Chikungunya Virus
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A Zika Virus Envelope Mutation Preceding the 2015 Epidemic Enhances Virulence and Fitness for Transmission
A Zika virus envelope mutation preceding the 2015 epidemic enhances virulence and fitness for transmission Chao Shana,b,1,2, Hongjie Xiaa,1, Sherry L. Hallerc,d,e, Sasha R. Azarc,d,e, Yang Liua, Jianying Liuc,d, Antonio E. Muruatoc, Rubing Chenc,d,e,f, Shannan L. Rossic,d,f, Maki Wakamiyaa, Nikos Vasilakisd,f,g,h,i, Rongjuan Peib, Camila R. Fontes-Garfiasa, Sanjay Kumar Singhj, Xuping Xiea, Scott C. Weaverc,d,e,k,l,2, and Pei-Yong Shia,d,e,k,l,2 aDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555; bState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, 430071 Wuhan, China; cDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555; dInstitute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX 77555; eInstitute for Translational Science, University of Texas Medical Branch, Galveston, TX 77555; fDepartment of Pathology, University of Texas Medical Branch, Galveston, TX 77555; gWorld Reference Center of Emerging Viruses and Arboviruses, University of Texas Medical Branch, Galveston, TX 77555; hCenter for Biodefence and Emerging Infectious Diseases, University of Texas Medical Branch, Galveston, TX 77555; iCenter for Tropical Diseases, University of Texas Medical Branch, Galveston, TX 77555; jDepartment of Neurosurgery-Research, The University of Texas MD Anderson Cancer Center, Houston, TX 77030; kSealy Institute for Vaccine Sciences, University of Texas Medical Branch, Galveston, TX 77555; and lSealy Center for Structural Biology and Molecular Biophysics, University of Texas Medical Branch, Galveston, TX 77555 Edited by Peter Palese, Icahn School of Medicine at Mount Sinai, New York, NY, and approved July 2, 2020 (received for review March 26, 2020) Arboviruses maintain high mutation rates due to lack of proof- recently been shown to orchestrate flavivirus assembly through reading ability of their viral polymerases, in some cases facilitating recruiting structural proteins and viral RNA (8, 9). -
Following Acute Encephalitis, Semliki Forest Virus Is Undetectable in the Brain by Infectivity Assays but Functional Virus RNA C
viruses Article Following Acute Encephalitis, Semliki Forest Virus is Undetectable in the Brain by Infectivity Assays but Functional Virus RNA Capable of Generating Infectious Virus Persists for Life Rennos Fragkoudis 1,2, Catherine M. Dixon-Ballany 1, Adrian K. Zagrajek 1, Lukasz Kedzierski 3 and John K. Fazakerley 1,3,* ID 1 The Roslin Institute and Royal (Dick) School of Veterinary Studies, College of Medicine & Veterinary Medicine, University of Edinburgh, Edinburgh, Midlothian EH25 9RG, UK; [email protected] (R.F.); [email protected] (C.M.D.-B.); [email protected] (A.K.Z.) 2 The School of Veterinary Medicine and Science, the University of Nottingham, Sutton Bonington Campus, Leicestershire LE12 5RD, UK 3 Department of Microbiology and Immunology, Faculty of Medicine, Dentistry and Health Sciences at The Peter Doherty Institute for Infection and Immunity and the Melbourne Veterinary School, Faculty of Veterinary and Agricultural Sciences, the University of Melbourne, 792 Elizabeth Street, Melbourne 3000, Australia; [email protected] * Correspondence: [email protected]; Tel.: +61-3-9731-2281 Received: 25 April 2018; Accepted: 17 May 2018; Published: 18 May 2018 Abstract: Alphaviruses are mosquito-transmitted RNA viruses which generally cause acute disease including mild febrile illness, rash, arthralgia, myalgia and more severely, encephalitis. In the mouse, peripheral infection with Semliki Forest virus (SFV) results in encephalitis. With non-virulent strains, infectious virus is detectable in the brain, by standard infectivity assays, for around ten days. As we have shown previously, in severe combined immunodeficient (SCID) mice, infectious virus is detectable for months in the brain. -
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DATOS PERSONALES Apellido y Nombres: Diaz, Luis Adrián DNI: 24630504 Domicilio Laboral: Laboratorio de Arbovirus - Instituto de Virología - Facultad de Ciencias Médicas - Universidad Nacional de Córdoba. Córdoba, Argentina. Correo electrónico: [email protected], [email protected] Teléfono laboral: 0351-4334022 Título/s de grado obtenidos: BIÓLOGO. FCEFyN – UNC. Promedio general con y sin aplazos: 8,64. Título/s de Post-Grado obtenidos: DOCTOR en Ciencias Biológicas. FCEFyN. Cargo docente actual: Profesor Adjunto. Dedicación simple. CONCURSADO. Instituto de Virología “Dr. J. M. Vanella”, Facultad Ciencias Médicas, Universidad Nacional de Córdoba. Cargo/s en investigación: Investigador Asistente. Carrera Investigador Científico CONICET. Dedicación Exclusiva. Fecha de ingreso: Septiembre de 2010 Subsidios obtenidos como responsable en los últimos 5 (cinco) años: Virus transmitidos por artrópodos (Arbovirus) de importancia sanitaria en Argentina: estudios ecoepidemiológicos. Código proyecto: 30720130100631CB. Res. SECYT 203/14, Res. Rec UNC: 1565/14. SECYT-UNC. 2014-2016. Evaluación de infección por flavivirus y ricketsias en aves y garrapatas de importancia sanitaria. Cooperación internacional CONICET-FAPESP. Director. 2014-2016. Interacciones ecológicas e inmunológicas entre los virus St. Louis encephalitis y West Nile de importancia médica y veterinaria en Argentina. DIRECTOR. PICT 627/2010. Subsidio otorgado por Ministerio de Ciencia y Tecnología de la Nación, Programa FONCyT. Lugar de trabajo: Instituto de Virología “Dr. J. M. Vanella”. Período: 2012-2014. Interacciones ecológicas e inmunológicas entre los virus St. Louis encephalitis y West Nile de importancia médica y veterinaria en Argentina. DIRECTOR. Fundación Bunge y Born. Lugar de trabajo: Instituto de Virología “Dr. J. M. Vanella”. Período: 2011-2013. Vigilancia epidemiológica de Flavivirus (Arbovirus) y sus posibles vectores y hospedadores asociados en la ciudad de Córdoba. -
Replication of Semliki Forest Virus: Polyadenylate in Plus- Strand RNA and Polyuridylate in Minus-Strand RNA
JOURNAL OF VIROLOGY, Nov. 1976, p. 446-464 Vol. 20, No. 2 Copyright X) 1976 American Society for Microbiology Printed in U.S.A. Replication of Semliki Forest Virus: Polyadenylate in Plus- Strand RNA and Polyuridylate in Minus-Strand RNA DOROTHEA L. SAWICKI* AND PETER J. GOMATOS Division of Virology, The Sloan-Kettering Institute, New York, New York 10021 Received for publication 4 June 1976 The 42S RNA from Semliki Forest virus contains a polyadenylate [poly(A)] sequence that is 80 to 90 residues long and is the 3'-terminus of the virion RNA. A poly(A) sequence of the same length was found in the plus strand of the replicative forms (RFs) and replicative intermediates (RIs) isolated 2 h after infection. In addition, both RFs and RIs contained a polyuridylate [poly(U)] sequence. No poly(U) was found in virion RNA, and thus the poly(U) sequence is in minus-strand RNA. The poly(U) from RFs was on the average 60 residues long, whereas that isolated from the RIs was 80 residues long. Poly(U) sequences isolated from RFs and RIs by digestion with RNase Ti contained 5'-phosphoryl- ated pUp and ppUp residues, indicating that the poly(U) sequence was the 5'- terminus of the minus-strand RNA. The poly(U) sequence in RFs or RIs was free to bind to poly(A)-Sepharose only after denaturation of the RNAs, indicating that the poly(U) was hydrogen bonded to the poly(A) at the 3'-terminus of the plus-strand RNA in these molecules. When treated with 0.02 g.g of RNase A per ml, both RFs and RIs yielded the same distribution of the three cores, RFI, RFII, and RFIII. -
Identification of Novel Antiviral Compounds Targeting Entry Of
viruses Article Identification of Novel Antiviral Compounds Targeting Entry of Hantaviruses Jennifer Mayor 1,2, Giulia Torriani 1,2, Olivier Engler 2 and Sylvia Rothenberger 1,2,* 1 Institute of Microbiology, University Hospital Center and University of Lausanne, Rue du Bugnon 48, CH-1011 Lausanne, Switzerland; [email protected] (J.M.); [email protected] (G.T.) 2 Spiez Laboratory, Swiss Federal Institute for NBC-Protection, CH-3700 Spiez, Switzerland; [email protected] * Correspondence: [email protected]; Tel.: +41-21-314-51-03 Abstract: Hemorrhagic fever viruses, among them orthohantaviruses, arenaviruses and filoviruses, are responsible for some of the most severe human diseases and represent a serious challenge for public health. The current limited therapeutic options and available vaccines make the development of novel efficacious antiviral agents an urgent need. Inhibiting viral attachment and entry is a promising strategy for the development of new treatments and to prevent all subsequent steps in virus infection. Here, we developed a fluorescence-based screening assay for the identification of new antivirals against hemorrhagic fever virus entry. We screened a phytochemical library containing 320 natural compounds using a validated VSV pseudotype platform bearing the glycoprotein of the virus of interest and encoding enhanced green fluorescent protein (EGFP). EGFP expression allows the quantitative detection of infection and the identification of compounds affecting viral entry. We identified several hits against four pseudoviruses for the orthohantaviruses Hantaan (HTNV) and Citation: Mayor, J.; Torriani, G.; Andes (ANDV), the filovirus Ebola (EBOV) and the arenavirus Lassa (LASV). Two selected inhibitors, Engler, O.; Rothenberger, S. -
Chikungunya Vaccine Candidates Elicit Protective Immunity in C57BL/6 Mice
Novel attenuated chikungunya vaccine candidates elicit protective immunity in C57BL/6 mice Author Hallengard, David, Kakoulidou, Maria, Lulla, Aleksei, Kummerer, Beate M., Johansson, Daniel X., Mutso, Margit, Lulla, Valeria, Fazakerley, John K., Roques, Pierre, Le Grand, Roger, Merits, Andres, Liljestrom, Peter Published 2014 Journal Title Journal of Virology Version Version of Record (VoR) DOI https://doi.org/10.1128/JVI.03453-13 Copyright Statement © 2013 American Society for Microbiology. The attached file is reproduced here in accordance with the copyright policy of the publisher. Please refer to the journal's website for access to the definitive, published version. Downloaded from http://hdl.handle.net/10072/343708 Griffith Research Online https://research-repository.griffith.edu.au Novel Attenuated Chikungunya Vaccine Candidates Elicit Protective Immunity in C57BL/6 mice David Hallengärd,a Maria Kakoulidou,a Aleksei Lulla,b Beate M. Kümmerer,c Daniel X. Johansson,a Margit Mutso,b Valeria Lulla,b John K. Fazakerley,d Pierre Roques,e,f Roger Le Grand,e,f Andres Merits,b Peter Liljeströma Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Swedena; Institute of Technology, University of Tartu, Tartu, Estoniab; Institute of Virology, University of Bonn Medical Centre, Bonn, Germanyc; The Pirbright Institute, Pirbright, United Kingdomd; Division of Immuno-Virology, iMETI, CEA, Paris, Francee; UMR-E1, University Paris-Sud XI, Orsay, Francef ABSTRACT Chikungunya virus (CHIKV) is a reemerging mosquito-borne alphavirus that has caused severe epidemics in Africa and Asia and occasionally in Europe. As of today, there is no licensed vaccine available to prevent CHIKV infection. Here we describe the development and evaluation of novel CHIKV vaccine candidates that were attenuated by deleting a large part of the gene encod- ing nsP3 or the entire gene encoding 6K and were administered as viral particles or infectious genomes launched by DNA. -
Early Events in Chikungunya Virus Infection—From Virus Cell Binding to Membrane Fusion
Viruses 2015, 7, 3647-3674; doi:10.3390/v7072792 OPEN ACCESS viruses ISSN 1999-4915 www.mdpi.com/journal/viruses Review Early Events in Chikungunya Virus Infection—From Virus Cell Binding to Membrane Fusion Mareike K. S. van Duijl-Richter, Tabitha E. Hoornweg, Izabela A. Rodenhuis-Zybert and Jolanda M. Smit * Department of Medical Microbiology, University of Groningen and University Medical Center Groningen, 9700 RB Groningen, The Netherlands; E-Mails: [email protected] (M.K.S.D.-R.); [email protected] (T.E.H.); [email protected] (I.A.R.-Z.) * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +31-50-3632738. Academic Editors: Yorgo Modis and Stephen Graham Received: 4 May 2015 / Accepted: 29 June 2015 / Published: 7 July 2015 Abstract: Chikungunya virus (CHIKV) is a rapidly emerging mosquito-borne alphavirus causing millions of infections in the tropical and subtropical regions of the world. CHIKV infection often leads to an acute self-limited febrile illness with debilitating myalgia and arthralgia. A potential long-term complication of CHIKV infection is severe joint pain, which can last for months to years. There are no vaccines or specific therapeutics available to prevent or treat infection. This review describes the critical steps in CHIKV cell entry. We summarize the latest studies on the virus-cell tropism, virus-receptor binding, internalization, membrane fusion and review the molecules and compounds that have been described to interfere with virus cell entry. The aim of the review is to give the reader a state-of-the-art overview on CHIKV cell entry and to provide an outlook on potential new avenues in CHIKV research. -
RNA Interference Restricts Rift Valley Fever Virus in Multiple Insect Systems
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Enlighten RESEARCH ARTICLE Host-Microbe Biology crossm RNA Interference Restricts Rift Valley Fever Virus in Multiple Insect Systems Isabelle Dietrich,a* Stephanie Jansen,b Gamou Fall,c Stephan Lorenzen,b Martin Rudolf,b Katrin Huber,b,d Anna Heitmann,b Sabine Schicht,h El Hadji Ndiaye,e Mick Watson,f Ilaria Castelli,g Benjamin Brennan,a a e c g Richard M. Elliott, Mawlouth Diallo, Amadou A. Sall, Anna-Bella Failloux, Downloaded from Esther Schnettler,a,b Alain Kohl,a Stefanie C. Beckerb,h MRC-University of Glasgow Centre for Virus Research, Glasgow, Scotland, United Kingdoma; Bernhard-Nocht- Institut für Tropenmedizin, Hamburg, Germanyb; Institut Pasteur de Dakar, Arbovirus and Viral Hemorrhagic Fever Unit, Dakar, Senegalc; German Mosquito Control Association (KABS/GFS), Waldsee, Germanyd; Institut Pasteur de Dakar, Medical Entomology Unit, Dakar, Senegale; The Roslin Institute, Royal (Dick) School of Veterinary Studies, Division of Genetics and Genomics, University of Edinburgh, Easter Bush, Edinburgh, United Kingdomf; Department of Virology, Arboviruses and Insect Vectors, Institut Pasteur, Paris, Franceg; Institute for Parasitology, University of Veterinary Medicine Hannover, Hannover, Germanyh http://msphere.asm.org/ ABSTRACT The emerging bunyavirus Rift Valley fever virus (RVFV) is transmitted to humans and livestock by a large number of mosquito species. RNA interference Received 23 February 2017 Accepted 31 March 2017 Published 3 May 2017 (RNAi) has been characterized as an important innate immune defense mechanism Citation Dietrich I, Jansen S, Fall G, Lorenzen S, used by mosquitoes to limit replication of positive-sense RNA flaviviruses and toga- Rudolf M, Huber K, Heitmann A, Schicht S, viruses; however, little is known about its role against negative-strand RNA viruses Ndiaye EH, Watson M, Castelli I, Brennan B, such as RVFV. -
Pan American Health Organization PAHO/ACMR 14/2 Original: English
Pan American Health Organization PAHO/ACMR 14/2 Original: English FOURTEENTH MEETING OF THE ADVISORY COMMITTEE ON MEDICAL RESEARCH Washington, D.C. 7-10 July 1975 ECOLOGY OF ARBOVIRUSES AND THEIR DISEASES IN FRENCH GUIANA The issue of this document does not constitute formal publication. It should not be reviewed, abstracted, or quoted without the consent of the Pan American Health Organization. The authors alone are responsible for statements expressed in signed papers. ECOLOGY OF ARBOVIRUSES AND THEIR DISEASES IN FRENCH GUIANA Approaching the study of the Arbovirus in French Guiana we tried to make manifest the ecological foci, where by the only fact of the presence at the same time of virus reservoirs and of a population of vectors particularly abondant we had some chance of isolating some arbovirus which can cause a disease to man. In order to identify these ecological foci we had to do a certain number of serological investigation trying to use man as a revelator of this arbovirus circu- lation. The serological investigation were executed first by using a series of antigen chosen because they have been isolated before in French Guiana - for the A group, Mucambo and Pixuna virus. - for the B group, Yellow fever virus, St-Louis, Dengue II and Dengue III. After the isolation of two virus : one, seeming new, belonging to the Venezuelan Encephalitis group, the other belonging to group B and recognized as similar to Ilheus, we have also included them in the series of antigens. Military coming from different territories and in particular from Martinica and Guadaloupe seemed to us to be excellent sentinel. -
Chikungunya Virus
CHIKUNGUNYA VIRUS Prepared for the Swine Health Information Center By the Center for Food Security and Public Health, College of Veterinary Medicine, Iowa State University July 2016 SUMMARY Etiology • Chikungunya virus (CHIKV) is an Old World alphavirus within the family Togaviridae that mainly causes disease in humans. • There are three genotypes: West African, East Central South African (ECSA), and Asian. The ECSA genotype has caused human epidemics in Africa and the Indian Ocean Region. The Asian genotype circulates in Asia and has recently emerged in the Americas (Caribbean, Latin America, and the U.S.). Cleaning and Disinfection • The efficacy of most disinfectants against CHIKV is not known. As a lipid-enveloped virus, CHIKV is expected to be destroyed by detergents, acids, alcohols (70% ethanol), aldehydes (formaldehyde, glutaraldehyde), beta-propiolactone, halogens (sodium hypochlorite and iodophors), phenols, quaternary ammonium compounds, and lipid solvents. Exposure to heat (58°C [137°F]), ultraviolent light, or radiation is also sufficient to render togaviruses inactive. Epidemiology • Humans act as hosts during CHIKV epidemics. Animal species including monkeys, rodents, and birds are also capable hosts. • Natural CHIKV infection has not been documented in pigs. There is some evidence that pigs can mount an antibody response to the virus. • In humans CHIKV causes fever, myalgia, and polyarthritis that can persist for years. A maculopapular, pruritic rash, lasting about one week, is seen in about half of human patients. Neonates infected with CHIKV can develop serious disease affecting the heart, skin, and brain. Bleeding and disseminated intravascular coagulation have also been observed in humans. Morbidity is high, but CHIKV rarely causes death. -
Mayaro: an Emerging Viral Threat?
Emerging Microbes & Infections ISSN: (Print) 2222-1751 (Online) Journal homepage: https://www.tandfonline.com/loi/temi20 Mayaro: an emerging viral threat? Yeny Acosta-Ampudia, Diana M. Monsalve, Yhojan Rodríguez, Yovana Pacheco, Juan-Manuel Anaya & Carolina Ramírez-Santana To cite this article: Yeny Acosta-Ampudia, Diana M. Monsalve, Yhojan Rodríguez, Yovana Pacheco, Juan-Manuel Anaya & Carolina Ramírez-Santana (2018) Mayaro: an emerging viral threat?, Emerging Microbes & Infections, 7:1, 1-11, DOI: 10.1038/s41426-018-0163-5 To link to this article: https://doi.org/10.1038/s41426-018-0163-5 © The Author(s) 2018 Published online: 26 Sep 2018. Submit your article to this journal Article views: 1317 View related articles View Crossmark data Citing articles: 31 View citing articles Full Terms & Conditions of access and use can be found at https://www.tandfonline.com/action/journalInformation?journalCode=temi20 Acosta-Ampudia et al. Emerging Microbes & Infections (2018) 7:163 Emerging Microbes & Infections DOI 10.1038/s41426-018-0163-5 www.nature.com/emi REVIEW ARTICLE Open Access Mayaro: an emerging viral threat? Yeny Acosta-Ampudia1, Diana M. Monsalve1, Yhojan Rodríguez1, Yovana Pacheco 1,Juan-ManuelAnaya1 and Carolina Ramírez-Santana1 Abstract Mayaro virus (MAYV), an enveloped RNA virus, belongs to the Togaviridae family and Alphavirus genus. This arthropod- borne virus (Arbovirus) is similar to Chikungunya (CHIKV), Dengue (DENV), and Zika virus (ZIKV). The term “ChikDenMaZika syndrome” has been coined for clinically suspected arboviruses, which have arisen as a consequence of the high viral burden, viral co-infection, and co-circulation in South America. In most cases, MAYV disease is nonspecific, mild, and self-limited. -
Structural Studies of Chikungunya Virus Maturation
Structural studies of Chikungunya virus maturation Moh Lan Yapa,b, Thomas Klosea, Akane Urakamic, S. Saif Hasana, Wataru Akahatac, and Michael G. Rossmanna,1 aDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907; bDepartment of Biological Science, Faculty of Science, Universiti Tunku Abdul Rahman, 31900 Kampar, Perak, Malaysia; and cVLP Therapeutics, Gaithersburg, MD 20878 Edited by Robert M. Stroud, University of California, San Francisco, California, and approved November 10, 2017 (received for review July 25, 2017) Cleavage of the alphavirus precursor glycoprotein p62 into the process. Flaviviruses are assembled as “immature” noninfectious E2 and E3 glycoproteins before assembly with the nucleocapsid is particles in the ER of the host cell that are then proteolytically the key to producing fusion-competent mature spikes on alphavi- modified to produce infectious viruses on leaving the host cell. ruses. Here we present a cryo-EM, 6.8-Å resolution structure of an However, alphavirus components are proteolytically modified “ ” immature Chikungunya virus in which the cleavage site has been before assembly into mature viruses on the plasma membrane. mutated to inhibit proteolysis. The spikes in the immature virus In addition, a regular, icosahedral capsid shell is observed only have a larger radius and are less compact than in the mature virus. in alphaviruses. During infection, a conserved sequence on the Furthermore, domains B on the E2 glycoproteins have less free- ’ dom of movement in the immature virus, keeping the fusion loops N-terminal regions of the capsid proteins binds to the host cell s protected under domain B. In addition, the nucleocapsid of the 60S ribosomal subunits, initiating the dissociation of the nu- immature virus is more compact than in the mature virus, protect- cleocapsid and the release of the RNA from the nucleocapsid ing a conserved ribosome-binding site in the capsid protein from (14).