downloaded from SUMMARY ..................................................................................................................................................278 INTRODUCTION ............................................................................................................................................278 PREVALENCE OF REPLICATION SYSTEM COMPONENTS COMPARED TO CAPSID PROTEINS AMONG VIRUS HALLMARK GENES.......................279 CLASSIFICATION OF VIRUSES BY REPLICATION-EXPRESSION STRATEGY: TYPICAL VIRUSES AND CAPSIDLESS FORMS ................................279 EVOLUTIONARY RELATIONSHIPS BETWEEN VIRUSES AND CAPSIDLESS VIRUS-LIKE GENETIC ELEMENTS ..............................................280 Capsidless Derivatives of Positive-Strand RNA Viruses....................................................................................................280 -
University of California, Irvine
UNIVERSITY OF CALIFORNIA, IRVINE Deciphering the mechanism of TDP2/VPg unlinkase activity during picornavirus infections DISSERTATION Submitted in partial satisfaction of the requirements for the degree of DOCTOR OF PHILOSOPHY in Biomedical Sciences by Autumn Candace Holmes Dissertation Committee: Dr. Bert L. Semler, Chair Dr. Paul Gershon Dr. Michael McClelland Dr. Suzanne Sandmeyer 2019 © 2019 Autumn C. Holmes TABLE OF CONTENTS Page List of figures iii List of tables v Acknowledgements vi Curriculum vitae vii Abstract of the dissertation ix CHAPTER 1: Introduction Summary 1 Significance 2 Picornavirus translation, RNA synthesis, and role of VPg 9 5’ tyrosyl-DNA phosphodiesterase 2 as VPg unlinkase 20 Biological significance of VPg unlinkase during picornavirus infections 27 CHAPTER 2: Post-translational effects of TDP2 VPg unlinkase activity during picornavirus infection in a human cell model Summary 30 Introduction 31 Results 36 Discussion 71 Materials and Methods 77 CHAPTER 3: Differential patterns of TDP2 and VP1 subcellular localization during picornavirus infections of multiple human cell lines Summary 84 Introduction 85 Results 88 Discussion 106 Materials and Methods 110 CHAPTER 4: Final conclusions and overall significance 112 REFERENCES 120 ii LIST OF FIGURES Page Figure 1.1 Schematic of the picornavirus genome 11 Figure 1.2 Forms of the viral RNA that arise during picornavirus infections and their linkage to VPg 19 Figure 1.3 Cellular roles of TDP2 beyond DNA repair 26 Figure 2.1 Binding of PCBP and 3CDpro to the poliovirus -
Noroviruses Subvert the Core Stress Granule Component G3BP1 to Promote Viral Vpg-Dependent Translation
Washington University School of Medicine Digital Commons@Becker Open Access Publications 8-12-2019 Noroviruses subvert the core stress granule component G3BP1 to promote viral VPg-dependent translation Myra Hosmillo Jia Lu Michael R. McAllaster James B. Eaglesham Xinjie Wang See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Authors Myra Hosmillo, Jia Lu, Michael R. McAllaster, James B. Eaglesham, Xinjie Wang, Edward Emmott, Patricia Domingues, Yasmin Chaudhry, Tim J. Fitzmaurice, Matthew K.H. Tung, Marc Dominik Panas, Gerald McInerney, Nicolas Locker, Craig B. Wilen, and Ian G. Goodfellow RESEARCH ARTICLE Noroviruses subvert the core stress granule component G3BP1 to promote viral VPg-dependent translation Myra Hosmillo1†, Jia Lu1†, Michael R McAllaster2†, James B Eaglesham1,3, Xinjie Wang1,4, Edward Emmott1,5,6, Patricia Domingues1, Yasmin Chaudhry1, Tim J Fitzmaurice1, Matthew KH Tung1, Marc Dominik Panas7, Gerald McInerney7, Nicolas Locker8, Craig B Wilen9*, Ian G Goodfellow1* 1Division of Virology, Department of Pathology, University of Cambridge, Cambridge, United Kingdom; 2Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, United States; 3Department of Microbiology, Harvard Medical School, Boston, United States; 4Institute for Brain Research and Rehabilitation, South China Normal University, Guangzhou, China; 5Department of Bioengineering, Northeastern University, Boston, United States; 6Barnett Institute for Chemical -
The Interaction Between Human Antimicrobial Use and the Risk of Foodborne Zoonotic Bacteria
Downloaded from orbit.dtu.dk on: Dec 20, 2017 The interaction between human antimicrobial use and the risk of foodborne zoonotic bacteria Koningstein, Maike; Hald, Tine; Mølbak, Kåre Publication date: 2014 Document Version Peer reviewed version Link back to DTU Orbit Citation (APA): Koningstein, M., Hald, T., & Mølbak, K. (2014). The interaction between human antimicrobial use and the risk of foodborne zoonotic bacteria. National Food Institute, Technical University of Denmark. General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. • Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. The interaction between human antimicrobial use and the risk of foodborne zoonotic bacteria Maike Koningstein, M.Sc. PhD Thesis 2013 Statens Serum Institute Department of Infectious Disease Epidemiology Artillerivej 5, 2300 Copenhagen, Denmark and National Food Institute, DTU Department for Microbiology -
Isolation and Characterization of a New Vesivirus from Rabbits
Virology 337 (2005) 373 – 383 www.elsevier.com/locate/yviro Isolation and characterization of a new Vesivirus from rabbits Jose´ M. Martı´n-Alonsoa, Douglas E. Skillingb, Lorenzo Gonza´lez-Molledaa, Gloria del Barrioa,A´ ngeles Machı´na, Nathan K. Keeferb, David O. Matsonc, Patrick L. Iversend, Alvin W. Smithb, Francisco Parraa,* aDepartamento de Bioquı´mica y Biologı´a Molecular, Instituto Universitario de Biotecnologı´a de Asturias, Edificio Santiago Gasco´n, Campus El Cristo, Universidad de Oviedo, 33006 Oviedo, Spain bLaboratory for Calicivirus Studies, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331, USA cChildren’s Hospital of The King’s Daughters, Eastern Virginia Medical School, Norfolk, VA 23507, USA dAVI BioPharma 4575 SW Research Way, Corvallis, OR 97333, USA Received 8 March 2005; returned to author for revision 4 April 2005; accepted 19 April 2005 Available online 17 May 2005 Abstract This report describes the isolation, cDNA cloning, complete genome nucleotide sequence, and partial characterization of a new cultivable calicivirus isolated from juvenile feeder European rabbits (Oryctolagus cuniculus) showing symptoms of diarrhea. Absence of neutralization by type-specific neutralizing antibodies for 40 caliciviruses and phylogenetic sequence comparisons of the open reading frame 1-encoded polyprotein with those of other caliciviruses demonstrate that this new calicivirus is a putative novel member of the Vesivirus genus which is closely related to the marine calicivirus subgroup. According to -
Investigating the Role of PIR1 and CD200R1 in the Innate Immune Response to Viral Pathogens
University of Massachusetts Medical School eScholarship@UMMS GSBS Dissertations and Theses Graduate School of Biomedical Sciences 2017-05-30 Investigating the Role of PIR1 and CD200R1 in the Innate Immune Response to Viral Pathogens Christopher R. MacKay University of Massachusetts Medical School Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/gsbs_diss Part of the Immunity Commons, Immunology of Infectious Disease Commons, Pathogenic Microbiology Commons, and the Virology Commons Repository Citation MacKay CR. (2017). Investigating the Role of PIR1 and CD200R1 in the Innate Immune Response to Viral Pathogens. GSBS Dissertations and Theses. https://doi.org/10.13028/M2602R. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/901 Creative Commons License This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in GSBS Dissertations and Theses by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. INVESTIGATING THE ROLE OF PIR1 AND CD200R1 IN THE INNATE IMMUNE RESPONSE TO VIRAL PATHOGENS A Dissertation Presented by CHRISTOPHER ROBERT MACKAY Submitted to the Faculty of the University of Massachusetts Graduate School of Biomedical Sciences, Worcester in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY May 30, 2017 M.D./Ph.D. Program INVESTIGATING THE ROLE OF PIR1 AND CD200R1 IN THE INNATE IMMUNE RESPONSE TO VIRAL PATHOGENS A Dissertation Presented by CHRISTOPHER ROBERT MACKAY The signatures of the Dissertation Defense Committee signifies completion and approval as to style and content of the Dissertation Evelyn A.