Unit-I CLASSIFICATION of VIRUSES
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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. -
Microtubule-Dependent Trafficking of Alphaherpesviruses in the Nervous
viruses Review Microtubule-Dependent Trafficking of Alphaherpesviruses in the Nervous System: The Ins and Outs Drishya Diwaker 1 and Duncan W. Wilson 1,2,* 1 Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA; [email protected] 2 Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA * Correspondence: [email protected]; Tel.: +1-(718)-430-2305 Received: 29 November 2019; Accepted: 15 December 2019; Published: 17 December 2019 Abstract: The Alphaherpesvirinae include the neurotropic pathogens herpes simplex virus and varicella zoster virus of humans and pseudorabies virus of swine. These viruses establish lifelong latency in the nuclei of peripheral ganglia, but utilize the peripheral tissues those neurons innervate for productive replication, spread, and transmission. Delivery of virions from replicative pools to the sites of latency requires microtubule-directed retrograde axonal transport from the nerve terminus to the cell body of the sensory neuron. As a corollary, during reactivation newly assembled virions must travel along axonal microtubules in the anterograde direction to return to the nerve terminus and infect peripheral tissues, completing the cycle. Neurotropic alphaherpesviruses can therefore exploit neuronal microtubules and motors for long distance axonal transport, and alternate between periods of sustained plus end- and minus end-directed motion at different stages of their infectious cycle. This review summarizes our current understanding of the molecular details by which this is achieved. Keywords: herpes simplex virus; pseudorabies virus; neurons; anterograde axonal transport; retrograde axonal transport; microtubules; motors 1. -
Where Do We Stand After Decades of Studying Human Cytomegalovirus?
microorganisms Review Where do we Stand after Decades of Studying Human Cytomegalovirus? 1, 2, 1 1 Francesca Gugliesi y, Alessandra Coscia y, Gloria Griffante , Ganna Galitska , Selina Pasquero 1, Camilla Albano 1 and Matteo Biolatti 1,* 1 Laboratory of Pathogenesis of Viral Infections, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy; [email protected] (F.G.); gloria.griff[email protected] (G.G.); [email protected] (G.G.); [email protected] (S.P.); [email protected] (C.A.) 2 Complex Structure Neonatology Unit, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy; [email protected] * Correspondence: [email protected] These authors contributed equally to this work. y Received: 19 March 2020; Accepted: 5 May 2020; Published: 8 May 2020 Abstract: Human cytomegalovirus (HCMV), a linear double-stranded DNA betaherpesvirus belonging to the family of Herpesviridae, is characterized by widespread seroprevalence, ranging between 56% and 94%, strictly dependent on the socioeconomic background of the country being considered. Typically, HCMV causes asymptomatic infection in the immunocompetent population, while in immunocompromised individuals or when transmitted vertically from the mother to the fetus it leads to systemic disease with severe complications and high mortality rate. Following primary infection, HCMV establishes a state of latency primarily in myeloid cells, from which it can be reactivated by various inflammatory stimuli. Several studies have shown that HCMV, despite being a DNA virus, is highly prone to genetic variability that strongly influences its replication and dissemination rates as well as cellular tropism. In this scenario, the few currently available drugs for the treatment of HCMV infections are characterized by high toxicity, poor oral bioavailability, and emerging resistance. -
WHO Immunological Basis for Immunization Series
WHO Immunological Basis for Immunization Series Module 21: Rotavirus Update 2019 Department of Immunization, Vaccines and Biologicals World Health Organization 20, Avenue Appia CH-1211 Geneva 27, Switzerland [email protected] http://www.who.int/immunization/en/ Immunization, Vaccines and Biologicals WHO Immunological Basis for Immunization Series Module 21: Rotavirus Update 2019 Immunization, Vaccines and Biologicals The immunological basis for immunization series: module 21: Rotavirus Vaccines (Immunological basis for immunization series; module 21) ISBN 978-92-4-000235-7 © World Health Organization 2020 Some rights reserved. This work is available under the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 IGO licence (CC BY-NC-SA 3.0 IGO; https://creativecommons.org/licenses/by-nc-sa/3.0/igo). Under the terms of this licence, you may copy, redistribute and adapt the work for non-commercial purposes, provided the work is appropriately cited, as indicated below. In any use of this work, there should be no suggestion that WHO endorses any specific organization, products or services. The use of the WHO logo is not permitted. If you adapt the work, then you must license your work under the same or equivalent Creative Commons licence. If you create a translation of this work, you should add the following disclaimer along with the suggested citation: “This translation was not created by the World Health Organization (WHO). WHO is not responsible for the content or accuracy of this translation. The original English edition shall be the binding and authentic edition”. Any mediation relating to disputes arising under the licence shall be conducted in accordance with the mediation rules of the World Intellectual Property Organization. -
Topics in Viral Immunology Bruce Campell Supervisory Patent Examiner Art Unit 1648 IS THIS METHOD OBVIOUS?
Topics in Viral Immunology Bruce Campell Supervisory Patent Examiner Art Unit 1648 IS THIS METHOD OBVIOUS? Claim: A method of vaccinating against CPV-1 by… Prior art: A method of vaccinating against CPV-2 by [same method as claimed]. 2 HOW ARE VIRUSES CLASSIFIED? Source: Seventh Report of the International Committee on Taxonomy of Viruses (2000) Edited By M.H.V. van Regenmortel, C.M. Fauquet, D.H.L. Bishop, E.B. Carstens, M.K. Estes, S.M. Lemon, J. Maniloff, M.A. Mayo, D. J. McGeoch, C.R. Pringle, R.B. Wickner Virology Division International Union of Microbiological Sciences 3 TAXONOMY - HOW ARE VIRUSES CLASSIFIED? Example: Potyvirus family (Potyviridae) Example: Herpesvirus family (Herpesviridae) 4 Potyviruses Plant viruses Filamentous particles, 650-900 nm + sense, linear ssRNA genome Genome expressed as polyprotein 5 Potyvirus Taxonomy - Traditional Host range Transmission (fungi, aphids, mites, etc.) Symptoms Particle morphology Serology (antibody cross reactivity) 6 Potyviridae Genera Bymovirus – bipartite genome, fungi Rymovirus – monopartite genome, mites Tritimovirus – monopartite genome, mites, wheat Potyvirus – monopartite genome, aphids Ipomovirus – monopartite genome, whiteflies Macluravirus – monopartite genome, aphids, bulbs 7 Potyvirus Taxonomy - Molecular Polyprotein cleavage sites % similarity of coat protein sequences Genomic sequences – many complete genomic sequences, >200 coat protein sequences now available for comparison 8 Coat Protein Sequence Comparison (RNA) 9 Potyviridae Species Bymovirus – 6 species Rymovirus – 4-5 species Tritimovirus – 2 species Potyvirus – 85 – 173 species Ipomovirus – 1-2 species Macluravirus – 2 species 10 Higher Order Virus Taxonomy Nature of genome: RNA or DNA; ds or ss (+/-); linear, circular (supercoiled?) or segmented (number of segments?) Genome size – 11-383 kb Presence of envelope Morphology: spherical, filamentous, isometric, rod, bacilliform, etc. -
Is the ZIKV Congenital Syndrome and Microcephaly Due to Syndemism with Latent Virus Coinfection?
viruses Review Is the ZIKV Congenital Syndrome and Microcephaly Due to Syndemism with Latent Virus Coinfection? Solène Grayo Institut Pasteur de Guinée, BP 4416 Conakry, Guinea; [email protected] or [email protected] Abstract: The emergence of the Zika virus (ZIKV) mirrors its evolutionary nature and, thus, its ability to grow in diversity or complexity (i.e., related to genome, host response, environment changes, tropism, and pathogenicity), leading to it recently joining the circle of closed congenital pathogens. The causal relation of ZIKV to microcephaly is still a much-debated issue. The identification of outbreak foci being in certain endemic urban areas characterized by a high-density population emphasizes that mixed infections might spearhead the recent appearance of a wide range of diseases that were initially attributed to ZIKV. Globally, such coinfections may have both positive and negative effects on viral replication, tropism, host response, and the viral genome. In other words, the possibility of coinfection may necessitate revisiting what is considered to be known regarding the pathogenesis and epidemiology of ZIKV diseases. ZIKV viral coinfections are already being reported with other arboviruses (e.g., chikungunya virus (CHIKV) and dengue virus (DENV)) as well as congenital pathogens (e.g., human immunodeficiency virus (HIV) and cytomegalovirus (HCMV)). However, descriptions of human latent viruses and their impacts on ZIKV disease outcomes in hosts are currently lacking. This review proposes to select some interesting human latent viruses (i.e., herpes simplex virus 2 (HSV-2), Epstein–Barr virus (EBV), human herpesvirus 6 (HHV-6), human parvovirus B19 (B19V), and human papillomavirus (HPV)), whose virological features and Citation: Grayo, S. -
Aujeszky's Disease Control in Pigs? Cattle Exposed to Asymptomatically Infected Pigs
Aujeszky’s Importance Aujeszky’s disease (pseudorabies) is a highly contagious, economically significant Disease disease of pigs. This viral infection tends to cause central nervous system (CNS) signs in young animals, respiratory illness in older pigs, and reproductive losses in sows. Pseudorabies, Mad Itch Mortality rates in very young piglets can be high, although older animals typically recover. Recovered swine can carry the virus latently, and may resume shedding it at a later time. Other species can be infected when they contact infected pigs or eat raw Last Updated: January 2017 porcine tissues, resulting in neurological signs that are usually fatal within a few days. Serious outbreaks were seen in cattle exposed to infected swine in the past, and thousands of farmed mink and foxes in China recently died after being fed contaminated pig liver. Why animals other than pigs do not typically survive this infection is not clear. Aujeszky’s disease can result in trade restrictions, as well as economic losses, in countries where it is endemic. It remains a significant problem among domesticated pigs in some parts of the world. Variants that recently caused outbreaks among vaccinated pigs in China may be a particular concern. Eradication programs have eliminated this disease from domesticated swine in many nations, including the U.S.. The disease has never been reported in Canada. However, viruses are often still maintained in feral pigs and wild boar, and could be reintroduced to domesticated pigs from this source. Viruses from wild suids have also sporadically caused Aujeszky’s disease in other animals, particularly hunting dogs. -
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. -
Type D Primate Retroviruses: a Review1
[CANCER RESEARCH 38, 3123-3139, October 1978] Type D Primate Retroviruses: A Review1 Donald Fine and Gerald Schochetman Viral Oncology Program, Frederick Cancer Research Center. Frederick, Maryland 21701 Abstract The prototype virus of the type D retroviruses is the techniques. The retrovirus associated with the induction of Mason-Pfizer monkey virus (MPMV). MPMV was originally mammary cancer in mice, MMTV,2 is morphologically dis isolated from a breast carcinoma of a female rhesus tinct from the type C viruses and is the prototype of the type monkey (an Old World monkey). MPMV is of obvious B virus group (30). A retrovirus group of primate origin, importance in that it is the only retrovirus thus far isolated which has properties similar to the type C and type B from a mammary tumor of a primate and has been shown viruses but is morphologically distinct from them, has been to have transforming potential for primate cells in vitro. designated genus Oncornavirus D (30). The prototype virus Subsequent to the isolation of MPMV, viruses morpholog of this genus is the MPMV. MPMV was originally isolated ically and ¡mmunologicallyindistinguishable from MPMV from a mammary carcinoma of a female rhesus monkey (an have been isolated from normal placenta and lactating Old World monkey) (19, 60). Because mammary carcinomas mammary glands of other rhesus monkeys in captivity. represent the most prevalent form of neoplasia in humans Recently, viruses morphologically resembling MPMV have and, furthermore, because the incidence of mammary tu been isolated from a langur monkey (another Old World mors in subhuman primates is rare (61, 62, 70, 78), MPMV monkey) and from squirrel monkeys (a New World mon is of obvious potential importance because it is the only key). -
Herpesviral Latency—Common Themes
pathogens Review Herpesviral Latency—Common Themes Magdalena Weidner-Glunde * , Ewa Kruminis-Kaszkiel and Mamata Savanagouder Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research of Polish Academy of Sciences, Tuwima Str. 10, 10-748 Olsztyn, Poland; [email protected] (E.K.-K.); [email protected] (M.S.) * Correspondence: [email protected] Received: 22 January 2020; Accepted: 14 February 2020; Published: 15 February 2020 Abstract: Latency establishment is the hallmark feature of herpesviruses, a group of viruses, of which nine are known to infect humans. They have co-evolved alongside their hosts, and mastered manipulation of cellular pathways and tweaking various processes to their advantage. As a result, they are very well adapted to persistence. The members of the three subfamilies belonging to the family Herpesviridae differ with regard to cell tropism, target cells for the latent reservoir, and characteristics of the infection. The mechanisms governing the latent state also seem quite different. Our knowledge about latency is most complete for the gammaherpesviruses due to previously missing adequate latency models for the alpha and beta-herpesviruses. Nevertheless, with advances in cell biology and the availability of appropriate cell-culture and animal models, the common features of the latency in the different subfamilies began to emerge. Three criteria have been set forth to define latency and differentiate it from persistent or abortive infection: 1) persistence of the viral genome, 2) limited viral gene expression with no viral particle production, and 3) the ability to reactivate to a lytic cycle. This review discusses these criteria for each of the subfamilies and highlights the common strategies adopted by herpesviruses to establish latency. -
Basic Properties of Viruses and Virus–Cell Interaction
WBV5 6/27/03 10:28 PM Page 49 Basic Properties of Viruses and Virus–Cell II Interaction PART ✷ VIRUS STRUCTURE AND CLASSIFICATION ✷ CLASSIFICATION SCHEMES ✷ THE BEGINNING AND END OF THE VIRUS REPLICATION CYCLE ✷ LATE EVENTS IN VIRAL INFECTION: CAPSID ASSEMBLY AND VIRION RELEASE ✷ HOST IMMUNE RESPONSE TO VIRAL INFECTION: THE NATURE OF THE VERTEBRATE IMMUNE RESPONSE ✷ PRESENTATION OF VIRAL ANTIGENS TO IMMUNE REACTIVE CELLS ✷ CONTROL AND DYSFUNCTION OF IMMUNITY ✷ MEASUREMENT OF THE IMMUNE REACTION ✷ STRATEGIES TO PROTECT AGAINST AND COMBAT VIRAL INFECTION ✷ VACCINATION — INDUCTION OF IMMUNITY TO PREVENT VIRUS INFECTION ✷ EUKARYOTIC CELL-BASED DEFENSES AGAINST VIRAL REPLICATION ✷ ANTIVIRAL DRUGS ✷ BACTERIAL ANTIVIRAL SYSTEMS — RESTRICTION ENDONUCLEASES ✷ PROBLEMS FOR PART II ✷ ADDITIONAL READING FOR PART II WBV5 6/27/03 10:28 PM Page 50 WBV5 6/27/03 3:35 PM Page 51 Virus Structure and Classification ✷ 5 Viral genomes ✷ Viral capsids ✷ Viral membrane envelopes ✷ CLASSIFICATION SCHEMES CHAPTER ✷ The Baltimore scheme of virus classification ✷ Disease-based classification schemes for viruses ✷ QUESTIONS FOR CHAPTER 5 Viruses are small compared to the wavelength of visible light; indeed, while the largest virus can be discerned in a good light microscope, viruses can only be visualized in detail using an electron microscope. A size scale with some important landmarks is shown in Fig. 5.1. Viruses are composed of a nucleic acid genomeor core, which is the genetic material of the virus, surrounded by a capsid made up of virus-encoded proteins. Viral genetic material encodes the structural proteins of the capsid and other viral proteins essential for other functions in initiating virus replication. The entire structure of the virus (the genome, the capsid, and — where present — the envelope) make up the virion or virus particle. -
Herpes Simplex Virus 1 (HSV-1) for Cancer Treatment Y Shen and J Nemunaitis Mary Crowley Medical Research Center, Dallas, TX, USA
Cancer Gene Therapy (2006) 13, 975–992 r 2006 Nature Publishing Group All rights reserved 0929-1903/06 $30.00 www.nature.com/cgt REVIEW Herpes simplex virus 1 (HSV-1) for cancer treatment Y Shen and J Nemunaitis Mary Crowley Medical Research Center, Dallas, TX, USA Cancer remains a serious threat to human health, causing over 500 000 deaths each year in US alone, exceeded only by heart diseases. Many new technologies are being developed to fight cancer, among which are gene therapies and oncolytic virotherapies. Herpes simplex virus type 1 (HSV-1) is a neurotropic DNA virus with many favorable properties both as a delivery vector for cancer therapeutic genes and as a backbone for oncolytic viruses. Herpes simplex virus type 1 is highly infectious, so HSV-1 vectors are efficient vehicles for the delivery of exogenous genetic materials to cells. The inherent cytotoxicity of this virus, if harnessed and made to be selective by genetic manipulations, makes this virus a good candidate for developing viral oncolytic approach. Furthermore, its large genome size, ability to infect cells with a high degree of efficiency, and the presence of an inherent replication controlling mechanism, the thymidine kinase gene, add to its potential capabilities. This review briefly summarizes the biology of HSV-1, examines various strategies that have been used to genetically modify the virus, and discusses preclinical as well as clinical results of the HSV-1-derived vectors in cancer treatment. Cancer Gene Therapy (2006) 13, 975–992. doi:10.1038/sj.cgt.7700946; published online 7 April 2006 Keywords: herpes simplex virus; HSV-1; cancer; oncolytic virus; clinical; gene therapy Introduction anti-HSV antibodies during the replication process.