Everything You Always Wanted to Know About Rabies Virus ♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣♣ (But Were Afraid to Ask) Benjamin M
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JOURNAL of VIROLOGY VOLUME 54 * JUNE 1985 * NUMBER 3 Arnold J
JOURNAL OF VIROLOGY VOLUME 54 * JUNE 1985 * NUMBER 3 Arnold J. Levine, Editor in Chief Michael B. A. Oldstone, Editor (1988) (1989) Scripps Clinic & Research Foundation Princeton University La Jolla, Calif. Princeton, N.J. Thomas E. Shenk, Editor (1989) David T. Denhardt, Editor (1987) Princeton University University of Western Ontario Princeton, N.J. London, Ontario, Canada Anna Marie Skalka, Editor (1989) Bernard N. Fields, Editor (1988) Hoffmann-La Roche Inc. Harvard Medical School Nutley, N.J. Boston, Mass. Robert A. Weisberg, Editor (1988) Robert M. Krug, Editor (1987) National Institute of Child Health Sloan-Kettering Institute and Human Development New York, N.Y. Bethesda, Md. EDITORIAL BOARD David Baltimore (1987) Hidesaburo Hanafusa (1986) Lois K. Miller (1985) Priscilla A. Schaffer (1987) Amiya K. Banerjee (1985) William S. Hayward (1987) Peter Model (1986) Sondra Schlesinger (1986) Andrew Becker (1985) Roger Hendrix (1987) Bernard Moss (1986) June R. Scott (1986) Tamar Ben-Porat (1987) Martin Hirsch (1986) Fred Murphy (1986) Bart Sefton (1985) Kenneth I. Berns (1985) John J. Holland (1987) Nancy G. Nossal (1987) Phillip A. Sharp (1985) Michael Botchan (1986) Ian H. Holmes (1986) Abner Notkins (1986) Charles J. Sherr (1987) David Botstein (1985) Robert W. Honess (1986) J. Thomas Parsons (1986) Saul J. Silverstein (1985) Barrie J. Carter (1987) Nancy Hopkins (1986) Ulf G. Pettersson (1986) Purnell Choppin (1986) Peter M. Howley (1987) Lennart Philipson (1987) Patricia G. Spear (1987) John M. Coffin (1986) Alice S. Huang (1987) Lewis I. Pizer (1987) Nat Sternberg (1986) Geoffrey M. Cooper (1987) Tony Hunter (1986) Craig R. Pringle (1986) Mark F. Stinski (1986) Donald Court (1987) Masayori Inouye (1985) Carol Prives (1986) James Strauss (1987) Richard Courtney (1986) Robert Kamen (1985) Robert Purcell (1986) F. -
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. -
Antibody-Mediated Enhancement of Rabies Virus
542 Nature Vol. 290 16 April 1981 rearranged, K-chain gene, for example; region than the salivary gland mRNA. It is Are these findings at all relevant to the only one of these is destined to appear in possible that this affects the translation rabies 'early death' effect? Rabies viruses the mRNA, the remainder being removed efficiences of the mRNA (see 'Discussion' were thought to be serologically identical, by differential splicing. in Young et al.). Although the explanation but a number of rabies-related viruses are Why does the mouse go to all this for this fascinating genetic mechanism is now knownl2 , and antigenic variation trouble? Any explanation should consider the subject of future work, it is, of course, between rabies virus strains has been estab the fact that a-amylase mRNA accounts likely to be tied up with the primary lished I3 • Mice inoculated with Lagos Bat or for 2 per cent of the cytoplasmic mRNA in question - what determines the different Mokola viruses, two of the rabies-related the salivary gland, but only 0.02 per cent in level of a-amylase in two different tissues? viruses, and subsequently challenged with liver. This level may reflect the transcrip In the rat (and other mammals) the rabies virus, also died more quicklyl4. tion rate from the two genes; the 'salivary situation may be even more complicated. These findings suggest that it is not gland' promoter would then be consider MacDonald and his co-workers (Nature essential to have homologous neutralizing ably stronger than the 'liver' promoter. 287, 17; 1980) have analysed the rat antibodies to produce the rabies 'early Alternatively, the rate of RNA processing a-amylase genes and these studies point to death' effect, but that cross-reacting sera andlor export to the cytoplasm may be at least five non-allelic a-amylase genes or may also be active in this system as in the different for the two mRNAs. -
Interactions in Escherichia Coli NAT STERNBERG Central Research and Development Department Experimental Station, E
JOURNAL OF BACTERIOLOGY, OCt. 1985, p. 490(493 Vol. 164, No. 1 0021-9193/85/100490-04$02.00/0 Copyright © 1985, American Society for Microbiology Evidence that Adenine Methylation Influences DNA-Protein Interactions in Escherichia coli NAT STERNBERG Central Research and Development Department Experimental Station, E. l. Du Pont de Nemours and Co., Inc., Wilmington, Delaware 19898 In this review, most of the information presented will be functional recA gene. K. R. Peterson, K. F. Wertman, derived from studies with Escherichia coli K-12 (E. coli) and D. W. Mount, and M. G. Marinus have recently found that its related bacteriophages, simply because more is known the genes of the SOS regulon could be induced (1.7- to about methylation in these organisms than in any other. The 6-fold) by introducing a dam mutation into E. coli. The two methylated bases that have been detected in E. coli are affected genes include recA, lexA, uvrA, uvrB, sulA, dinD, 6-methyladenine (6-meAde) and 5-methylcytosine (7, 18). and dinF. The only SOS gene not effected is uvrD. Except Since little is known about the biological function of 6- for lexA and uvrB, none of the genes are fully induced. In methylcytosine, I will deal exclusively here with the studies essence, the cell adjusts the basal level of the SOS response on 6-meAde. to that needed without fully inducing the regulon. In this 6-meAde is the product of a reaction catalyzed by a case, the control of gene expression is probably an indirect methylase coded for by the bacterial dam gene (21). -
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. -
Characterizing and Evaluating the Zoonotic Potential of Novel Viruses Discovered in Vampire Bats
viruses Article Characterizing and Evaluating the Zoonotic Potential of Novel Viruses Discovered in Vampire Bats Laura M. Bergner 1,2,* , Nardus Mollentze 1,2 , Richard J. Orton 2 , Carlos Tello 3,4, Alice Broos 2, Roman Biek 1 and Daniel G. Streicker 1,2 1 Institute of Biodiversity, Animal Health and Comparative Medicine, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK; [email protected] (N.M.); [email protected] (R.B.); [email protected] (D.G.S.) 2 MRC–University of Glasgow Centre for Virus Research, Glasgow G61 1QH, UK; [email protected] (R.J.O.); [email protected] (A.B.) 3 Association for the Conservation and Development of Natural Resources, Lima 15037, Peru; [email protected] 4 Yunkawasi, Lima 15049, Peru * Correspondence: [email protected] Abstract: The contemporary surge in metagenomic sequencing has transformed knowledge of viral diversity in wildlife. However, evaluating which newly discovered viruses pose sufficient risk of infecting humans to merit detailed laboratory characterization and surveillance remains largely speculative. Machine learning algorithms have been developed to address this imbalance by ranking the relative likelihood of human infection based on viral genome sequences, but are not yet routinely Citation: Bergner, L.M.; Mollentze, applied to viruses at the time of their discovery. Here, we characterized viral genomes detected N.; Orton, R.J.; Tello, C.; Broos, A.; through metagenomic sequencing of feces and saliva from common vampire bats (Desmodus rotundus) Biek, R.; Streicker, D.G. and used these data as a case study in evaluating zoonotic potential using molecular sequencing Characterizing and Evaluating the data. -
Rabies Information for Dog Owners
Rabies Information for Dog Owners Key Facts Disease in dogs: • During initial days of illness, signs can be nonspecific, such as fever, anxiety and consumption of foreign items (e.g. blankets) • Progresses to more severe signs, such as: • Behavioral change (e.g. aggression, excitability) • Incoordination, loss of balance, disorientation, weakness • Hypersalivation • Seizures • Death results within 10 days of first signs of illness Rabies in dogs is not treatable. Vaccination is key to prevention: • Rabies vaccines are protective if given before exposure to the rabies virus. • Proof of dog vaccination is mandated by many jurisdictions and required for international travel. • Dogs not current on vaccination that are likely exposed to the rabies virus may be required to be euthanized or undergo a long and expensive quarantine. What is it? Rabies is caused by infection with the rabies virus. In North America, the most common wildlife rabies The virus lives in various species of mammals and species (termed reservoirs) vary regionally and is most commonly spread through bites from one include raccoons, skunks, foxes, coyotes, and animal to another or to a human (i.e. in an infected bats. Each year in the United States over 4,000 animal’s saliva). rabid animals are reported, including several Disease in dogs may begin with vague signs of hundred rabid dogs and cats, other domestic illness, but rapidly progresses to severe neurologic species (e.g., horses, cattle, sheep, goats) and signs (e.g. aggression, incoordination). Typically, thousands of wildlife animals. death occurs within 10 days of the first signs of illness. Where is it? The rabies virus is present in nearly all parts of the world. -
Viral Zoonotic Encephalitis: Australian Bat Lyssavirus and Hendra
Viral zoonotic encephalitis: Australian Bat Lyssavirus and Hendra Bev Paterson Hunter© by Medicalauthor Research Institute University of Newcastle Australia ESCMID OnlineEmail: [email protected] Library Encephalitis in Australia Causes substantial morbidity and mortality Herpes simplex virus is the most commonly identified causative pathogen 70% of adult encephalitis hospitalisations no pathogen identified 57% of deaths no pathogen identified (Reference: Huppatz et al. CDI,© 2009; by Huppatzauthor et al. EID, 2009) ESCMID Online Lecture Library Viral zoonotic encphalitis Several recently emerged or resurging pathogens are known to cause an encephalitis syndrome Vectorborne and transmitted flaviviruses – MVEV, WNEV-KUN and JEV © by author Bat-borne viruses – Australian Bat Lyssavirus (ABLV) and Hendra virus ESCMID Online Lecture Library Impact of climatic conditions © by author ESCMID Online Lecture Library Australian Bat Lyssavirus Australia has no endemic rabies ABLV is a member of the family Rhabdoviridae, genus Lyssavirus ABLV is very closely related to rabies (genotype 7 of the Lyssavirus genus) Reservoir is bats © by author Two deaths from ABLV ESCMID Online Lecture Library Human exposure © by author ESCMID Online Lecture Library Epidemiology of human disease Two fatal human cases – coastal Qld – encephalitis indistinguishable from classic rabies 1996 – 39yr female, a few weeks after scratches from bat 1998 – 37yr female, 27 months after bite from bat © by author References (Samaratunga -
Echohealth and the Identification of New Viruses
954 Microsc Microanal 11(Suppl 2), 2005 DOI: 10.1017/S1431927605504811 Copyright 2005 Microscopy Society of America ECOHEALTH AND THE IDENTIFICATIOIN OF NEW VIRUSES Dr Alex Hyatt BSc(Hons), DipEd, PhD Senior Principal Research Scientist Project Leader "Electron Microscopy & Iridoviruses" CSIRO, Livestock Industries, Australian Animal Health Laboratory 5 Portarlington Road, Geelong Vic 3220 During the past decade many new diseases have emerged from the environment and into society where there have been impacts on human and/or veterinary health, trade and the ‘health’ of the environment. In nearly all cases the emergence can be attributed to environmental perturbations via some aspect of human behaviour. Examples of such environmental perturbations can include altered habitat (changes in the number of vector breeding sites and/or host reservoirs), niche invasions (interspecies host-transfers), changes in biodiversity, human-induced genetic changes of disease vectors or pathogens (e.g. mosquito resistance , emergence of disease resistant strains of microbes) and environmental contamination of infectious agents (e.g. dissemination of microbes into water bodies). Whilst the significance of this area of ‘health’ is emerging in terms of politics, general health and trade there is a requirement to provide an infrastructure for the rapid and accurate identification of infectious agents that can be redistributed to new hosts and give rise to new diseases; these diseases are often referred to as emerging diseases. In virology, the recognised technologies associated with identification and charcterisation of infectious agents associated with emerging diseases include classical virology, serology, histopathology, and electron microscopy. Recent advances in molecular biology in areas such as real time PCR, genomic subtraction, microchip arrays in addition to other multiplex-based assays have caused some people to become confused about the on-going relevance of electron microscopy. -
Progressive Multifocal Leukoencephalopathy and the Spectrum of JC Virus-Related Disease
REVIEWS Progressive multifocal leukoencephalopathy and the spectrum of JC virus- related disease Irene Cortese 1 ✉ , Daniel S. Reich 2 and Avindra Nath3 Abstract | Progressive multifocal leukoencephalopathy (PML) is a devastating CNS infection caused by JC virus (JCV), a polyomavirus that commonly establishes persistent, asymptomatic infection in the general population. Emerging evidence that PML can be ameliorated with novel immunotherapeutic approaches calls for reassessment of PML pathophysiology and clinical course. PML results from JCV reactivation in the setting of impaired cellular immunity, and no antiviral therapies are available, so survival depends on reversal of the underlying immunosuppression. Antiretroviral therapies greatly reduce the risk of HIV-related PML, but many modern treatments for cancers, organ transplantation and chronic inflammatory disease cause immunosuppression that can be difficult to reverse. These treatments — most notably natalizumab for multiple sclerosis — have led to a surge of iatrogenic PML. The spectrum of presentations of JCV- related disease has evolved over time and may challenge current diagnostic criteria. Immunotherapeutic interventions, such as use of checkpoint inhibitors and adoptive T cell transfer, have shown promise but caution is needed in the management of immune reconstitution inflammatory syndrome, an exuberant immune response that can contribute to morbidity and death. Many people who survive PML are left with neurological sequelae and some with persistent, low-level viral replication in the CNS. As the number of people who survive PML increases, this lack of viral clearance could create challenges in the subsequent management of some underlying diseases. Progressive multifocal leukoencephalopathy (PML) is for multiple sclerosis. Taken together, HIV, lymphopro- a rare, debilitating and often fatal disease of the CNS liferative disease and multiple sclerosis account for the caused by JC virus (JCV). -
Congenital Cytomegalovirus Infection Alters Olfaction Before Hearing Deterioration in Mice
10424 • The Journal of Neuroscience, December 5, 2018 • 38(49):10424–10437 Development/Plasticity/Repair Congenital Cytomegalovirus Infection Alters Olfaction Before Hearing Deterioration In Mice X Franc¸oise Lazarini,1,2 Lida Katsimpardi,1,2* Sarah Levivien,1,2,3*Se´bastien Wagner,1,2 XPierre Gressens,3,4,5 Natacha Teissier,3,4,6† and Pierre-Marie Lledo1,2† 1Institut Pasteur, Perception and Memory Unit, F-75015 Paris, France, 2Centre National de la Recherche Scientifique, Unite´ Mixte de Recherche 3571, F-75015 Paris, France, 3PROTECT, INSERM, Unite´ 1141, F-75019 Paris, France, 4Paris Diderot University, Sorbonne Paris Cite´, F-75018 Paris, France, 5Center for Developing Brain, King’s College, London, WC2R2LS United Kingdom, and 6Pediatric Otorhinolaryngology Department, Robert Debre´ Hospital, Assistance Publique–Hoˆpitaux de Paris, F-75019 Paris, France In developed countries, cytomegalovirus (CMV)-infected newborns are at high risk of developing sensorineural handicaps such as hearing loss, requiring extensive follow-up. However, early prognostic tools for auditory damage in children are not yet available. In the fetus, CMV infection leads to early olfactory bulb (OB) damage, suggesting that olfaction might represent a valuable prognosis for neurological outcome of this viral infection. Here, we demonstrate that in utero CMV inoculation causes fetal infection and growth retardation in mice of both sexes. It disrupts OB normal development, leading to disproportionate OB cell layers and rapid major olfactory deficits. Olfaction is impaired as early as day 6 after birth in both sexes, long before the emergence of auditory deficits. Olfactometry in males reveals a long-lasting alteration in olfactory perception and discrimination, particularly in binary mixtures of monomolecular odorants. -
Eye-Opening Approach to Norovirus Surveillance
LETTERS Rapid collaboration between pub- DOI: 10.3201/eid1608.091380 of norovirus infections in society. lic health authorities in the Philippines We therefore present a new approach and Finland led to appropriate action References to estimate the number of cases and at the site of origin of the rabies case spread of norovirus infections in the 1. Meslin FX. Rabies as a traveler’s risk, es- within a few days. In a country in pecially in high-endemicity areas. J Travel community. which rabies is not endemic, diagnos- Med. 2005;Suppl 1:S30–40. We plotted the number of queries ing rabies and implementing control 2. Srinivasan A, Burton EC, Kuehnert MJ, for *vomit* (asterisks denote any pre- measures in healthcare settings are of- Rupprecht C, Sutker WL, Ksiazek TG, et fi x or suffi x) submitted to the search al. Rabies in Transplant Recipients Inves- ten diffi cult because of limited experi- tigation Team. Transmission of rabies vi- engine on a medical website in Swe- ence with this disease. The last human rus from an organ donor to four transplant den (www.vardguiden.se). This num- rabies case in Finland was diagnosed recipients. N Engl J Med. 2005;352:1103– ber was normalized to account for in 1985, when a bat researcher died 11. DOI: 10.1056/NEJMoa043018 the increasing use of the website over 3. Metlin AE, Rybakov SS, Gruzdev KN, after being bitten by bats abroad and Neuvonen E, Cox J, Huovilainen A. An- time and aggregated by week, starting in Finland (5). For imported cases, pa- tigenic and molecular characterization of with week 40 in 2005.