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Characterization of the Matrix Proteins of the Fish Rhabdovirus, Infectious Hematopoietic Necrosis Virus
AN ABSTRACT OF THE THESIS OF Patricia A. Ormonde for the degree of Master of Science presented on April 14. 1995. Title: Characterization of the Matrix Proteins of the Fish Rhabdovinis, Infectious Hematopoietic Necrosis Virus. Redacted for Privacy Abstract approved: Jo-Ann C. ong Infectious hematopoietic necrosis virus (1HNV) is an important fish pathogen enzootic in salmon and trout populations of the Pacific Northwestern United States. Occasional epizootics in fish hatcheries can result in devastating losses of fish stocks. The complete nucleotide sequence of IHNV has not yet been determined. This knowledge is the first step towards understanding the roles viral proteins play in IHNV infection, and is necessary for determining the relatedness of IHNV to other rhabdoviruses. The glycoprotein, nucleocapsid and non-virion genes of IHNV have been described previously; however, at the initiation of this study, very little was known about the matrix protein genes. Rhabdoviral matrix proteins have been found to be important in viral transcription and virion assembly. This thesis describes the preliminary characterization of the M1 and M2 matrix proteins of IHNV. In addition, the trout humoral immune response to M1 and M2 proteins expressed from plasmid DNA injected into the fish was investigated. This work may prove useful in designing future vaccines against IHN. The sequences of M1 phosphoprotein and M2 matrix protein genes of IHNV were determined from both genomic and mRNA clones. Analysis of the sequences indicated that the predicted open reading frame of M1 gene encoded a 230 amino acid protein with a estimated molecular weight of 25.6 kDa. Further analysis revealed a second open reading frame encoding a 42 amino acid protein with a calculated molecular weight of 4.8 kDa. -
10.2.2 Nomenclature of Viruses and Taxonomic Groups Bacterial Viruses Such As T1, T2 and Φx174
Classification and nomenclature of viruses History of virus classification • Type of host • Type of disease • Transmition by an arthropod vector • Nucleic acid type • SS or DS • Segmented • Size of the virion • Capsid simmetry • Envelope Nomenclature • Small, icosahedral, single-stranded DNA viruses of animals were called parvoviruses (Latin parvus = small) • Nematode-transmitted polyhedral (icosahedral) viruses of plants were called nepoviruses • Phages T2, T4 and T6 were called T even phages • Serological relationships between viruses were investigated • Distinct strains (serotypes) could be distinguished in serological tests • Antisera against purified virions • Serotypes reflect differences in virus proteins International Committee on Taxonomy of Viruses • Order had to be brought • ICTV was formed in 1966 • Many working groups and is advised by virologists around the world • Rules for the nomenclature and classification of viruses • Considers proposals for new taxonomic groups and virus names • Approved are published in book form and on the web Modern virus classification and nomenclature • Each order, family, subfamily and genus is defined by viral characteristics that are necessary for membership of that group. Classification based on genome sequences • Similarity is represented in diagrams known as phylogenetic trees. • Rooted- the tree begins at a root which is assumed to be the ancestor of the viruses in the tree. • Unrooted- no assumption is made about the ancestor of the viruses in the tree. 10.2.2 Nomenclature of viruses and taxonomic groups Bacterial viruses such as T1, T2 and ϕX174. Viruses of humans and other vertebrates diseases that they cause Examples: measles virus, smallpox virus, foot and mouth disease virus Some viruses city, town or river Examples: Newcastle disease virus, Norwalk virus, Ebola virus Insect viruses Many insect viruses were named after the insect, with an indication of the effect of infection on the host. -
2020 Taxonomic Update for Phylum Negarnaviricota (Riboviria: Orthornavirae), Including the Large Orders Bunyavirales and Mononegavirales
Archives of Virology https://doi.org/10.1007/s00705-020-04731-2 VIROLOGY DIVISION NEWS 2020 taxonomic update for phylum Negarnaviricota (Riboviria: Orthornavirae), including the large orders Bunyavirales and Mononegavirales Jens H. Kuhn1 · Scott Adkins2 · Daniela Alioto3 · Sergey V. Alkhovsky4 · Gaya K. Amarasinghe5 · Simon J. Anthony6,7 · Tatjana Avšič‑Županc8 · María A. Ayllón9,10 · Justin Bahl11 · Anne Balkema‑Buschmann12 · Matthew J. Ballinger13 · Tomáš Bartonička14 · Christopher Basler15 · Sina Bavari16 · Martin Beer17 · Dennis A. Bente18 · Éric Bergeron19 · Brian H. Bird20 · Carol Blair21 · Kim R. Blasdell22 · Steven B. Bradfute23 · Rachel Breyta24 · Thomas Briese25 · Paul A. Brown26 · Ursula J. Buchholz27 · Michael J. Buchmeier28 · Alexander Bukreyev18,29 · Felicity Burt30 · Nihal Buzkan31 · Charles H. Calisher32 · Mengji Cao33,34 · Inmaculada Casas35 · John Chamberlain36 · Kartik Chandran37 · Rémi N. Charrel38 · Biao Chen39 · Michela Chiumenti40 · Il‑Ryong Choi41 · J. Christopher S. Clegg42 · Ian Crozier43 · John V. da Graça44 · Elena Dal Bó45 · Alberto M. R. Dávila46 · Juan Carlos de la Torre47 · Xavier de Lamballerie38 · Rik L. de Swart48 · Patrick L. Di Bello49 · Nicholas Di Paola50 · Francesco Di Serio40 · Ralf G. Dietzgen51 · Michele Digiaro52 · Valerian V. Dolja53 · Olga Dolnik54 · Michael A. Drebot55 · Jan Felix Drexler56 · Ralf Dürrwald57 · Lucie Dufkova58 · William G. Dundon59 · W. Paul Duprex60 · John M. Dye50 · Andrew J. Easton61 · Hideki Ebihara62 · Toufc Elbeaino63 · Koray Ergünay64 · Jorlan Fernandes195 · Anthony R. Fooks65 · Pierre B. H. Formenty66 · Leonie F. Forth17 · Ron A. M. Fouchier48 · Juliana Freitas‑Astúa67 · Selma Gago‑Zachert68,69 · George Fú Gāo70 · María Laura García71 · Adolfo García‑Sastre72 · Aura R. Garrison50 · Aiah Gbakima73 · Tracey Goldstein74 · Jean‑Paul J. Gonzalez75,76 · Anthony Grifths77 · Martin H. Groschup12 · Stephan Günther78 · Alexandro Guterres195 · Roy A. -
The LUCA and Its Complex Virome in Another Recent Synthesis, We Examined the Origins of the Replication and Structural Mart Krupovic , Valerian V
PERSPECTIVES archaea that form several distinct, seemingly unrelated groups16–18. The LUCA and its complex virome In another recent synthesis, we examined the origins of the replication and structural Mart Krupovic , Valerian V. Dolja and Eugene V. Koonin modules of viruses and posited a ‘chimeric’ scenario of virus evolution19. Under this Abstract | The last universal cellular ancestor (LUCA) is the most recent population model, the replication machineries of each of of organisms from which all cellular life on Earth descends. The reconstruction of the four realms derive from the primordial the genome and phenotype of the LUCA is a major challenge in evolutionary pool of genetic elements, whereas the major biology. Given that all life forms are associated with viruses and/or other mobile virion structural proteins were acquired genetic elements, there is no doubt that the LUCA was a host to viruses. Here, by from cellular hosts at different stages of evolution giving rise to bona fide viruses. projecting back in time using the extant distribution of viruses across the two In this Perspective article, we combine primary domains of life, bacteria and archaea, and tracing the evolutionary this recent work with observations on the histories of some key virus genes, we attempt a reconstruction of the LUCA virome. host ranges of viruses in each of the four Even a conservative version of this reconstruction suggests a remarkably complex realms, along with deeper reconstructions virome that already included the main groups of extant viruses of bacteria and of virus evolution, to tentatively infer archaea. We further present evidence of extensive virus evolution antedating the the composition of the virome of the last universal cellular ancestor (LUCA; also LUCA. -
Link of a Ubiquitous Human Coronavirus to Dromedary Camels
Link of a ubiquitous human coronavirus to dromedary camels Victor M. Cormana,b,1, Isabella Eckerlea,1, Ziad A. Memishc, Anne M. Liljanderd, Ronald Dijkmane,f, Hulda Jonsdottire,f, Kisi J. Z. Juma Ngeiywag, Esther Kamaug, Mario Younanh, Malakita Al Masrii, Abdullah Assirii, Ilona Gluecksj, Bakri E. Musak, Benjamin Meyera, Marcel A. Müllera, Mosaad Hilalil, Set Bornsteinm, Ulrich Werneryn, Volker Thiele,f, Joerg Joresd,o, Jan Felix Drexlera,b,2, and Christian Drostena,b,2 aUniversity of Bonn Medical Centre, 53127 Bonn, Germany; bGerman Centre for Infection Research, partner site Bonn–Cologne, Germany; cCollege of Medicine, Alfaisal University, 11533 Riyadh, Kingdom of Saudi Arabia; dInternational Livestock Research Institute, Nairobi, Kenya; eDepartment of Infectious Diseases and Pathobiology, Vetsuisse Faculty Bern, University of Bern, 3012 Bern, Switzerland; fFederal Department of Home Affairs, Institute of Virology and Immunology, Bern and Mittelhausern, Switzerland; gMinistry of Agriculture, Livestock, and Fisheries, State Department of Livestock, Department of Veterinary Services, Nairobi, Kenya; hVétérinaires Sans Frontières Germany, Nairobi, Kenya; iMinistry of Health, 11176 Riyadh, Kingdom of Saudi Arabia; jVétérinaires Sans Frontières Suisse, Nairobi, Kenya; kMinistry of Science and Communication, Khartoum, Sudan; lCairo University, 12613 Giza, Egypt; mNational Veterinary Institute, 75189 Uppsala, Sweden; nCentral Veterinary Research Laboratory, Dubai, United Arab Emirates; and oInstitute of Veterinary Bacteriology, University of Bern, 3001 Bern, Switzerland Edited by Luis Enjuanes, Centro Nacional de Biotecnología-Consejo Superior de Investigaciones Cientificas, Madrid, Spain, and accepted by Editorial Board Member Diane E. Griffin June 27, 2016 (received for review March 17, 2016) The four human coronaviruses (HCoVs) are globally endemic respiratory ecological history of these ubiquitous human pathogens. -
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]. -
Everything You Always Wanted to Know About Rabies Virus ♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣ (But Were Afraid to Ask) Benjamin M
ANNUAL REVIEWS Further Click here to view this article's online features: t%PXOMPBEmHVSFTBT115TMJEFT t/BWJHBUFMJOLFESFGFSFODFT t%PXOMPBEDJUBUJPOT Everything You Always Wanted t&YQMPSFSFMBUFEBSUJDMFT t4FBSDILFZXPSET to Know About Rabies Virus (But Were Afraid to Ask) Benjamin M. Davis,1 Glenn F. Rall,2 and Matthias J. Schnell1,2,3 1Department of Microbiology and Immunology and 3Jefferson Vaccine Center, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania, 19107; email: [email protected] 2Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111 Annu. Rev. Virol. 2015. 2:451–71 Keywords First published online as a Review in Advance on rabies virus, lyssaviruses, neurotropic virus, neuroinvasive virus, viral June 24, 2015 transport The Annual Review of Virology is online at virology.annualreviews.org Abstract This article’s doi: The cultural impact of rabies, the fatal neurological disease caused by in- 10.1146/annurev-virology-100114-055157 fection with rabies virus, registers throughout recorded history. Although Copyright c 2015 by Annual Reviews. ⃝ rabies has been the subject of large-scale public health interventions, chiefly All rights reserved through vaccination efforts, the disease continues to take the lives of about 40,000–70,000 people per year, roughly 40% of whom are children. Most of Access provided by Thomas Jefferson University on 11/13/15. For personal use only. Annual Review of Virology 2015.2:451-471. Downloaded from www.annualreviews.org these deaths occur in resource-poor countries, where lack of infrastructure prevents timely reporting and postexposure prophylaxis and the ubiquity of domestic and wild animal hosts makes eradication unlikely. Moreover, al- though the disease is rarer than other human infections such as influenza, the prognosis following a bite from a rabid animal is poor: There is cur- rently no effective treatment that will save the life of a symptomatic rabies patient. -
Rapid Protein Sequence Evolution Via Compensatory Frameshift Is Widespread in RNA Virus Genomes
Park and Hahn BMC Bioinformatics (2021) 22:251 https://doi.org/10.1186/s12859-021-04182-9 RESEARCH Open Access Rapid protein sequence evolution via compensatory frameshift is widespread in RNA virus genomes Dongbin Park and Yoonsoo Hahn* *Correspondence: [email protected] Abstract Department of Life Science, Background: RNA viruses possess remarkable evolutionary versatility driven by the Chung-Ang University, Seoul 06794, South Korea high mutability of their genomes. Frameshifting nucleotide insertions or deletions (indels), which cause the premature termination of proteins, are frequently observed in the coding sequences of various viral genomes. When a secondary indel occurs near the primary indel site, the open reading frame can be restored to produce functional proteins, a phenomenon known as the compensatory frameshift. Results: In this study, we systematically analyzed publicly available viral genome sequences and identifed compensatory frameshift events in hundreds of viral protein- coding sequences. Compensatory frameshift events resulted in large-scale amino acid diferences between the compensatory frameshift form and the wild type even though their nucleotide sequences were almost identical. Phylogenetic analyses revealed that the evolutionary distance between proteins with and without a compensatory frameshift were signifcantly overestimated because amino acid mismatches caused by compensatory frameshifts were counted as substitutions. Further, this could cause compensatory frameshift forms to branch in diferent locations in the protein and nucleotide trees, which may obscure the correct interpretation of phylogenetic rela- tionships between variant viruses. Conclusions: Our results imply that the compensatory frameshift is one of the mecha- nisms driving the rapid protein evolution of RNA viruses and potentially assisting their host-range expansion and adaptation. -
The Multi-Functional Reovirus Σ3 Protein Is a Virulence Factor That Suppresses Stress Granule Formation to Allow Viral Replicat
bioRxiv preprint doi: https://doi.org/10.1101/2021.03.22.436456; this version posted March 22, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 The multi-functional reovirus σ3 protein is a 2 virulence factor that suppresses stress granule 3 formation to allow viral replication and myocardial 4 injury 5 6 Yingying Guo1, Meleana Hinchman1, Mercedes Lewandrowski1, Shaun Cross1,2, Danica 7 M. Sutherland3,4, Olivia L. Welsh3, Terence S. Dermody3,4,5, and John S. L. Parker1* 8 9 1Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University, 10 Ithaca, New York 14853; 2Cornell Institute of Host-Microbe Interactions and Disease, 11 Cornell University, Ithaca, New York 14853; Departments of 3Pediatrics and 12 4Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, 13 Pittsburgh, PA 15224; and 5Institute of Infection, Inflammation, and Immunity, UPMC 14 Children’s Hospital of Pittsburgh, PA 15224 15 16 17 Running head: REOVIRUS SIGMA3 PROTEIN SUPPRESSES STRESS GRANULES 18 DURING INFECTION 19 20 * Corresponding author. Mailing address: Baker Institute for Animal Health, College 21 of Veterinary Medicine, Cornell University, Hungerford Hill Road; Ithaca, NY 14853. 22 Phone: (607) 256-5626. Fax: (607) 256-5608. E-mail: [email protected] 23 Word count for abstract: 261 24 Word count for text: 12282 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.03.22.436456; this version posted March 22, 2021. -
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 -
Structure and Function of the Influenza a Virus Non-Structural Protein 1 Chang Woo Han1†, Mi Suk Jeong2†, and Se Bok Jang1*
J. Microbiol. Biotechnol. (2019), 29(8), 1184–1192 https://doi.org/10.4014/jmb.1903.03053 Research Article Review jmb Structure and Function of the Influenza A Virus Non-Structural Protein 1 Chang Woo Han1†, Mi Suk Jeong2†, and Se Bok Jang1* 1Department of Molecular Biology, College of Natural Sciences, Pusan National University, Busan 46241, Republic of Korea 2Korea Nanobiotechnology Center, Pusan National University, Busan 46241, Republic of Korea Received: March 25, 2019 Revised: May 27, 2019 The influenza A virus is a highly infectious respiratory pathogen that sickens many people Accepted: June 3, 2019 with respiratory disease annually. To prevent outbreaks of this viral infection, an First published online understanding of the characteristics of virus-host interaction and development of an anti-viral June 4, 2019 agent is urgently needed. The influenza A virus can infect mammalian species including *Corresponding author humans, pigs, horses and seals. Furthermore, this virus can switch hosts and form a novel Phone: +82-51-510-2523; lineage. This so-called zoonotic infection provides an opportunity for virus adaptation to the Fax: +82-51-581-2544; E-mail: [email protected] new host and leads to pandemics. Most influenza A viruses express proteins that antagonize the antiviral defense of the host cell. The non-structural protein 1 (NS1) of the influenza A † These authors contributed virus is the most important viral regulatory factor controlling cellular processes to modulate equally to this work. host cell gene expression and double-stranded RNA (dsRNA)-mediated antiviral response. This review focuses on the influenza A virus NS1 protein and outlines current issues including the life cycle of the influenza A virus, structural characterization of the influenza A virus NS1, interaction between NS1 and host immune response factor, and design of inhibitors resistant pISSN 1017-7825, eISSN 1738-8872 to the influenza A virus. -
Introduction to Viroids and Prions
Harriet Wilson, Lecture Notes Bio. Sci. 4 - Microbiology Sierra College Introduction to Viroids and Prions Viroids – Viroids are plant pathogens made up of short, circular, single-stranded RNA molecules (usually around 246-375 bases in length) that are not surrounded by a protein coat. They have internal base-pairs that cause the formation of folded, three-dimensional, rod-like shapes. Viroids apparently do not code for any polypeptides (proteins), but do cause a variety of disease symptoms in plants. The mechanism for viroid replication is not thoroughly understood, but is apparently dependent on plant enzymes. Some evidence suggests they are related to introns, and that they may also infect animals. Disease processes may involve RNA-interference or activities similar to those involving mi-RNA. Prions – Prions are proteinaceous infectious particles, associated with a number of disease conditions such as Scrapie in sheep, Bovine Spongiform Encephalopathy (BSE) or Mad Cow Disease in cattle, Chronic Wasting Disease (CWD) in wild ungulates such as muledeer and elk, and diseases in humans including Creutzfeld-Jacob disease (CJD), Gerstmann-Straussler-Scheinker syndrome (GSS), Alpers syndrome (in infants), Fatal Familial Insomnia (FFI) and Kuru. These diseases are characterized by loss of motor control, dementia, paralysis, wasting and eventually death. Prions can be transmitted through ingestion, tissue transplantation, and through the use of comtaminated surgical instruments, but can also be transmitted from one generation to the next genetically. This is because prion proteins are encoded by genes normally existing within the brain cells of various animals. Disease is caused by the conversion of normal cell proteins (glycoproteins) into prion proteins.