70 results on '"Victoria Wahl-Jensen"'
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2. Filovirus RefSeq Entries: Evaluation and Selection of Filovirus Type Variants, Type Sequences, and Names
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Jens H. Kuhn, Kristian G. Andersen, Yīmíng Bào, Sina Bavari, Stephan Becker, Richard S. Bennett, Nicholas H. Bergman, Olga Blinkova, Steven Bradfute, J. Rodney Brister, Alexander Bukreyev, Kartik Chandran, Alexander A. Chepurnov, Robert A. Davey, Ralf G. Dietzgen, Norman A. Doggett, Olga Dolnik, John M. Dye, Sven Enterlein, Paul W. Fenimore, Pierre Formenty, Alexander N. Freiberg, Robert F. Garry, Nicole L. Garza, Stephen K. Gire, Jean-Paul Gonzalez, Anthony Griffiths, Christian T. Happi, Lisa E. Hensley, Andrew S. Herbert, Michael C. Hevey, Thomas Hoenen, Anna N. Honko, Georgy M. Ignatyev, Peter B. Jahrling, Joshua C. Johnson, Karl M. Johnson, Jason Kindrachuk, Hans-Dieter Klenk, Gary Kobinger, Tadeusz J. Kochel, Matthew G. Lackemeyer, Daniel F. Lackner, Eric M. Leroy, Mark S. Lever, Elke Mühlberger, Sergey V. Netesov, Gene G. Olinger, Sunday A. Omilabu, Gustavo Palacios, Rekha G. Panchal, Daniel J. Park, Jean L. Patterson, Janusz T. Paweska, Clarence J. Peters, James Pettitt, Louise Pitt, Sheli R. Radoshitzky, Elena I. Ryabchikova, Erica Ollmann Saphire, Pardis C. Sabeti, Rachel Sealfon, Aleksandr M. Shestopalov, Sophie J. Smither, Nancy J. Sullivan, Robert Swanepoel, Ayato Takada, Jonathan S. Towner, Guido van der Groen, Viktor E. Volchkov, Valentina A. Volchkova, Victoria Wahl-Jensen, Travis K. Warren, Kelly L. Warfield, Manfred Weidmann, and Stuart T. Nichol
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Bundibugyo virus ,cDNA clone ,cuevavirus ,Ebola ,Ebola virus ,ebolavirus ,filovirid ,Filoviridae ,filovirus ,genome annotation ,ICTV ,International Committee on Taxonomy of Viruses ,Lloviu virus ,Marburg virus ,marburgvirus ,mononegavirad ,Mononegavirales ,mononegavirus ,Ravn virus ,RefSeq ,Reston virus ,reverse genetics ,Sudan virus ,Taï Forest virus ,virus classification ,virus isolate ,virus nomenclature ,virus strain ,virus taxonomy ,virus variant ,Microbiology ,QR1-502 - Abstract
Sequence determination of complete or coding-complete genomes of viruses is becoming common practice for supporting the work of epidemiologists, ecologists, virologists, and taxonomists. Sequencing duration and costs are rapidly decreasing, sequencing hardware is under modification for use by non-experts, and software is constantly being improved to simplify sequence data management and analysis. Thus, analysis of virus disease outbreaks on the molecular level is now feasible, including characterization of the evolution of individual virus populations in single patients over time. The increasing accumulation of sequencing data creates a management problem for the curators of commonly used sequence databases and an entry retrieval problem for end users. Therefore, utilizing the data to their fullest potential will require setting nomenclature and annotation standards for virus isolates and associated genomic sequences. The National Center for Biotechnology Information’s (NCBI’s) RefSeq is a non-redundant, curated database for reference (or type) nucleotide sequence records that supplies source data to numerous other databases. Building on recently proposed templates for filovirus variant naming [ ()////-], we report consensus decisions from a majority of past and currently active filovirus experts on the eight filovirus type variants and isolates to be represented in RefSeq, their final designations, and their associated sequences.
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- 2014
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3. ABSL-4 Aerobiology Biosafety and Technology at the NIH/NIAID Integrated Research Facility at Fort Detrick
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Matthew G. Lackemeyer, Fabian de Kok-Mercado, Jiro Wada, Laura Bollinger, Jason Kindrachuk, Victoria Wahl-Jensen, Jens H. Kuhn, and Peter B. Jahrling
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ABSL-4 ,aerobiology ,biosafety level 4 ,class III biosafety cabinet ,BSL-4 ,high-consequence viral pathogens ,medical countermeasure ,viral hemorrhagic fever ,Microbiology ,QR1-502 - Abstract
The overall threat of a viral pathogen to human populations is largely determined by the modus operandi and velocity of the pathogen that is transmitted among humans. Microorganisms that can spread by aerosol are considered a more challenging enemy than those that require direct body-to-body contact for transmission, due to the potential for infection of numerous people rather than a single individual. Additionally, disease containment is much more difficult to achieve for aerosolized viral pathogens than for pathogens that spread solely via direct person-to-person contact. Thus, aerobiology has become an increasingly necessary component for studying viral pathogens that are naturally or intentionally transmitted by aerosol. The goal of studying aerosol viral pathogens is to improve public health preparedness and medical countermeasure development. Here, we provide a brief overview of the animal biosafety level 4 Aerobiology Core at the NIH/NIAID Integrated Research Facility at Fort Detrick, Maryland, USA.
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- 2014
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4. Use of the Syrian Hamster as a New Model of Ebola Virus Disease and Other Viral Hemorrhagic Fevers
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Hideki Ebihara, Victoria Wahl-Jensen, Fabian de Kok-Mercado, Dana P. Scott, Laura Bollinger, and David Safronetz
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Ebola ,filovirus ,hamster model ,rodent model ,pathogenesis ,Microbiology ,QR1-502 - Abstract
Historically, mice and guinea pigs have been the rodent models of choice for therapeutic and prophylactic countermeasure testing against Ebola virus disease (EVD). Recently, hamsters have emerged as a novel animal model for the in vivo study of EVD. In this review, we discuss the history of the hamster as a research laboratory animal, as well as current benefits and challenges of this model. Availability of immunological reagents is addressed. Salient features of EVD in hamsters, including relevant pathology and coagulation parameters, are compared directly with the mouse, guinea pig and nonhuman primate models.
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- 2012
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5. Divergent Simian Arteriviruses Cause Simian Hemorrhagic Fever of Differing Severities in Macaques
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Victoria Wahl-Jensen, Joshua C. Johnson, Michael Lauck, Jason T. Weinfurter, Louise H. Moncla, Andrea M. Weiler, Olivia Charlier, Oscar Rojas, Russell Byrum, Dan R. Ragland, Louis Huzella, Erika Zommer, Melanie Cohen, John G. Bernbaum, Yíngyún Caì, Hannah B. Sanford, Steven Mazur, Reed F. Johnson, Jing Qin, Gustavo F. Palacios, Adam L. Bailey, Peter B. Jahrling, Tony L. Goldberg, David H. O’Connor, Thomas C. Friedrich, and Jens H. Kuhn
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Microbiology ,QR1-502 - Abstract
ABSTRACT Simian hemorrhagic fever (SHF) is a highly lethal disease in captive macaques. Three distinct arteriviruses are known etiological agents of past SHF epizootics, but only one, simian hemorrhagic fever virus (SHFV), has been isolated in cell culture. The natural reservoir(s) of the three viruses have yet to be identified, but African nonhuman primates are suspected. Eleven additional divergent simian arteriviruses have been detected recently in diverse and apparently healthy African cercopithecid monkeys. Here, we report the successful isolation in MARC-145 cell culture of one of these viruses, Kibale red colobus virus 1 (KRCV-1), from serum of a naturally infected red colobus (Procolobus [Piliocolobus] rufomitratus tephrosceles) sampled in Kibale National Park, Uganda. Intramuscular (i.m.) injection of KRCV-1 into four cynomolgus macaques (Macaca fascicularis) resulted in a self-limiting nonlethal disease characterized by depressive behavioral changes, disturbance in coagulation parameters, and liver enzyme elevations. In contrast, i.m. injection of SHFV resulted in typical lethal SHF characterized by mild fever, lethargy, lymphoid depletion, lymphoid and hepatocellular necrosis, low platelet counts, increased liver enzyme concentrations, coagulation abnormalities, and increasing viral loads. As hypothesized based on the genetic and presumed antigenic distance between KRCV-1 and SHFV, all four macaques that had survived KRCV-1 injection died of SHF after subsequent SHFV injection, indicating a lack of protective heterotypic immunity. Our data indicate that SHF is a disease of macaques that in all likelihood can be caused by a number of distinct simian arteriviruses, although with different severity depending on the specific arterivirus involved. Consequently, we recommend that current screening procedures for SHFV in primate-holding facilities be modified to detect all known simian arteriviruses. IMPORTANCE Outbreaks of simian hemorrhagic fever (SHF) have devastated captive Asian macaque colonies in the past. SHF is caused by at least three viruses of the family Arteriviridae: simian hemorrhagic fever virus (SHFV), simian hemorrhagic encephalitis virus (SHEV), and Pebjah virus (PBJV). Nine additional distant relatives of these three viruses were recently discovered in apparently healthy African nonhuman primates. We hypothesized that all simian arteriviruses are potential causes of SHF. To test this hypothesis, we inoculated cynomolgus macaques with a highly divergent simian arterivirus (Kibale red colobus virus 1 [KRCV-1]) from a wild Ugandan red colobus. Despite being only distantly related to red colobuses, all of the macaques developed disease. In contrast to SHFV-infected animals, KRCV-1-infected animals survived after a mild disease presentation. Our study advances the understanding of an important primate disease. Furthermore, our data indicate a need to include the full diversity of simian arteriviruses in nonhuman primate SHF screening assays.
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- 2016
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6. Differences in the Comparative Stability of Ebola Virus Makona-C05 and Yambuku-Mayinga in Blood.
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Michael Schuit, David M Miller, Mary S Reddick-Elick, Carly B Wlazlowski, Claire Marie Filone, Artemas Herzog, Leremy A Colf, Victoria Wahl-Jensen, Michael Hevey, and James W Noah
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Medicine ,Science - Abstract
In support of the response to the 2013-2016 Ebola virus disease (EVD) outbreak in Western Africa, we investigated the persistence of Ebola virus/H.sapiens-tc/GIN/2014/Makona-C05 (EBOV/Mak-C05) on non-porous surfaces that are representative of hospitals, airplanes, and personal protective equipment. We performed persistence studies in three clinically-relevant human fluid matrices (blood, simulated vomit, and feces), and at environments representative of in-flight airline passenger cabins, environmentally-controlled hospital rooms, and open-air Ebola treatment centers in Western Africa. We also compared the surface stability of EBOV/Mak-C05 to that of the prototype Ebola virus/H.sapiens-tc/COD/1976/Yambuku-Mayinga (EBOV/Yam-May), in a subset of these conditions. We show that on inert, non-porous surfaces, EBOV decay rates are matrix- and environment-dependent. Among the clinically-relevant matrices tested, EBOV persisted longest in dried human blood, had limited viability in dried simulated vomit, and did not persist in feces. EBOV/Mak-C05 and EBOV/Yam-May decay rates in dried matrices were not significantly different. However, during the drying process in human blood, EBOV/Yam-May showed significantly greater loss in viability than EBOV/Mak-C05 under environmental conditions relevant to the outbreak region, and to a lesser extent in conditions relevant to an environmentally-controlled hospital room. This factor may contribute to increased communicability of EBOV/Mak-C05 when surfaces contaminated with dried human blood are the vector and may partially explain the magnitude of the most recent outbreak, compared to prior outbreaks. These EBOV persistence data will improve public health efforts by informing risk assessments, structure remediation decisions, and response procedures for future EVD outbreaks.
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- 2016
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7. Implementation of Objective PASC-Derived Taxon Demarcation Criteria for Official Classification of Filoviruses
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Yīmíng Bào, Gaya K. Amarasinghe, Christopher F. Basler, Sina Bavari, Alexander Bukreyev, Kartik Chandran, Olga Dolnik, John M. Dye, Hideki Ebihara, Pierre Formenty, Roger Hewson, Gary P. Kobinger, Eric M. Leroy, Elke Mühlberger, Sergey V. Netesov, Jean L. Patterson, Janusz T. Paweska, Sophie J. Smither, Ayato Takada, Jonathan S. Towner, Viktor E. Volchkov, Victoria Wahl-Jensen, and Jens H. Kuhn
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cuevavirus ,Ebola ,ebolavirus ,Filoviridae ,filovirus ,marburgvirus ,Mononegavirales ,virus taxonomy ,virus classification ,ICTV ,Microbiology ,QR1-502 - Abstract
The mononegaviral family Filoviridae has eight members assigned to three genera and seven species. Until now, genus and species demarcation were based on arbitrarily chosen filovirus genome sequence divergence values (≈50% for genera, ≈30% for species) and arbitrarily chosen phenotypic virus or virion characteristics. Here we report filovirus genome sequence-based taxon demarcation criteria using the publicly accessible PAirwise Sequencing Comparison (PASC) tool of the US National Center for Biotechnology Information (Bethesda, MD, USA). Comparison of all available filovirus genomes in GenBank using PASC revealed optimal genus demarcation at the 55–58% sequence diversity threshold range for genera and at the 23–36% sequence diversity threshold range for species. Because these thresholds do not change the current official filovirus classification, these values are now implemented as filovirus taxon demarcation criteria that may solely be used for filovirus classification in case additional data are absent. A near-complete, coding-complete, or complete filovirus genome sequence will now be required to allow official classification of any novel “filovirus.” Classification of filoviruses into existing taxa or determining the need for novel taxa is now straightforward and could even become automated using a presented algorithm/flowchart rooted in RefSeq (type) sequences.
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- 2017
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8. Endothelial cell permeability during hantavirus infection involves factor XII-dependent increased activation of the kallikrein-kinin system.
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Shannon L Taylor, Victoria Wahl-Jensen, Anna Maria Copeland, Peter B Jahrling, and Connie S Schmaljohn
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Immunologic diseases. Allergy ,RC581-607 ,Biology (General) ,QH301-705.5 - Abstract
Hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS) are diseases caused by hantavirus infections and are characterized by vascular leakage due to alterations of the endothelial barrier. Hantavirus-infected endothelial cells (EC) display no overt cytopathology; consequently, pathogenesis models have focused either on the influx of immune cells and release of cytokines or on increased degradation of the adherens junction protein, vascular endothelial (VE)-cadherin, due to hantavirus-mediated hypersensitization of EC to vascular endothelial growth factor (VEGF). To examine endothelial leakage in a relevant in vitro system, we co-cultured endothelial and vascular smooth muscle cells (vSMC) to generate capillary blood vessel-like structures. In contrast to results obtained in monolayers of cultured EC, we found that despite viral replication in both cell types as well as the presence of VEGF, infected in vitro vessels neither lost integrity nor displayed evidence of VE-cadherin degradation. Here, we present evidence for a novel mechanism of hantavirus-induced vascular leakage involving activation of the plasma kallikrein-kinin system (KKS). We show that incubation of factor XII (FXII), prekallikrein (PK), and high molecular weight kininogen (HK) plasma proteins with hantavirus-infected EC results in increased cleavage of HK, higher enzymatic activities of FXIIa/kallikrein (KAL) and increased liberation of bradykinin (BK). Measuring cell permeability in real-time using electric cell-substrate impedance sensing (ECIS), we identified dramatic increases in endothelial cell permeability after KKS activation and liberation of BK. Furthermore, the alterations in permeability could be prevented using inhibitors that directly block BK binding, the activity of FXIIa, or the activity of KAL. Lastly, FXII binding and autoactivation is increased on the surface of hantavirus-infected EC. These data are the first to demonstrate KKS activation during hantavirus infection and could have profound implications for treatment of hantavirus infections.
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- 2013
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9. Ebola virion attachment and entry into human macrophages profoundly effects early cellular gene expression.
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Victoria Wahl-Jensen, Sabine Kurz, Friedericke Feldmann, Lukas K Buehler, Jason Kindrachuk, Victor DeFilippis, Jean da Silva Correia, Klaus Früh, Jens H Kuhn, Dennis R Burton, and Heinz Feldmann
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Arctic medicine. Tropical medicine ,RC955-962 ,Public aspects of medicine ,RA1-1270 - Abstract
Zaire ebolavirus (ZEBOV) infections are associated with high lethality in primates. ZEBOV primarily targets mononuclear phagocytes, which are activated upon infection and secrete mediators believed to trigger initial stages of pathogenesis. The characterization of the responses of target cells to ZEBOV infection may therefore not only further understanding of pathogenesis but also suggest possible points of therapeutic intervention. Gene expression profiles of primary human macrophages exposed to ZEBOV were determined using DNA microarrays and quantitative PCR to gain insight into the cellular response immediately after cell entry. Significant changes in mRNA concentrations encoding for 88 cellular proteins were observed. Most of these proteins have not yet been implicated in ZEBOV infection. Some, however, are inflammatory mediators known to be elevated during the acute phase of disease in the blood of ZEBOV-infected humans. Interestingly, the cellular response occurred within the first hour of Ebola virion exposure, i.e. prior to virus gene expression. This observation supports the hypothesis that virion binding or entry mediated by the spike glycoprotein (GP(1,2)) is the primary stimulus for an initial response. Indeed, ZEBOV virions, LPS, and virus-like particles consisting of only the ZEBOV matrix protein VP40 and GP(1,2) (VLP(VP40-GP)) triggered comparable responses in macrophages, including pro-inflammatory and pro-apoptotic signals. In contrast, VLP(VP40) (particles lacking GP(1,2)) caused an aberrant response. This suggests that GP(1,2) binding to macrophages plays an important role in the immediate cellular response.
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- 2011
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10. Progression of pathogenic events in cynomolgus macaques infected with variola virus.
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Victoria Wahl-Jensen, Jennifer A Cann, Kathleen H Rubins, John W Huggins, Robert W Fisher, Anthony J Johnson, Fabian de Kok-Mercado, Thomas Larsen, Jo Lynne Raymond, Lisa E Hensley, and Peter B Jahrling
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Medicine ,Science - Abstract
Smallpox, caused by variola virus (VARV), is a devastating human disease that affected millions worldwide until the virus was eradicated in the 1970 s. Subsequent cessation of vaccination has resulted in an immunologically naive human population that would be at risk should VARV be used as an agent of bioterrorism. The development of antivirals and improved vaccines to counter this threat would be facilitated by the development of animal models using authentic VARV. Towards this end, cynomolgus macaques were identified as adequate hosts for VARV, developing ordinary or hemorrhagic smallpox in a dose-dependent fashion. To further refine this model, we performed a serial sampling study on macaques exposed to doses of VARV strain Harper calibrated to induce ordinary or hemorrhagic disease. Several key differences were noted between these models. In the ordinary smallpox model, lymphoid and myeloid hyperplasias were consistently found whereas lymphocytolysis and hematopoietic necrosis developed in hemorrhagic smallpox. Viral antigen accumulation, as assessed immunohistochemically, was mild and transient in the ordinary smallpox model. In contrast, in the hemorrhagic model antigen distribution was widespread and included tissues and cells not involved in the ordinary model. Hemorrhagic smallpox developed only in the presence of secondary bacterial infections - an observation also commonly noted in historical reports of human smallpox. Together, our results support the macaque model as an excellent surrogate for human smallpox in terms of disease onset, acute disease course, and gross and histopathological lesions.
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- 2011
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11. Demonstration of cross-protective vaccine immunity against an emerging pathogenic Ebolavirus Species.
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Lisa E Hensley, Sabue Mulangu, Clement Asiedu, Joshua Johnson, Anna N Honko, Daphne Stanley, Giulia Fabozzi, Stuart T Nichol, Thomas G Ksiazek, Pierre E Rollin, Victoria Wahl-Jensen, Michael Bailey, Peter B Jahrling, Mario Roederer, Richard A Koup, and Nancy J Sullivan
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Immunologic diseases. Allergy ,RC581-607 ,Biology (General) ,QH301-705.5 - Abstract
A major challenge in developing vaccines for emerging pathogens is their continued evolution and ability to escape human immunity. Therefore, an important goal of vaccine research is to advance vaccine candidates with sufficient breadth to respond to new outbreaks of previously undetected viruses. Ebolavirus (EBOV) vaccines have demonstrated protection against EBOV infection in nonhuman primates (NHP) and show promise in human clinical trials but immune protection occurs only with vaccines whose antigens are matched to the infectious challenge species. A 2007 hemorrhagic fever outbreak in Uganda demonstrated the existence of a new EBOV species, Bundibugyo (BEBOV), that differed from viruses covered by current vaccine candidates by up to 43% in genome sequence. To address the question of whether cross-protective immunity can be generated against this novel species, cynomolgus macaques were immunized with DNA/rAd5 vaccines expressing ZEBOV and SEBOV glycoprotein (GP) prior to lethal challenge with BEBOV. Vaccinated subjects developed robust, antigen-specific humoral and cellular immune responses against the GP from ZEBOV as well as cellular immunity against BEBOV GP, and immunized macaques were uniformly protected against lethal challenge with BEBOV. This report provides the first demonstration of vaccine-induced protective immunity against challenge with a heterologous EBOV species, and shows that Ebola vaccines capable of eliciting potent cellular immunity may provide the best strategy for eliciting cross-protection against newly emerging heterologous EBOV species.
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- 2010
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12. Two-Center Evaluation of Disinfectant Efficacy against Ebola Virus in Clinical and Laboratory Matrices
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Michael Hevey, Sophie J. Smither, Michael Schuit, Claire Marie Filone, Mary S. Reddick-Elick, Amy L. Reese, Lin Eastaugh, David M. Miller, Dana Mitzel, M. Stephen Lever, Victoria Wahl-Jensen, Denise Freeburger, Artemas Herzog, James W. Noah, and Carly Wlazlowski
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filovirus ,laboratory matrix ,0301 basic medicine ,Microbiology (medical) ,Epidemiology ,Virus transmission ,viruses ,Disinfectant ,030106 microbiology ,lcsh:Medicine ,medicine.disease_cause ,lcsh:Infectious and parasitic diseases ,Bleaching Agents ,Ebola virus ,03 medical and health sciences ,chemistry.chemical_compound ,peracetic acid ,Disinfectant Efficacy against Ebola Virus ,Peracetic acid ,medicine ,Humans ,Two-Center Evaluation of Disinfectant Efficacy against Ebola Virus in Clinical and Laboratory Matrices ,lcsh:RC109-216 ,Dried blood ,disinfection ,Cells, Cultured ,Dried Blood Spot Testing ,Ebolavirus ,clinical matrix ,business.industry ,lcsh:R ,Dispatch ,bleach ,Virology ,Titer ,030104 developmental biology ,Infectious Diseases ,chemistry ,two-center evaluation ,Laboratories ,disinfectant efficacy ,business ,Disinfectants - Abstract
Ebola virus (EBOV) in body fluids poses risk for virus transmission. However, there are limited experimental data for such matrices on the disinfectant efficacy against EBOV. We evaluated the effectiveness of disinfectants against EBOV in blood on surfaces. Only 5% peracetic acid consistently reduced EBOV titers in dried blood to the assay limit of quantification.
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- 2018
13. Simian Hemorrhagic Fever Virus Cell Entry Is Dependent on CD163 and Uses a Clathrin-Mediated Endocytosis-Like Pathway
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John G. Bernbaum, Thomas C. Friedrich, Adam L. Bailey, Volker Haucke, David H. O’Connor, Peter B. Jahrling, Shuǐqìng Yú, Nicole Deiuliis, Matthew G. Lackemeyer, Yíngyún Caì, Steven Mazur, Tony L. Goldberg, Michael Lauck, Jens H. Kuhn, Elena Postnikova, Adam McCluskey, Phillip J. Robinson, Sheli R. Radoshitzky, and Victoria Wahl-Jensen
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Simian hemorrhagic fever virus ,Arterivirus ,Immunology ,Antigens, Differentiation, Myelomonocytic ,Receptors, Cell Surface ,Endocytosis ,medicine.disease_cause ,Microbiology ,Cell Line ,Antigens, CD ,Virology ,Chlorocebus aethiops ,medicine ,Animals ,Dynamin ,biology ,Pinocytosis ,Receptor-mediated endocytosis ,Virus Internalization ,Porcine reproductive and respiratory syndrome virus ,biology.organism_classification ,Virus-Cell Interactions ,Cell biology ,Lassa virus ,Insect Science ,Host-Pathogen Interactions ,Receptors, Virus - Abstract
Simian hemorrhagic fever virus (SHFV) causes a severe and almost uniformly fatal viral hemorrhagic fever in Asian macaques but is thought to be nonpathogenic for humans. To date, the SHFV life cycle is almost completely uncharacterized on the molecular level. Here, we describe the first steps of the SHFV life cycle. Our experiments indicate that SHFV enters target cells by low-pH-dependent endocytosis. Dynamin inhibitors, chlorpromazine, methyl-β-cyclodextrin, chloroquine, and concanamycin A dramatically reduced SHFV entry efficiency, whereas the macropinocytosis inhibitors EIPA, blebbistatin, and wortmannin and the caveolin-mediated endocytosis inhibitors nystatin and filipin III had no effect. Furthermore, overexpression and knockout study and electron microscopy results indicate that SHFV entry occurs by a dynamin-dependent clathrin-mediated endocytosis-like pathway. Experiments utilizing latrunculin B, cytochalasin B, and cytochalasin D indicate that SHFV does not hijack the actin polymerization pathway. Treatment of target cells with proteases (proteinase K, papain, α-chymotrypsin, and trypsin) abrogated entry, indicating that the SHFV cell surface receptor is a protein. Phospholipases A2 and D had no effect on SHFV entry. Finally, treatment of cells with antibodies targeting CD163, a cell surface molecule identified as an entry factor for the SHFV-related porcine reproductive and respiratory syndrome virus, diminished SHFV replication, identifying CD163 as an important SHFV entry component. IMPORTANCE Simian hemorrhagic fever virus (SHFV) causes highly lethal disease in Asian macaques resembling human illness caused by Ebola or Lassa virus. However, little is known about SHFV's ecology and molecular biology and the mechanism by which it causes disease. The results of this study shed light on how SHFV enters its target cells. Using electron microscopy and inhibitors for various cellular pathways, we demonstrate that SHFV invades cells by low-pH-dependent, actin-independent endocytosis, likely with the help of a cellular surface protein.
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- 2015
14. A Semi-automated High-Throughput Microtitration Assay for Filoviruses
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Claire Marie, Filone, David, Miller, and Victoria, Wahl-Jensen
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Cell Survival ,Humans ,Filoviridae ,High-Throughput Screening Assays - Abstract
The 50% tissue culture infectious dose (TCID
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- 2017
15. Within-Host Evolution of Simian Arteriviruses in Crab-Eating Macaques
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Yíngyún Caì, Chase W. Nelson, Louise H. Moncla, Victoria Wahl-Jensen, Jens H. Kuhn, Peter B. Jahrling, Adam L. Bailey, Jason T. Weinfurter, Jorge M. Dinis, Andrea M. Weiler, Gabrielle L. Barry, David H. O’Connor, Michael Lauck, Thomas C. Friedrich, Olivia K. Charlier, Tony L. Goldberg, and Joshua C. Johnson
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0301 basic medicine ,Simian hemorrhagic fever virus ,Arterivirus ,viruses ,Immunology ,Biology ,Simian ,Virus Replication ,Polymorphism, Single Nucleotide ,Microbiology ,Genome ,Virus ,Viral hemorrhagic fever ,Open Reading Frames ,03 medical and health sciences ,Virology ,medicine ,Animals ,Selection, Genetic ,ORFS ,Red colobus ,Arterivirus Infections ,Monkey Diseases ,Virus Internalization ,biology.organism_classification ,medicine.disease ,Biological Evolution ,Macaca fascicularis ,030104 developmental biology ,Genetic Diversity and Evolution ,Insect Science ,Viral evolution ,Host-Pathogen Interactions ,RNA, Viral - Abstract
Simian arteriviruses are a diverse clade of viruses infecting captive and wild nonhuman primates. We recently reported that Kibale red colobus virus 1 (KRCV-1) causes a mild and self-limiting disease in experimentally infected crab-eating macaques, while simian hemorrhagic fever virus (SHFV) causes lethal viral hemorrhagic fever. Here we characterize how these viruses evolved during replication in cell culture and in experimentally infected macaques. During passage in cell culture, 68 substitutions that were localized in open reading frames (ORFs) likely associated with host cell entry and exit became fixed in the KRCV-1 genome. However, we did not detect any strong signatures of selection during replication in macaques. We uncovered patterns of evolution that were distinct from those observed in surveys of wild red colobus monkeys, suggesting that these species may exert different adaptive challenges for KRCV-1. During SHFV infection, we detected signatures of selection on ORF 5a and on a small subset of sites in the genome. Overall, our data suggest that patterns of evolution differ markedly among simian arteriviruses and among host species. IMPORTANCE Certain RNA viruses can cross species barriers and cause disease in new hosts. Simian arteriviruses are a diverse group of related viruses that infect captive and wild nonhuman primates, with associated disease severity ranging from apparently asymptomatic infections to severe, viral hemorrhagic fevers. We infected nonhuman primate cell cultures and then crab-eating macaques with either simian hemorrhagic fever virus (SHFV) or Kibale red colobus virus 1 (KRCV-1) and assessed within-host viral evolution. We found that KRCV-1 quickly acquired a large number of substitutions in its genome during replication in cell culture but that evolution in macaques was limited. In contrast, we detected selection focused on SHFV ORFs 5a and 5, which encode putative membrane proteins. These patterns suggest that in addition to diverse pathogenic phenotypes, these viruses may also exhibit distinct patterns of within-host evolution both in vitro and in vivo .
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- 2017
16. Taxonomy of the order Mononegavirales : update 2017
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Andrew J. Easton, Gael Kurath, Jonathan S. Towner, Qi Fang, Calogero Terregino, Noël Tordo, Jean L. Patterson, John H. Werren, John M. Dye, Andrea Maisner, Qisheng Song, Peter J. Walker, Benhur Lee, Pierre Formenty, Richard E. Randall, Ralf Dürrwald, Kim R. Blasdell, Alisa Bochnowski, Bertus K. Rima, Robert A. Lamb, Paul A. Rota, Kartik Chandran, Ralf G. Dietzgen, David M. Stone, Norbert Nowotny, Hideki Kondo, Roger Hewson, Anna E. Whitfield, Janusz T. Paweska, Masayuki Horie, Peter L. Collins, Keizo Tomonaga, Martin Schwemmle, Anthony P. James, Olga Dolnik, Gary P. Kobinger, Beibei Wang, Michael N. Pearson, Nicolás Bejerman, Susan Payne, Ming Li, Jian Hong, Fei Wang, Christopher F. Basler, Robert M. Harding, Jens H. Kuhn, Ron A. M. Fouchier, Charles H. Calisher, Eric M. Leroy, Viktor E. Volchkov, Hideki Ebihara, Lin-Fa Wang, Dàohóng Jiāng, Sina Bavari, Gaya K. Amarasinghe, Ayato Takada, Sergey V. Netesov, Elke Mühlberger, Sophie J. Smither, David Wang, Gongyin Ye, Peter Revill, Martin Beer, Colleen M. Higgins, Yīmíng Bào, Robert B. Tesh, Victoria Wahl-Jensen, Thomas Briese, Zhichao Yan, Dennis Rubbenstroth, Elodie Ghedin, Alexander Bukreyev, Nikos Vasilakis, Virology, Washington University School of Medicine (WUSM), University of Washington [Seattle], National Center for Biotechnology Information (NCBI), Georgia State University, University System of Georgia (USG), Army Medical Research Institute of Infectious Diseases [USA] (USAMRIID), Institute of Diagnostic Virology (IVD), Friedrich-Loeffler-Institut (FLI), Instituto Nacional de Tecnología Agropecuaria, Universidad Nacional de la Patagonia Austral (UNPA), Consejo Nacional de Investigaciones Científicas y Técnicas [Buenos Aires] (CONICET), Commonwealth Scientific and Industrial Research Organisation [Canberra] (CSIRO), Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Columbia Mailman School of Public Health, The University of Texas Medical Branch (UTMB), College of Veterinary Medicine and Biomedical Sciences, Colorado State University [Fort Collins] (CSU), Albert Einstein College of Medicine [New York], National Institute of Allergy and Infectious Diseases [Bethesda] (NIAID-NIH), National Institutes of Health [Bethesda] (NIH), Queensland Alliance for Agriculture and Food Innovation (QAAFI), University of Queensland [Brisbane], Philipps University of Marburg, IDT Biologika, School of Life Sciences, Warwick University, Department of Biochemistry and Molecular Biology, University of Rochester [USA], State Key Laboratory of Rice Biology, China National Rice Research Institute, Chinese Academy of Agricultural Sciences (CAAS), Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Department of Viroscience [Rotterdam, The Netherlands], Erasmus University Medical Center [Rotterdam] (Erasmus MC), Center for Genomics and Systems Biology, Department of Biology [New York], New York University [New York] (NYU), NYU System (NYU)-NYU System (NYU)-New York University [New York] (NYU), NYU System (NYU)-NYU System (NYU), Centre for Tropical Crops and Biocommodities, Queensland University of Technology, Public Health England [Salisbury] (PHE), Auckland University of Technology (AUT), Infections Virales et Pathologie Comparée - UMR 754 (IVPC), Institut National de la Recherche Agronomique (INRA)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon, Kagoshima University, State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Research Centre in Infectious Diseases, CHUL Research Centre and Department of Microbiology and Immunology, Université Laval [Québec] (ULaval)-Faculty of Medicine, Institute of Plant Science and Resources, Okayama University, US Geological Survey [Seattle], United States Geological Survey [Reston] (USGS), Northwestern University [Evanston], Icahn School of Medicine at Mount Sinai [New York] (MSSM), Centre International de Recherches Médicales de Franceville (CIRMF), Institute for Applied Ecology New Zealand (AENZ), Boston University School of Medicine (BUSM), Boston University [Boston] (BU), Novosibirsk State University (NSU), University of Veterinary Medicine [Vienna] (Vetmeduni), Mohammed Bin Rashid University of Medicine and Health Sciences (MBRU), Texas Biomedical Research Institute [San Antonio, TX], Texas A&M University System, National Institute for Communicable Diseases [Johannesburg] (NICD), University of Auckland [Auckland], Biomedical Sciences Research Complex [St Andrews, Scotland] (BSRC), University of St Andrews [Scotland], Victorian Infectious Diseases Reference Laboratory, Queen's University [Belfast] (QUB), National Center for Immunization and Respiratory Diseases, CDC, Centers for Disease Control and Prevention (CDC), University of Freiburg [Freiburg], Defence Science and Technology Laboratory (Dstl), Ministry of Defence (UK) (MOD), University of Missouri School of Medicine, University of Missouri System, Centre for Environment, Fisheries and Aquaculture Science [Weymouth] (CEFAS), Hokkaido University [Sapporo, Japan], Istituto Zooprofilattico Sperimentale delle Venezie (IZSVe), Institute for Virus Research, Kyoto University [Kyoto], Stratégies antivirales, Institut Pasteur [Paris], Institut Pasteur de Guinée, Réseau International des Instituts Pasteur (RIIP), Viral Special Pathogens Branch, Centers for Disease Control and Prevention-WHO Collaborative Centre for Viral Hemorrhagic Fevers, Bases moléculaires de la pathogénicité virale – Molecular Basis of Viral Pathogenicity (BMPV), Centre International de Recherche en Infectiologie - UMR (CIRI), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), National Biodefense Analysis and Countermeasures Center [Frederick], U.S. Social Security Administration, CSIRO Health & Biosecurity, Washington University School of Medicine, Department of Agriculture, Fisheries and Forestry, Ecoscience Precinct, GPO Box 267, Brisbane, Duke-NUS Medical School [Singapore], Department of Biology, Kansas State University, Albert Einstein College of Medicine, Queensland Alliance for Agriculture and Food Innovation, University of Queensland (UQ), Public Health England [Porton Down, Salisbury], Institut National de la Recherche Agronomique (INRA)-École pratique des hautes études (EPHE)-Université Claude Bernard Lyon 1 (UCBL), Faculty of Medicine-Laval University [Québec], Okayama University [Okayama], Centre International de Recherches Médicales de Franceville, Institute for Applied Ecology New Zealand, Texas Biomedical Research Institute [San Antonio, Texas], A&M University, National Institute for Communicable Diseases (NICD), The University of Auckland, Centre for Experimental Medicine [Queen’s University of Belfast], Hokkaido University, Istituto Zooprofilattico Sperimentale delle Venezie, Bases moléculaires de la pathogénicité virale – Molecular Basis of Viral Pathogenicity, Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Duke NUS Medical School, U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID), Columbia University [New York], Philipps Universität Marburg = Philipps University of Marburg, University of Warwick [Coventry], Queensland University of Technology [Brisbane] (QUT), Institut National de la Recherche Agronomique (INRA)-École Pratique des Hautes Études (EPHE), Huazhong Agricultural University [Wuhan] (HZAU), Victorian Infectious Diseases Reference Laboratory [Melbourne, Australia] (VIDRL), Kyoto University, Institut Pasteur [Paris] (IP), Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Biomedical Sciences Research Complex
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0301 basic medicine ,030106 microbiology ,Genome, Viral ,Article ,03 medical and health sciences ,Species Specificity ,Genus ,Phylogenetics ,Virology ,Gene Order ,Viral ,Mononegavirales ,Phylogeny ,Order Mononegavirales ,Genome ,biology ,General Medicine ,Pneumovirus ,biology.organism_classification ,[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology ,030104 developmental biology ,Evolutionary biology ,[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Taxonomy (biology) - Abstract
International audience; In 2017, the order Mononegavirales was expanded by the inclusion of a total of 69 novel species. Five new rhabdovirus genera and one new nyamivirus genus were established to harbor 41 of these species, whereas the remaining new species were assigned to already established genera. Furthermore, non-Latinized binomial species names replaced all paramyxovirus and pneumovirus species names, thereby accomplishing application of binomial species names throughout the entire order. This article presents the updated taxonomy of the order Mononegavirales as now accepted by the International Committee on Taxonomy of Viruses (ICTV).
- Published
- 2017
17. A Semi-automated High-Throughput Microtitration Assay for Filoviruses
- Author
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Victoria Wahl-Jensen, Claire Marie Filone, and David M. Miller
- Subjects
0301 basic medicine ,ENDPOINT DILUTION ASSAY ,03 medical and health sciences ,030104 developmental biology ,Chromatography ,Chemistry ,030106 microbiology ,Viability assay ,Gold standard (test) ,Throughput (business) ,Plate reader - Abstract
The 50% tissue culture infectious dose (TCID50) endpoint dilution assay is one of the gold standard methods for measuring filovirus infectivity. We have increased virology microtitration assay throughput at biosafety level (BSL)-4 by implementing automated liquid handling and semi-automated assay endpoint readout. Utilization of automated liquid handling for cell plating and virus dilution along with optimization of the assay endpoint readout, using a luminescent-based cell viability assay and an automated plate reader, has improved workflow efficiency, reduced operator burden and assay time, decreased assay variability, and increased data return.
- Published
- 2017
18. Implementation of Objective PASC-Derived Taxon Demarcation Criteria for Official Classification of Filoviruses
- Author
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Janusz T. Paweska, Elke Mühlberger, Jonathan S. Towner, Sina Bavari, Kartik Chandran, Eric M. Leroy, Gary P. Kobinger, Ayato Takada, Olga Dolnik, Gaya K. Amarasinghe, Roger Hewson, Victoria Wahl-Jensen, Sophie J. Smither, Christopher F. Basler, Jean L. Patterson, Viktor E. Volchkov, Jens H. Kuhn, Pierre Formenty, Hideki Ebihara, Sergey V. Netesov, John M. Dye, Alexander Bukreyev, Yīmíng Bào, Beijing Institute of Genomics, Chinese Academy of Sciences [Beijing] (CAS)-China Graduate University of the Chinese Academy of Sciences, Department of Pathology and Immunology, Washington University School of Medicine, Georgia State University, University System of Georgia (USG), Army Medical Research Institute of Infectious Diseases [USA] (USAMRIID), The University of Texas Medical Branch (UTMB), Albert Einstein College of Medicine, Philipps University of Marburg, Department of Biochemistry and Molecular Biology, University of Rochester [USA], Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Public Health England [Porton Down, Salisbury], Département de Biochimie et Microbiologie, Université Laval, Centre International de Recherches Médicales de Franceville (CIRMF), Centre International de Recherches Médicales de Franceville, National Emerging Infectious Diseases Laboratories (NEIDL), Boston University [Boston] (BU), Novosibirsk State University (NSU), Texas Biomedical Research Institute [San Antonio, Texas], National Institute for Communicable Diseases (NICD), Defence Science and Technology Laboratory (Dstl), Ministry of Defence (UK) (MOD), Hokkaido University, Viral Special Pathogens Branch, Centers for Disease Control and Prevention-WHO Collaborative Centre for Viral Hemorrhagic Fevers, Bases moléculaires de la pathogénicité virale – Molecular Basis of Viral Pathogenicity, Centre International de Recherche en Infectiologie - UMR (CIRI), Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), National Biodefense Analysis and Countermeasures Center [Frederick], U.S. Social Security Administration, Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Beijing Genomics Institute [Shenzhen] (BGI), Albert Einstein College of Medicine [New York], Public Health England [Salisbury] (PHE), Université Laval [Québec] (ULaval), Texas Biomedical Research Institute [San Antonio, TX], National Institute for Communicable Diseases [Johannesburg] (NICD), Hokkaido University [Sapporo, Japan], Bases moléculaires de la pathogénicité virale – Molecular Basis of Viral Pathogenicity (BMPV), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID), Philipps Universität Marburg = Philipps University of Marburg, Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), and Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)
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0301 basic medicine ,Letter ,marburgvirus ,lcsh:QR1-502 ,lcsh:Microbiology ,ICTV ,Genus ,Software Design ,RefSeq ,Viral ,virus classification ,Phylogeny ,Genome ,Ebolavirus ,Cuevavirus ,Infectious Diseases ,GenBank ,Ebola ,[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Databases, Nucleic Acid ,cuevavirus ,Sequence Analysis ,Algorithms ,filovirus ,030106 microbiology ,Genome, Viral ,Biology ,virus taxonomy ,03 medical and health sciences ,Databases ,Type (biology) ,Species Specificity ,Virology ,ebolavirus ,Virus classification ,Whole genome sequencing ,Base Sequence ,Nucleic Acid ,Whole Genome Sequencing ,Genetic Variation ,Sequence Analysis, DNA ,DNA ,biology.organism_classification ,Filoviridae ,[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology ,030104 developmental biology ,Taxon ,Marburgvirus ,Evolutionary biology ,Mononegavirales - Abstract
The mononegaviral family Filoviridae has eight members assigned to three genera and seven species. Until now, genus and species demarcation were based on arbitrarily chosen filovirus genome sequence divergence values (approximate to 50% for genera, approximate to 30% for species) and arbitrarily chosen phenotypic virus or virion characteristics. Here we report filovirus genome sequence-based taxon demarcation criteria using the publicly accessible PAirwise Sequencing Comparison (PASC) tool of the US National Center for Biotechnology Information (Bethesda, MD, USA). Comparison of all available filovirus genomes in GenBank using PASC revealed optimal genus demarcation at the 55-58% sequence diversity threshold range for genera and at the 23-36% sequence diversity threshold range for species. Because these thresholds do not change the current official filovirus classification, these values are now implemented as filovirus taxon demarcation criteria that may solely be used for filovirus classification in case additional data are absent. A near-complete, coding-complete, or complete filovirus genome sequence will now be required to allow official classification of any novel "filovirus." Classification of filoviruses into existing taxa or determining the need for novel taxa is now straightforward and could even become automated using a presented algorithm/flowchart rooted in RefSeq (type) sequences.
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- 2017
19. Filovirus RefSeq Entries: Evaluation and Selection of Filovirus Type Variants, Type Sequences, and Names
- Author
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Stephen K. Gire, Kristian G. Andersen, James Pettitt, Victoria Wahl-Jensen, Rachel Sealfon, Peter B. Jahrling, Janusz T. Paweska, Mark S. Lever, Eric M. Leroy, Nancy J. Sullivan, Louise Pitt, Erica Ollmann Saphire, Jonathan S. Towner, Olga Dolnik, Viktor E. Volchkov, Alexander N. Freiberg, Jean-Paul Gonzalez, Guido van der Groen, Lisa E. Hensley, Gary P. Kobinger, Christian T. Happi, Clarence J. Peters, Pardis C. Sabeti, Stuart T. Nichol, Kelly L. Warfield, Nicole L. Garza, Sina Bavari, Sunday Omilabu, Pierre Formenty, J. Rodney Brister, Jean L. Patterson, Stephan Becker, Aleksandr M. Shestopalov, Michael Hevey, Sophie J. Smither, Valentina A. Volchkova, Jason Kindrachuk, Yiming Bao, Kartik Chandran, Ralf G. Dietzgen, Sheli R. Radoshitzky, Elke Mühlberger, Robert F. Garry, Thomas Hoenen, Robert Swanepoel, Daniel J. Park, Steven B. Bradfute, Paul W. Fenimore, Jens H. Kuhn, Alexander A. Chepurnov, Tadeusz J. Kochel, Manfred Weidmann, Anna N. Honko, Elena I. Ryabchikova, John M. Dye, Karl M. Johnson, Nicholas H. Bergman, Gustavo Palacios, Ayato Takada, Daniel F. Lackner, Gene G. Olinger, Hans-Dieter Klenk, Olga Blinkova, Sven Enterlein, Robert A. Davey, Sergey V. Netesov, Andrew S. Herbert, Richard S. Bennett, Rekha G. Panchal, Norman A. Doggett, Georgy M. Ignatyev, Matthew G. Lackemeyer, Joshua C. Johnson, Alexander Bukreyev, Travis K. Warren, and Anthony Griffiths
- Subjects
virus strain ,Letter ,genome annotation ,marburgvirus ,lcsh:QR1-502 ,virus nomenclature ,medicine.disease_cause ,lcsh:Microbiology ,virus variant ,Ebola virus ,ICTV ,Bundibugyo virus ,RefSeq ,Lloviu virus ,cDNA clone ,virus classification ,Ravn virus ,Marburg virus ,biology ,Genome project ,Cuevavirus ,Sudan virus ,Infectious Diseases ,Ebola ,Reston virus ,Databases, Nucleic Acid ,cuevavirus ,filovirus ,filovirid ,Computational biology ,virus taxonomy ,International Committee on Taxonomy of Viruses ,Evolution, Molecular ,Annotation ,reverse genetics ,Virology ,medicine ,Humans ,virus isolate ,Selection, Genetic ,Virus classification ,ebolavirus ,Sequence (medicine) ,mononegavirus ,mononegavirad ,biology.organism_classification ,Filoviridae ,Mononegavirales ,Taï Forest virus - Abstract
Sequence determination of complete or coding-complete genomes of viruses is becoming common practice for supporting the work of epidemiologists, ecologists, virologists, and taxonomists. Sequencing duration and costs are rapidly decreasing, sequencing hardware is under modification for use by non-experts, and software is constantly being improved to simplify sequence data management and analysis. Thus, analysis of virus disease outbreaks on the molecular level is now feasible, including characterization of the evolution of individual virus populations in single patients over time. The increasing accumulation of sequencing data creates a management problem for the curators of commonly used sequence databases and an entry retrieval problem for end users. Therefore, utilizing the data to their fullest potential will require setting nomenclature and annotation standards for virus isolates and associated genomic sequences. The National Center for Biotechnology Information’s (NCBI’s) RefSeq is a non-redundant, curated database for reference (or type) nucleotide sequence records that supplies source data to numerous other databases. Building on recently proposed templates for filovirus variant naming [ ()////-], we report consensus decisions from a majority of past and currently active filovirus experts on the eight filovirus type variants and isolates to be represented in RefSeq, their final designations, and their associated sequences.
- Published
- 2014
20. Construction and Nonclinical Testing of a Puumala Virus Synthetic M Gene-Based DNA Vaccine
- Author
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Rebecca L. Brocato, Connie S. Schmaljohn, M. J. Josleyn, Victoria Wahl-Jensen, and Jay W. Hooper
- Subjects
Microbiology (medical) ,Orthohantavirus ,Hantavirus Infections ,Clinical Biochemistry ,Immunology ,Andes virus ,Viral Plaque Assay ,Cross Reactions ,Antibodies, Viral ,Puumala virus ,Cell Line ,DNA vaccination ,Viral Matrix Proteins ,Neutralization Tests ,Cricetinae ,Chlorocebus aethiops ,Vaccines, DNA ,Animals ,Immunology and Allergy ,Vector (molecular biology) ,Vero Cells ,Hantavirus ,Vaccines ,biology ,Viral Vaccine ,Vaccination ,virus diseases ,Viral Vaccines ,biology.organism_classification ,Antibodies, Neutralizing ,Macaca mulatta ,Virology ,Hemorrhagic Fever with Renal Syndrome ,COS Cells ,DNA, Viral ,Hantavirus Infection - Abstract
Puumala virus (PUUV) is a causative agent of hemorrhagic fever with renal syndrome (HFRS). Although PUUV-associated HFRS does not result in high case-fatality rates, the social and economic impact is considerable. There is no licensed vaccine or specific therapeutic to prevent or treat HFRS. Here we report the synthesis of a codon-optimized, full-length M segment open reading frame and its cloning into a DNA vaccine vector to produce the plasmid pWRG/PUU-M(s2). pWRG/PUU-M(s2) delivered by gene gun produced high-titer neutralizing antibodies in hamsters and nonhuman primates. Vaccination with pWRG/PUU-M(s2) protected hamsters against infection with PUUV but not against infection by related HFRS-associated hantaviruses. Unexpectedly, vaccination protected hamsters in a lethal disease model of Andes virus (ANDV) in the absence of ANDV cross-neutralizing antibodies. This is the first evidence that an experimental DNA vaccine for HFRS can provide protection in a hantavirus lethal disease model.
- Published
- 2013
21. Taxonomy of the order Mononegavirales: update 2016
- Author
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Ralf Dürrwald, Krisztián Bányai, Robert A. Lamb, Hideki Kondo, Alexander Bukreyev, Anna N. Clawson, Calogero Terregino, Robert B. Tesh, Andrew J. Easton, Andrea Maisner, Paul A. Rota, Gael Kurath, Kartik Chandran, Charles H. Calisher, Ralf G. Dietzgen, Janusz T. Paweska, Szilvia Marton, Dennis Rubbenstroth, Masayuki Horie, Juliana Freitas-Astúa, Bertus K. Rima, Jonathan S. Towner, Viktor E. Volchkov, Eric M. Leroy, David M. Stone, Susan Payne, Kwok-Yung Yuen, Hideki Ebihara, Lin-Fa Wang, Lìjiāng Liú, C. Li, Nikos Vasilakis, Olga Dolnik, Gaya K. Amarasinghe, Gary P. Kobinger, Jean L. Patterson, Sergio Lenardon, Xian Dan Lin, Leslie L. Domier, Mang Shi, Pierre Formenty, Ben Longdon, Anna E. Whitfield, Sina Bavari, Timothy H. Hyndman, Martin Verbeek, E. W. Kitajima, Elke Mühlberger, Peter J. Walker, Ayato Takada, Mark D. Stenglein, François Xavier Briand, David Wang, Elodie Ghedin, Jiāsēn Chéng, Keizo Tomonaga, Norbert Nowotny, Roger Hewson, Noël Tordo, Jun Hua Tian, Nicolás Bejerman, John M. Dye, Christopher F. Basler, Yong-Zhen Zhang, Kim R. Blasdell, Yanping Fu, Sophie J. Smither, Richard E. Randall, Jens H. Kuhn, Jiǎtāo Xiè, Victoria Wahl-Jensen, Thierry Wetzel, Martin Schwemmle, Michael M. Goodin, John A. Walsh, Thomas Briese, Yīmíng Bào, Peter L. Collins, Dàohóng Jiāng, Sergey V. Netesov, Ron A. M. Fouchier, Szilvia L. Farkas, Claudio L. Afonso, US Department of Agriculture, Washington University School of Medicine (WUSM), University of Washington [Seattle], Centre for Agricultural Research [Budapest] (ATK), Hungarian Academy of Sciences (MTA), National Center for Biotechnology Information (NCBI), Georgia State University, University System of Georgia (USG), Army Medical Research Institute of Infectious Diseases [USA] (USAMRIID), Instituto Nacional de Tecnología Agropecuaria, Universidad Nacional de la Patagonia Austral (UNPA), Consejo Nacional de Investigaciones Científicas y Técnicas [Buenos Aires] (CONICET), Commonwealth Scientific and Industrial Research Organisation [Canberra] (CSIRO), Laboratoire de Ploufragan-Plouzané-Niort [ANSES], Agence nationale de sécurité sanitaire de l'alimentation, de l'environnement et du travail (ANSES), Columbia Mailman School of Public Health, The University of Texas Medical Branch (UTMB), Department of Veterinary Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University System, Albert Einstein College of Medicine [New York], Huazhong Agricultural University, Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, National Institute of Allergy and Infectious Diseases [Bethesda] (NIAID-NIH), National Institutes of Health [Bethesda] (NIH), Queensland Alliance for Agriculture and Food Innovation - Centre for Animal Science, University of Queensland [Brisbane], Philipps University of Marburg, University of Illinois [Chicago] (UIC), University of Illinois System, IDT Biologika, School of Life Sciences, Warwick University, Laboratory of Persistent Viral Diseases, LABOKLIN, Embrapa Cassava and Fruits, Brazilian Agricultural Research Corporation (Embrapa), Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Department of Viroscience [Rotterdam, The Netherlands], Erasmus University Medical Center [Rotterdam] (Erasmus MC), Center for Genomics and Systems Biology, Department of Biology [New York], New York University [New York] (NYU), NYU System (NYU)-NYU System (NYU)-New York University [New York] (NYU), NYU System (NYU)-NYU System (NYU), Department of Plant Pathology, University of Kentucky, University of Kentucky, Public Health England [Salisbury] (PHE), Kagoshima University, School of Veterinary and Life Sciences [Murdoch], Murdoch University, State Key Laboratory of Agricultural Microbiology, Escola Superior de Agricultura 'Luiz de Queiroz' (ESALQ), Universidade de São Paulo (USP), Research Centre in Infectious Diseases, CHUL Research Centre and Department of Microbiology and Immunology, Université Laval [Québec] (ULaval)-Faculty of Medicine, Institute of Plant Science and Resources, Okayama University, US Geological Survey [Seattle], United States Geological Survey [Reston] (USGS), Northwestern University [Evanston], Centre International de Recherches Médicales de Franceville (CIRMF), State Key Laboratory for Infectious Disease prevention and Control, Beijing Institute of Technology (BIT), Wēnzhōu Center for Disease Control and Prevention, Department of Genetics University of Cambridge, University of Cambridge [UK] (CAM), Boston University School of Medicine (BUSM), Boston University [Boston] (BU), Novosibirsk State University (NSU), University of Veterinary Medicine [Vienna] (Vetmeduni), Mohammed Bin Rashid University of Medicine and Health Sciences (MBRU), Texas Biomedical Research Institute [San Antonio, TX], College of Veterinary Medicine and Biomedical Sciences, National Institute for Communicable Diseases [Johannesburg] (NICD), Biomedical Sciences Research Complex [St Andrews, Scotland] (BSRC), University of St Andrews [Scotland], Queen's University [Belfast] (QUB), National Center for Immunization and Respiratory Diseases, CDC, Centers for Disease Control and Prevention (CDC), University of Freiburg [Freiburg], Chinese Center for Disease Control and Prevention, Defence Science and Technology Laboratory (Dstl), Ministry of Defence (UK) (MOD), Department of Microbiology, Immunology and Pathology, Colorado State University [Fort Collins] (CSU), Centre for Environment, Fisheries and Aquaculture Science [Weymouth] (CEFAS), Hokkaido University [Sapporo, Japan], Istituto Zooprofilattico Sperimentale delle Venezie (IZSVe), Wǔhàn Center for Disease Control and Prevention, Institute for Virus Research, Kyoto University [Kyoto], Stratégies antivirales, Institut Pasteur [Paris], Institut Pasteur de Guinée, Réseau International des Instituts Pasteur (RIIP), Viral Special Pathogens Branch, Centers for Disease Control and Prevention-WHO Collaborative Centre for Viral Hemorrhagic Fevers, Wageningen University and Research [Wageningen] (WUR), Bases moléculaires de la pathogénicité virale – Molecular Basis of Viral Pathogenicity (BMPV), Centre International de Recherche en Infectiologie - UMR (CIRI), Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), National Biodefense Analysis and Countermeasures Center [Frederick], U.S. Social Security Administration, CSIRO Health & Biosecurity, Departments of Molecular Microbiology and Pathology & Immunology, Department of Agriculture, Fisheries and Forestry, Ecoscience Precinct, GPO Box 267, Brisbane, Duke-NUS Medical School [Singapore], Kansas State University, State Key Laboratory of Emerging Infectious Diseases & Department of Microbiology, The University of Hong Kong (HKU)-Li Ka Shing Faculty of Medicine, State Key Laboratory of Emerging Infectious Diseases, The University of Hong Kong (HKU), French Agency for Food, Environmental and Occupational Health & Safety (Anses) - Veterinary epidemiology, Albert Einstein College of Medicine, Public Health England [Porton Down, Salisbury], Faculty of Medicine-Laval University [Québec], Okayama University [Okayama], Centre International de Recherches Médicales de Franceville, Texas Biomedical Research Institute [San Antonio, Texas], A&M University, National Institute for Communicable Diseases (NICD), Centre for Experimental Medicine [Queen’s University of Belfast], Hokkaido University, Istituto Zooprofilattico Sperimentale delle Venezie [Padova], Wageningen University and Research Centre [Wageningen] (WUR), Bases moléculaires de la pathogénicité virale – Molecular Basis of Viral Pathogenicity, Duke NUS Medical School, U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID), Columbia University [New York], Huazhong Agricultural University [Wuhan] (HZAU), Philipps Universität Marburg = Philipps University of Marburg, University of Warwick [Coventry], University of Kentucky (UK), Universidade de São Paulo = University of São Paulo (USP), Kyoto University, Institut Pasteur [Paris] (IP), Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Virology, and Biomedical Sciences Research Complex
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0301 basic medicine ,030106 microbiology ,Zoology ,Genome, Viral ,Article ,03 medical and health sciences ,Genus ,Phylogenetics ,Virology ,Crustavirus ,Life Science ,Viral ,Mononegavirales ,Phylogeny ,Order Mononegavirales ,QR355 ,Genome ,biology ,Entomology & Disease Management ,General Medicine ,biology.organism_classification ,[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology ,Pneumoviridae ,Subfamily Pneumovirinae ,MONONEGAVIRALES ,030104 developmental biology ,Evolutionary biology ,Wildlife Ecology and Conservation ,[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Taxonomy (biology) ,RA ,RC - Abstract
International audience; In 2016, the order Mononegavirales was emended through the addition of two new families (Mymonaviridae and Sunviridae), the elevation of the paramyxoviral subfamily Pneumovirinae to family status (Pneumoviridae), the addition of five free-floating genera (Anphevirus, Arlivirus, Chengtivirus, Crustavirus, and Wastrivirus), and several other changes at the genus and species levels. This article presents the updated taxonomy of the order Mononegavirales as now accepted by the International Committee on Taxonomy of Viruses (ICTV).
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- 2016
22. Differences in the Comparative Stability of Ebola Virus Makona-C05 and Yambuku-Mayinga in Blood
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Carly Wlazlowski, Victoria Wahl-Jensen, Leremy A. Colf, James W. Noah, Michael Hevey, David M. Miller, Artemas Herzog, Michael Schuit, Claire Marie Filone, and Mary S. Reddick-Elick
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0301 basic medicine ,RNA viruses ,Physiology ,Polymers ,lcsh:Medicine ,medicine.disease_cause ,Pathology and Laboratory Medicine ,Feces ,Chlorocebus aethiops ,Medicine and Health Sciences ,lcsh:Science ,Viral Genomics ,Multidisciplinary ,Human blood ,Hematology ,Genomics ,Ebolavirus ,Body Fluids ,Viral Persistence and Latency ,Chemistry ,Blood ,Macromolecules ,Medical Microbiology ,Filoviruses ,Viral Pathogens ,Physical Sciences ,Metallurgy ,Viruses ,Biological Cultures ,Anatomy ,Pathogens ,Ebola Virus ,Polypropylene ,Research Article ,Materials by Structure ,Vomiting ,Materials Science ,Microbial Genomics ,Biology ,Research and Analysis Methods ,Microbiology ,03 medical and health sciences ,Species Specificity ,Virology ,medicine ,Alloys ,Genetics ,Animals ,Humans ,Microbial Pathogens ,Personal Protective Equipment ,Vero Cells ,Ebola virus ,Hemorrhagic Fever Viruses ,lcsh:R ,Organisms ,Outbreak ,Biology and Life Sciences ,Humidity ,Cell Cultures ,Stainless Steel ,Polymer Chemistry ,030104 developmental biology ,Steel ,Vector (epidemiology) ,lcsh:Q - Abstract
In support of the response to the 2013-2016 Ebola virus disease (EVD) outbreak in Western Africa, we investigated the persistence of Ebola virus/H.sapiens-tc/GIN/2014/Makona-C05 (EBOV/Mak-C05) on non-porous surfaces that are representative of hospitals, airplanes, and personal protective equipment. We performed persistence studies in three clinically-relevant human fluid matrices (blood, simulated vomit, and feces), and at environments representative of in-flight airline passenger cabins, environmentally-controlled hospital rooms, and open-air Ebola treatment centers in Western Africa. We also compared the surface stability of EBOV/Mak-C05 to that of the prototype Ebola virus/H.sapiens-tc/COD/1976/Yambuku-Mayinga (EBOV/Yam-May), in a subset of these conditions. We show that on inert, non-porous surfaces, EBOV decay rates are matrix- and environment-dependent. Among the clinically-relevant matrices tested, EBOV persisted longest in dried human blood, had limited viability in dried simulated vomit, and did not persist in feces. EBOV/Mak-C05 and EBOV/Yam-May decay rates in dried matrices were not significantly different. However, during the drying process in human blood, EBOV/Yam-May showed significantly greater loss in viability than EBOV/Mak-C05 under environmental conditions relevant to the outbreak region, and to a lesser extent in conditions relevant to an environmentally-controlled hospital room. This factor may contribute to increased communicability of EBOV/Mak-C05 when surfaces contaminated with dried human blood are the vector and may partially explain the magnitude of the most recent outbreak, compared to prior outbreaks. These EBOV persistence data will improve public health efforts by informing risk assessments, structure remediation decisions, and response procedures for future EVD outbreaks.
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- 2016
23. Minigenomes, transcription and replication competent virus-like particles and beyond: Reverse genetics systems for filoviruses and other negative stranded hemorrhagic fever viruses
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Thomas Hoenen, Fabian de Kok-Mercado, Jens H. Kuhn, Allison Groseth, and Victoria Wahl-Jensen
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DNA, Complementary ,Transcription, Genetic ,Bunyaviridae ,viruses ,Genome, Viral ,Biology ,Transfection ,Virus Replication ,Antiviral Agents ,Article ,Replication competent virus ,law.invention ,Viral Proteins ,Viral life cycle ,Genes, Reporter ,law ,Transcription (biology) ,Virology ,Arenaviridae ,Virus Release ,Pharmacology ,RNA ,Virus Internalization ,Filoviridae ,Reverse genetics ,Ribonucleoproteins ,Viral replication ,Recombinant DNA ,Viral genome replication - Abstract
Reverse-genetics systems are powerful tools enabling researchers to study the replication cycle of RNA viruses, including filoviruses and other hemorrhagic fever viruses, as well as to discover new antivirals. They include full-length clone systems as well as a number of life cycle modeling systems. Full-length clone systems allow for the generation of infectious, recombinant viruses, and thus are an important tool for studying the virus replication cycle in its entirety. In contrast, life cycle modeling systems such as minigenome and transcription and replication competent virus-like particle systems can be used to simulate and dissect parts of the virus life cycle outside of containment facilities. Minigenome systems are used to model viral genome replication and transcription, whereas transcription and replication competent virus-like particle systems also model morphogenesis and budding as well as infection of target cells. As such, these modeling systems have tremendous potential to further the discovery and screening of new antivirals targeting hemorrhagic fever viruses. This review provides an overview of currently established reverse genetics systems for hemorrhagic fever-causing negative-sense RNA viruses, with a particular emphasis on filoviruses, and the potential application of these systems for antiviral research.
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- 2011
24. Ebolavirus -Peptide Immunoadhesins Inhibit Marburgvirus and Ebolavirus Cell Entry
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M. Javad Aman, Xiaoli Chi, Kelly L. Warfield, Lian Dong, Sina Bavari, Michael Farzan, Peter B. Jahrling, Jens H. Kuhn, Jacqueline D. Gearhart, Sheli R. Radoshitzky, Cary Retterer, Victoria Wahl-Jensen, James M. Cunningham, Steven B. Bradfute, Viktor E. Volchkov, Krishna P. Kota, John Misasi, Philip J. Kranzusch, and Marc A. Hogenbirk
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viruses ,Recombinant Fusion Proteins ,Immunology ,Biology ,medicine.disease_cause ,Microbiology ,Antiviral Agents ,Virus ,Cell Line ,Marburg virus ,Viral Proteins ,Virology ,medicine ,Animals ,Humans ,Ebolavirus ,chemistry.chemical_classification ,Biological Products ,Ebola virus ,Virus Internalization ,Marburgvirus ,biology.organism_classification ,Fusion protein ,Bundibugyo virus ,Immunoglobulin Fc Fragments ,Virus-Cell Interactions ,chemistry ,Insect Science ,Glycoprotein - Abstract
With the exception of Reston and Lloviu viruses, filoviruses (marburgviruses, ebolaviruses, and “cuevaviruses”) cause severe viral hemorrhagic fevers in humans. Filoviruses use a class I fusion protein, GP 1,2 , to bind to an unknown, but shared, cell surface receptor to initiate virus-cell fusion. In addition to GP 1,2 , ebolaviruses and cuevaviruses, but not marburgviruses, express two secreted glycoproteins, soluble GP (sGP) and small soluble GP (ssGP). All three glycoproteins have identical N termini that include the receptor-binding region (RBR) but differ in their C termini. We evaluated the effect of the secreted ebolavirus glycoproteins on marburgvirus and ebolavirus cell entry, using Fc-tagged recombinant proteins. Neither sGP-Fc nor ssGP-Fc bound to filovirus-permissive cells or inhibited GP 1,2 -mediated cell entry of pseudotyped retroviruses. Surprisingly, several Fc-tagged Δ-peptides, which are small C-terminal cleavage products of sGP secreted by ebolavirus-infected cells, inhibited entry of retroviruses pseudotyped with Marburg virus GP 1,2 , as well as Marburg virus and Ebola virus infection in a dose-dependent manner and at low molarity despite absence of sequence similarity to filovirus RBRs. Fc-tagged Δ-peptides from three ebolaviruses (Ebola virus, Sudan virus, and Taï Forest virus) inhibited GP 1,2 -mediated entry and infection of viruses comparably to or better than the Fc-tagged RBRs, whereas the Δ-peptide-Fc of an ebolavirus nonpathogenic for humans (Reston virus) and that of an ebolavirus with lower lethality for humans (Bundibugyo virus) had little effect. These data indicate that Δ-peptides are functional components of ebolavirus proteomes. They join cathepsins and integrins as novel modulators of filovirus cell entry, might play important roles in pathogenesis, and could be exploited for the synthesis of powerful new antivirals.
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- 2011
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25. Being obsessive-compulsive about terminology and nomenclature is not a vice, but a virtue
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Jens H. Kuhn and Victoria Wahl-Jensen
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Virtue ,media_common.quotation_subject ,General Engineering ,Linguistics ,Terminology ,Obsessive compulsive ,Reading (process) ,General Earth and Planetary Sciences ,Natural (music) ,Syllabic verse ,Chinese characters ,Psychology ,Nomenclature ,General Environmental Science ,media_common - Abstract
At first glance, discussions among linguists seem utterly absurd to those without linguistic training. Scientific debates on the Chinese languages are a good example. For decades, linguists have been arguing over how many Chinese languages exist. Should Chinese characters be classified as ideographs or pictographs, and are they phonetic or rather syllabic in nature (DeFrancis 1984)? Reading linguistic treatises is reminiscent of reading any specialized scientific article—they are difficult to understand if one is not among the experts. It is only natural that non-experts ask sooner or later whether all of these linguistic discussions are of any practical use, and how much money, often derived from taxes, is spent on them. Of course these discussions are of practical use and money is well spent.
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- 2010
26. Immune Serum Produced by DNA Vaccination Protects Hamsters against Lethal Respiratory Challenge with Andes Virus
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Jay W. Hooper, Anthony M. Ferro, and Victoria Wahl-Jensen
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Male ,Orthohantavirus ,Hantavirus Infections ,Immunology ,Andes virus ,Biology ,Antibodies, Viral ,Microbiology ,Median lethal dose ,DNA vaccination ,Lethal Dose 50 ,Neutralization Tests ,Cricetinae ,Virology ,Vaccines and Antiviral Agents ,Vaccines, DNA ,Animals ,Hantavirus ,Hantavirus pulmonary syndrome ,Mesocricetus ,Lethal dose ,Immunization, Passive ,biology.organism_classification ,Insect Science ,Female ,Rabbits ,Hantavirus Infection - Abstract
Hantavirus pulmonary syndrome (HPS) is a highly pathogenic disease (40% case fatality rate) carried by rodents chronically infected with certain viruses within the genus Hantavirus of the family Bunyaviridae . The primary mode of transmission to humans is thought to be inhalation of excreta from infected rodents; however, ingestion of contaminated material and rodent bites are also possible modes of transmission. Person-to-person transmission of HPS caused by one species of hantavirus, Andes virus (ANDV), has been reported. Previously, we reported that ANDV injected intramuscularly causes a disease in Syrian hamsters that closely resembles HPS in humans. Here we tested whether ANDV was lethal in hamsters when it was administered by routes that more accurately model the most common routes of human infection, i.e., the subcutaneous, intranasal, and intragastric routes. We discovered that ANDV was lethal by all three routes. Remarkably, even at very low doses, ANDV was highly pathogenic when it was introduced by the mucosal routes (50% lethal dose [LD 50 ], ∼100 PFU). We performed passive transfer experiments to test the capacity of neutralizing antibodies to protect against lethal intranasal challenge. The neutralizing antibodies used in these experiments were produced in rabbits vaccinated by electroporation with a previously described ANDV M gene-based DNA vaccine, pWRG/AND-M. Hamsters that were administered immune serum on days −1 and +5 relative to challenge were protected against intranasal challenge (21 LD 50 ). These findings demonstrate the utility of using the ANDV hamster model to study transmission across mucosal barriers and provide evidence that neutralizing antibodies produced by DNA vaccine technology can be used to protect against challenge by the respiratory route.
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- 2008
27. Characterization of the Host Response to Pichinde Virus Infection in the Syrian Golden Hamster by Species-Specific Kinome Analysis*
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Reed F. Johnson, David Safronetz, Scott Napper, Shane D. Falcinelli, Peter B. Jahrling, Brian B. Gowen, Jason Kindrachuk, Anthony Kusalik, Joseph Prescott, Victoria Wahl-Jensen, and Brett Trost
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Vascular Endothelial Growth Factor A ,Proteome ,Viral pathogenesis ,Hamster ,Biology ,Biochemistry ,Hemorrhagic Fever, American ,Analytical Chemistry ,Viral hemorrhagic fever ,Immune system ,Species Specificity ,medicine ,Animals ,Kinome ,Phosphorylation ,Molecular Biology ,Lung ,Pichinde virus ,Mesocricetus ,Research ,Interleukins ,Toll-Like Receptors ,NF-kappa B ,medicine.disease ,biology.organism_classification ,Virology ,Disease Models, Animal ,Female ,Signal transduction ,Protein Kinases ,Golden hamster ,Signal Transduction - Abstract
The Syrian golden hamster has been increasingly used to study viral hemorrhagic fever (VHF) pathogenesis and countermeasure efficacy. As VHFs are a global health concern, well-characterized animal models are essential for both the development of therapeutics and vaccines as well as for increasing our understanding of the molecular events that underlie viral pathogenesis. However, the paucity of reagents or platforms that are available for studying hamsters at a molecular level limits the ability to extract biological information from this important animal model. As such, there is a need to develop platforms/technologies for characterizing host responses of hamsters at a molecular level. To this end, we developed hamster-specific kinome peptide arrays to characterize the molecular host response of the Syrian golden hamster. After validating the functionality of the arrays using immune agonists of defined signaling mechanisms (lipopolysaccharide (LPS) and tumor necrosis factor (TNF)-α), we characterized the host response in a hamster model of VHF based on Pichinde virus (PICV(1)) infection by performing temporal kinome analysis of lung tissue. Our analysis revealed key roles for vascular endothelial growth factor (VEGF), interleukin (IL) responses, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling, and Toll-like receptor (TLR) signaling in the response to PICV infection. These findings were validated through phosphorylation-specific Western blot analysis. Overall, we have demonstrated that hamster-specific kinome arrays are a robust tool for characterizing the species-specific molecular host response in a VHF model. Further, our results provide key insights into the hamster host response to PICV infection and will inform future studies with high-consequence VHF pathogens.
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- 2015
28. Structure-Function Analysis of the Soluble Glycoprotein, sGP, of Ebola Virus
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Heinz Feldmann, Darryl Falzarano, Jochen Seebach, Kristin Wolf, Hans-Joachim Schnittler, Oleg V. Krokhin, and Victoria Wahl-Jensen
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Glycosylation ,Protein Conformation ,Molecular Sequence Data ,Mutant ,Biochemistry ,Structure-Activity Relationship ,chemistry.chemical_compound ,Protein structure ,Viral Envelope Proteins ,Humans ,Amino Acid Sequence ,Cysteine ,Disulfides ,Molecular Biology ,Peptide sequence ,Cells, Cultured ,chemistry.chemical_classification ,Organic Chemistry ,Endothelial Cells ,Ebolavirus ,Transmembrane protein ,Amino acid ,chemistry ,Mutation ,Molecular Medicine ,Glycoprotein - Abstract
In addition to the transmembrane protein, GP(1,2), the Ebola virus glycoprotein gene encodes the soluble glycoproteins sGP and Delta-peptide. Two more soluble proteins, GP(1) and GP(1,2DeltaTM), are generated from GP(1,2) as a result of disulfide-bond instability and proteolytic cleavage, respectively, and are shed from the surface of infected cells. The sGP glycoprotein is secreted as a disulfide-linked homodimer, but there have been conflicting reports on whether it is arranged in a parallel or antiparallel orientation. Off-line HPLC-MALDI-TOF MS (MS/MS) was used to identify the arrangement of all disulfide bonds and simultaneously determine site-specific information regarding N-glycosylation. Our data prove that sGP is a parallel homodimer that contains C53-C53' and C306-C306' disulfide bonds, and although there are six predicted N-linked carbohydrate sites, only five are consistently glycosylated. The disulfide bond arrangement was confirmed by using cysteine to glycine mutations at amino acid positions 53 and 306. The mutants had a reduced ability to rescue the barrier function of TNF-alpha-treated endothelial cells--a function previously reported for sGP. This indicates that these disulfide bonds are critical for the proposed anti-inflammatory function of sGP.
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- 2006
29. Effects of Ebola Virus Glycoproteins on Endothelial Cell Activation and Barrier Function
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Ute Ströher, Heinz Feldmann, Victoria Wahl-Jensen, Tatiana Afanasieva, Hans-Joachim Schnittler, and Jochen Seebach
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viruses ,Immunology ,Vascular Cell Adhesion Molecule-1 ,Viral Nonstructural Proteins ,medicine.disease_cause ,Microbiology ,Virus ,VP40 ,Virology ,E-selectin ,medicine ,Humans ,RNA, Messenger ,Mononegavirales ,Cells, Cultured ,Barrier function ,Glycoproteins ,Ebola virus ,biology ,Tumor Necrosis Factor-alpha ,Virion ,Endothelial Cells ,Ebolavirus ,Intercellular Adhesion Molecule-1 ,biology.organism_classification ,Cell biology ,Endothelial stem cell ,Insect Science ,biology.protein ,Pathogenesis and Immunity ,E-Selectin ,Cell activation - Abstract
Ebola virus causes severe hemorrhagic fever with high mortality rates in humans and nonhuman primates. Vascular instability and dysregulation are disease-decisive symptoms during severe infection. While the transmembrane glycoprotein GP 1,2 has been shown to cause endothelial cell destruction, the role of the soluble glycoproteins in pathogenesis is largely unknown; however, they are hypothesized to be of biological relevance in terms of target cell activation and/or increase of endothelial permeability. Here we show that virus-like particles (VLPs) consisting of the Ebola virus matrix protein VP40 and GP 1,2 were able to activate endothelial cells and induce a decrease in barrier function as determined by impedance spectroscopy and hydraulic conductivity measurements. In contrast, the soluble glycoproteins sGP and Δ-peptide did not activate endothelial cells or change the endothelial barrier function. The VLP-induced decrease in barrier function was further enhanced by the cytokine tumor necrosis factor alpha (TNF-α), which is known to induce a long-lasting decrease in endothelial cell barrier function and is hypothesized to play a key role in Ebola virus pathogenesis. Surprisingly, sGP, but not Δ-peptide, induced a recovery of endothelial barrier function following treatment with TNF-α. Our results demonstrate that Ebola virus GP 1,2 in its particle-associated form mediates endothelial cell activation and a decrease in endothelial cell barrier function. Furthermore, sGP, the major soluble glycoprotein of Ebola virus, seems to possess an anti-inflammatory role by protecting the endothelial cell barrier function.
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- 2005
30. Properties of Replication-Competent Vesicular Stomatitis Virus Vectors Expressing Glycoproteins of Filoviruses and Arenaviruses
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Viktor E. Volchkov, Hans-Dieter Klenk, Victoria Wahl-Jensen, Ralf Wagner, Ryan Liebscher, Michael Garbutt, Heinz Feldmann, Peggy Möller, Ute Ströher, and Steven M. Jones
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viruses ,Genetic Vectors ,Immunology ,Virus Replication ,medicine.disease_cause ,Microbiology ,Vesicular stomatitis Indiana virus ,Virus ,Mice ,Viral Proteins ,VP40 ,Virology ,Vaccines and Antiviral Agents ,medicine ,Animals ,Humans ,Mononegavirales ,Glycoproteins ,Mice, Inbred BALB C ,Ebola virus ,biology ,Arenavirus ,Rhabdoviridae ,Filoviridae ,biology.organism_classification ,Recombinant Proteins ,Macaca fascicularis ,Lassa virus ,Viral replication ,Vesicular stomatitis virus ,Insect Science ,Female - Abstract
Replication-competent recombinant vesicular stomatitis viruses (rVSVs) expressing the type I transmembrane glycoproteins and selected soluble glycoproteins of several viral hemorrhagic fever agents (Marburg virus, Ebola virus, and Lassa virus) were generated and characterized. All recombinant viruses exhibited rhabdovirus morphology and replicated cytolytically in tissue culture. Unlike the rVSVs with an additional transcription unit expressing the soluble glycoproteins, the viruses carrying the foreign transmembrane glycoproteins in replacement of the VSV glycoprotein were slightly attenuated in growth. Biosynthesis and processing of the foreign glycoproteins were authentic, and the cell tropism was defined by the transmembrane glycoprotein. None of the rVSVs displayed pathogenic potential in animals. The rVSV expressing the Zaire Ebola virus transmembrane glycoprotein mediated protection in mice against a lethal Zaire Ebola virus challenge. Our data suggest that the recombinant VSV can be used to study the role of the viral glycoproteins in virus replication, immune response, and pathogenesis.
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- 2004
31. Ebola Virus Modulates Transforming Growth Factor β Signaling and Cellular Markers of Mesenchyme-Like Transition in Hepatocytes
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Joseph E. Blaney, Dawn Traynor, Thomas Hoenen, Friederike Feldmann, Victoria Wahl-Jensen, David Safronetz, Scott Napper, Jason Kindrachuk, Elena Postnikova, Anthony Kusalik, Peter B. Jahrling, Ryan J. Arsenault, Heinz Feldmann, and Brett Trost
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Cell signaling ,Cellular differentiation ,Immunology ,medicine.disease_cause ,Microbiology ,Mesoderm ,Downregulation and upregulation ,Transforming Growth Factor beta ,Virology ,medicine ,Animals ,Humans ,Kinome ,Ebolavirus ,Mice, Inbred BALB C ,Ebola virus ,biology ,Gene Expression Profiling ,Cell Differentiation ,Transforming growth factor beta ,Hemorrhagic Fever, Ebola ,Cell biology ,Virus-Cell Interactions ,Disease Models, Animal ,Insect Science ,Host-Pathogen Interactions ,biology.protein ,Hepatocytes ,Signal transduction ,Signal Transduction - Abstract
Ebola virus (EBOV) causes a severe hemorrhagic disease in humans and nonhuman primates, with a median case fatality rate of 78.4%. Although EBOV is considered a public health concern, there is a relative paucity of information regarding the modulation of the functional host response during infection. We employed temporal kinome analysis to investigate the relative early, intermediate, and late host kinome responses to EBOV infection in human hepatocytes. Pathway overrepresentation analysis and functional network analysis of kinome data revealed that transforming growth factor (TGF-β)-mediated signaling responses were temporally modulated in response to EBOV infection. Upregulation of TGF-β signaling in the kinome data sets correlated with the upregulation of TGF-β secretion from EBOV-infected cells. Kinase inhibitors targeting TGF-β signaling, or additional cell receptors and downstream signaling pathway intermediates identified from our kinome analysis, also inhibited EBOV replication. Further, the inhibition of select cell signaling intermediates identified from our kinome analysis provided partial protection in a lethal model of EBOV infection. To gain perspective on the cellular consequence of TGF-β signaling modulation during EBOV infection, we assessed cellular markers associated with upregulation of TGF-β signaling. We observed upregulation of matrix metalloproteinase 9, N-cadherin, and fibronectin expression with concomitant reductions in the expression of E-cadherin and claudin-1, responses that are standard characteristics of an epithelium-to-mesenchyme-like transition. Additionally, we identified phosphorylation events downstream of TGF-β that may contribute to this process. From these observations, we propose a model for a broader role of TGF-β-mediated signaling responses in the pathogenesis of Ebola virus disease. IMPORTANCE Ebola virus (EBOV), formerly Zaire ebolavirus, causes a severe hemorrhagic disease in humans and nonhuman primates and is the most lethal Ebola virus species, with case fatality rates of up to 90%. Although EBOV is considered a worldwide concern, many questions remain regarding EBOV molecular pathogenesis. As it is appreciated that many cellular processes are regulated through kinase-mediated phosphorylation events, we employed temporal kinome analysis to investigate the functional responses of human hepatocytes to EBOV infection. Administration of kinase inhibitors targeting signaling pathway intermediates identified in our kinome analysis inhibited viral replication in vitro and reduced EBOV pathogenesis in vivo . Further analysis of our data also demonstrated that EBOV infection modulated TGF-β-mediated signaling responses and promoted “mesenchyme-like” phenotypic changes. Taken together, these results demonstrated that EBOV infection specifically modulates TGF-β-mediated signaling responses in epithelial cells and may have broader implications in EBOV pathogenesis.
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- 2014
32. ABSL-4 Aerobiology Biosafety and Technology at the NIH/NIAID Integrated Research Facility at Fort Detrick
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Fabian de Kok-Mercado, Jiro Wada, Jason Kindrachuk, Matthew G. Lackemeyer, Jens H. Kuhn, Laura Bollinger, Victoria Wahl-Jensen, and Peter B. Jahrling
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Biosafety level 4 ,aerobiology ,medicine.medical_specialty ,Biomedical Research ,lcsh:QR1-502 ,Virus diseases ,biosafety level 4 ,Aerobiology ,Article ,lcsh:Microbiology ,ABSL-4 ,class III biosafety cabinet ,BSL-4 ,high-consequence viral pathogens ,medical countermeasure ,viral hemorrhagic fever ,Viral hemorrhagic fever ,Biosafety ,National Institute of Allergy and Infectious Diseases (U.S.) ,Virology ,medicine ,Animals ,Environmental planning ,Aerosols ,Inhalation Exposure ,Maryland ,business.industry ,Transmission (medicine) ,Extramural ,Containment of Biohazards ,medicine.disease ,United States ,Disease Models, Animal ,Infectious Diseases ,National Institutes of Health (U.S.) ,Virus Diseases ,business ,Public health preparedness - Abstract
The overall threat of a viral pathogen to human populations is largely determined by the modus operandi and velocity of the pathogen that is transmitted among humans. Microorganisms that can spread by aerosol are considered a more challenging enemy than those that require direct body-to-body contact for transmission, due to the potential for infection of numerous people rather than a single individual. Additionally, disease containment is much more difficult to achieve for aerosolized viral pathogens than for pathogens that spread solely via direct person-to-person contact. Thus, aerobiology has become an increasingly necessary component for studying viral pathogens that are naturally or intentionally transmitted by aerosol. The goal of studying aerosol viral pathogens is to improve public health preparedness and medical countermeasure development. Here, we provide a brief overview of the animal biosafety level 4 Aerobiology Core at the NIH/NIAID Integrated Research Facility at Fort Detrick, Maryland, USA.
- Published
- 2014
- Full Text
- View/download PDF
33. Virus nomenclature below the species level: a standardized nomenclature for filovirus strains and variants rescued from cDNA
- Author
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Sina Bavari, Sven Enterlein, Yíngyún Caì, Kristina Brauburger, Matthew G. Lackemeyer, Olga Dolnik, Nancy J. Sullivan, Sergewy V. Netesov, Gary P. Kobinger, Peter B. Jahrling, Erica Ollmann Saphire, Eric M. Leroy, Travis K. Warren, J. Rodney Brister, Elke Mühlberger, Steven B. Bradfute, Kelly L. Warfield, Yiming Bao, Guido van der Groen, Thomas Hoenen, Alexander N. Freiberg, Gustavo Palacios, Jean-Paul Gonzalez, Sheli R. Radoshitzky, Elena I. Ryabchikova, Ayato Takada, Alexander Bukreyev, Georgy M. Ignatyev, Mark S. Lever, Janusz T. Paweska, Lisa E. Hensley, Pierre Formenty, Viktor E. Volchkov, Robert A. Davey, Anna N. Honko, Stuart T. Nichol, John M. Dye, Kartik Chandran, Jonathan S. Towner, Valentina A. Volchkova, Hans-Dieter Klenk, Gene G. Olinger, Jens H. Kuhn, Victoria Wahl-Jensen, Karl M. Johnson, Manfre Weidmann, Louisa Pitt, Jean L. Patterson, Stephan Becker, Aleksandr M. Shestopalov, Sophie J. Smither, and Robert Swanepoel
- Subjects
Genetics ,Ebola virus ,biology ,Filoviridae ,Genome, Viral ,General Medicine ,Marburgvirus ,biology.organism_classification ,Recombinant virus ,medicine.disease_cause ,Virology ,Genome ,Article ,Virus ,Reassortant Viruses ,medicine ,Virus classification - Abstract
Specific alterations (mutations, deletions, insertions) of virus genomes are crucial for the functional characterization of their regulatory elements and their expression products, as well as a prerequisite for the creation of attenuated viruses that could serve as vaccine candidates. Virus genome tailoring can be performed either by using traditionally cloned genomes as starting materials, followed by site-directed mutagenesis, or by de novo synthesis of modified virus genomes or parts thereof. A systematic nomenclature for such recombinant viruses is necessary to set them apart from wild-type and laboratory-adapted viruses, and to improve communication and collaborations among researchers who may want to use recombinant viruses or create novel viruses based on them. A large group of filovirus experts has recently proposed nomenclatures for natural and laboratory animal-adapted filoviruses that aim to simplify the retrieval of sequence data from electronic databases. Here, this work is extended to include nomenclature for filoviruses obtained in the laboratory via reverse genetics systems. The previously developed template for natural filovirus genetic variant naming, < virus name > (< strain >/)< isolation host-suffix >/< country of sampling >/< year of sampling >/< genetic variant designation >-< isolate designation >, is retained, but we propose to adapt the type of information added to each field for cDNA clone-derived filoviruses. For instance, the full-length designation of an Ebola virus Kikwit variant rescued from a plasmid developed at the US Centers for Disease Control and Prevention could be akin to "Ebola virus H.sapiens-rec/COD/1995/Kikwit-abc1" (with the suffix "rec" identifying the recombinant nature of the virus and "abc1" being a placeholder for any meaningful isolate designator). Such a full-length designation should be used in databases and the methods section of publications. Shortened designations (such as "EBOV H.sap/COD/95/Kik-abc1") and abbreviations (such as "EBOV/Kik-abc1") could be used in the remainder of the text, depending on how critical it is to convey information contained in the full-length name. "EBOV" would suffice if only one EBOV strain/variant/isolate is addressed.
- Published
- 2013
34. General Disease Pathology in Filoviral and Arenaviral Infections
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Louis Huzella, Matthew G. Lackemeyer, Peter B. Jahrling, Victoria Wahl-Jensen, Jens H. Kuhn, Jennifer A. Cann, and Donna L. Perry
- Subjects
business.industry ,Immunology ,Medicine ,Disease ,business - Published
- 2013
35. Viral Hemorrhagic Fevers
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Anna N. Clawson, Victoria Wahl-Jensen, Peter B. Jahrling, Sina Bavari, Jens H. Kuhn, and Sheli R. Radoshitzky
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Hemorrhagic Fevers ,business.industry ,Immunology ,Medicine ,business - Published
- 2013
36. VIRUS NOMENCLATURE BELOW THE SPECIES LEVEL: A STANDARDIZED NOMENCLATURE FOR LABORATORY ANIMAL-ADAPTED STRAINS AND VARIANTS OF VIRUSES ASSIGNED TO THE FAMILY FILOVIRIDAE
- Author
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Eric M. Leroy, Travis K. Warren, Victoria Wahl-Jensen, Jonathan S. Towner, Kelly L. Warfield, Viktor E. Volchkov, Matthew G. Lackemeyer, Guido van der Groen, Erica Ollmann Saphire, Manfred Weidmann, Nancy J. Sullivan, Alexander N. Freiberg, Gene G. Olinger, Yíngyún Caì, Jean-Paul Gonzalez, Olga Dolnik, Alexander Bukreyev, Robert Swanepoel, Gary P. Kobinger, Pierre Formenty, Ayato Takada, Loreen L. Lofts, Louise Pitt, Jean L. Patterson, Steven B. Bradfute, Stephan Becker, Kartik Chandran, Aleksandr M. Shestopalov, Hans-Dieter Klenk, Sophie J. Smither, Robert A. Davey, Anna N. Honko, Jens H. Kuhn, Karl M. Johnson, Georgy M. Ignatyev, Mark S. Lever, Stuart T. Nichol, Lisa E. Hensley, John M. Dye, Elena I. Ryabchikova, J. Rodney Brister, Yiming Bao, Janusz T. Paweska, Elke Mühlberger, Gustavo Palacios, Sven Enterlein, Sergey V. Netesov, Sina Bavari, Peter B. Jahrling, and Sheli R. Radoshitzky
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Ebola virus ,Lloviu virus ,biology ,Filoviridae ,General Medicine ,medicine.disease_cause ,biology.organism_classification ,Virology ,Article ,Cuevavirus ,Marburg virus ,medicine ,Mononegavirales ,Nomenclature ,Virus classification - Abstract
The International Committee on Taxonomy of Viruses (ICTV) organizes the classification of viruses into taxa, but is not responsible for the nomenclature for taxa members. International experts groups, such as the ICTV Study Groups, recommend the classification and naming of viruses and their strains, variants, and isolates. The ICTV Filoviridae Study Group has recently introduced an updated classification and nomenclature for filoviruses. Subsequently, and together with numerous other filovirus experts, a consistent nomenclature for their natural genetic variants and isolates was developed that aims at simplifying the retrieval of sequence data from electronic databases. This is a first important step toward a viral genome annotation standard as sought by the US National Center for Biotechnology Information (NCBI). Here, this work is extended to include filoviruses obtained in the laboratory by artificial selection through passage in laboratory hosts. The previously developed template for natural filovirus genetic variant naming (< virus name > < isolation host-suffix >/< country of sampling >/< year of sampling >/< genetic variant designation >-< isolate designation >) is retained, but it is proposed to adapt the type of information added to each field for laboratory animal-adapted variants. For instance, the full-length designation of an Ebola virus Mayinga variant adapted at the State Research Center for Virology and Biotechnology "Vector" to cause disease in guinea pigs after seven passages would be akin to "Ebola virus VECTOR/C.porcellus-lab/COD/1976/Mayinga-GPA-P7". As was proposed for the names of natural filovirus variants, we suggest using the full-length designation in databases, as well as in the method section of publications. Shortened designations (such as "EBOV VECTOR/C.por/COD/76/May-GPA-P7") and abbreviations (such as "EBOV/May-GPA-P7") could be used in the remainder of the text depending on how critical it is to convey information contained in the full-length name. "EBOV" would suffice if only one EBOV strain/variant/isolate is addressed.
- Published
- 2013
37. Virus nomenclature below the species level: a standardized nomenclature for natural variants of viruses assigned to the family Filoviridae
- Author
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John M. Dye, Sergey V. Netesov, Janusz T. Paweska, Mark S. Lever, Travis K. Warren, Peter B. Jahrling, Jean L. Patterson, Stephan Becker, Alexander Bukreyev, Jens H. Kuhn, Lisa E. Hensley, Kartik Chandran, Eric M. Leroy, Sophie J. Smither, J. Rodney Brister, Erica Ollmann Saphire, Victoria Wahl-Jensen, Yiming Bao, Steven B. Bradfute, Manfred Weidmann, Robert Swanepoel, Karl M. Johnson, Jonathan S. Towner, Gene G. Olinger, Viktor E. Volchkov, Olga Dolnik, Anna N. Honko, Louise Pitt, Sina Bavari, Gary P. Kobinger, Guido van der Groen, Sheli R. Radoshitzky, Gustavo Palacios, Robert A. Davey, Sven Enterlein, Elke Mühlberger, Stuart T. Nichol, Institut für Virologie, Philipps University, Centre International de Recherches Médicales de Franceville (CIRMF), National Institute for Communicable Diseases [Johannesburg] (NICD), University of Göttingen - Georg-August-Universität Göttingen, Centers for Disease Control and Prevention [Atlanta] (CDC), and Centers for Disease Control and Prevention
- Subjects
MESH: Terminology as Topic ,[SDV]Life Sciences [q-bio] ,Filoviridae ,Computational biology ,medicine.disease_cause ,Article ,03 medical and health sciences ,Virology ,MESH: Filoviridae Infections ,medicine ,MESH: Animals ,Nomenclature ,Virus classification ,ComputingMilieux_MISCELLANEOUS ,030304 developmental biology ,Genetics ,0303 health sciences ,Ebola virus ,MESH: Humans ,biology ,030306 microbiology ,General Medicine ,Genome project ,biology.organism_classification ,3. Good health ,Gene nomenclature ,MESH: Classification ,MESH: Filoviridae ,Homo sapiens ,Taxonomy (biology) - Abstract
The task of international expert groups is to recommend the classification and naming of viruses. The International Committee on Taxonomy of Viruses Filoviridae Study Group and other experts have recently established an almost consistent classification and nomenclature for filoviruses. Here, further guidelines are suggested to include their natural genetic variants. First, this term is defined. Second, a template for full-length virus names (such as “Ebola virus H.sapiens-tc/COD/1995/Kikwit-9510621”) is proposed. These names contain information on the identity of the virus (e.g., Ebola virus), isolation host (e.g., members of the species Homo sapiens), sampling location (e.g., Democratic Republic of the Congo (COD)), sampling year, genetic variant (e.g., Kikwit), and isolate (e.g., 9510621). Suffixes are proposed for individual names that clarify whether a given genetic variant has been characterized based on passage zero material (-wt), has been passaged in tissue/cell culture (-tc), is known from consensus sequence fragments only (-frag), or does (most likely) not exist anymore (-hist). We suggest that these comprehensive names are to be used specifically in the methods section of publications. Suitable abbreviations, also proposed here, could then be used throughout the text, while the full names could be used again in phylograms, tables, or figures if the contained information aids the interpretation of presented data. The proposed system is very similar to the well-known influenzavirus nomenclature and the nomenclature recently proposed for rotaviruses. If applied consistently, it would considerably simplify retrieval of sequence data from electronic databases and be a first important step toward a viral genome annotation standard as sought by the National Center for Biotechnology Information (NCBI). Furthermore, adoption of this nomenclature would increase the general understanding of filovirus-related publications and presentations and improve figures such as phylograms, alignments, and diagrams. Most importantly, it would counter the increasing confusion in genetic variant naming due to the identification of ever more sequences through technological breakthroughs in high-throughput sequencing and environmental sampling.
- Published
- 2013
38. Pathology of experimental aerosol Zaire ebolavirus infection in rhesus macaques
- Author
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C. G. Robinson, M. E. Mattix, Nancy A. Twenhafel, C. Terry, William D. Pratt, Joshua C. Johnson, Lisa E. Hensley, Gene G. Olinger, Victoria Wahl-Jensen, Anna N. Honko, and Kathleen A. Cashman
- Subjects
Zaire ebolavirus ,Male ,Pathology ,medicine.medical_specialty ,Lymphoid Tissue ,Respiratory System ,Spleen ,Viremia ,Biological Warfare Agents ,Biology ,medicine.disease_cause ,Virus Replication ,Body Temperature ,medicine ,Animals ,Humans ,Respiratory system ,Lung ,Disseminated intravascular coagulation ,Ebolavirus ,Aerosols ,General Veterinary ,Hemorrhagic Fever, Ebola ,medicine.disease ,Macaca mulatta ,Neutrophilia ,medicine.anatomical_structure ,Liver ,Immunology ,Models, Animal ,Female ,Lymph Nodes ,Lymphocytopenia ,medicine.symptom - Abstract
There is limited knowledge of the pathogenesis of human ebolavirus infections and no reported human cases acquired by the aerosol route. There is a threat of ebolavirus as an aerosolized biological weapon, and this study evaluated the pathogenesis of aerosol infection in 18 rhesus macaques. Important and unique findings include early infection of the respiratory lymphoid tissues, early fibrin deposition in the splenic white pulp, and perivasculitis and vasculitis in superficial dermal blood vessels of haired skin with rash. Initial infection occurred in the respiratory lymphoid tissues, fibroblastic reticular cells, dendritic cells, alveolar macrophages, and blood monocytes. Virus spread to regional lymph nodes, where significant viral replication occurred. Virus secondarily infected many additional blood monocytes and spread from the respiratory tissues to multiple organs, including the liver and spleen. Viremia, increased temperature, lymphocytopenia, neutrophilia, thrombocytopenia, and increased alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transpeptidase, total bilirubin, serum urea nitrogen, creatinine, and hypoalbuminemia were measurable mid to late infection. Infection progressed rapidly with whole-body destruction of lymphoid tissues, hepatic necrosis, vasculitis, hemorrhage, and extravascular fibrin accumulation. Hypothermia and thrombocytopenia were noted in late stages with the development of disseminated intravascular coagulation and shock. This study provides unprecedented insight into pathogenesis of human aerosol Zaire ebolavirus infection and suggests development of a medical countermeasure to aerosol infection will be a great challenge due to massive early infection of respiratory lymphoid tissues. Rhesus macaques may be used as a model of aerosol infection that will allow the development of lifesaving medical countermeasures under the Food and Drug Administration’s animal rule.
- Published
- 2012
39. Filoviruses: Hemorrhagic Fevers
- Author
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Victoria Wahl-Jensen, Sina Bavari, Peter B. Jahrling, Jens H. Kuhn, and Sheli R. Radoshitzky
- Subjects
Ebolavirus ,Marburg virus ,Hemorrhagic Fevers ,biology ,business.industry ,medicine ,medicine.disease_cause ,Marburgvirus ,biology.organism_classification ,business ,Virology - Published
- 2012
40. Orthopoxviruses
- Author
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Peter Jahrling and Victoria Wahl-Jensen
- Published
- 2012
41. Comparative pathology of smallpox and monkeypox in man and macaques
- Author
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Lisa E. Hensley, Peter B. Jahrling, Jennifer A. Cann, and Victoria Wahl-Jensen
- Subjects
Gene Expression Regulation, Viral ,viruses ,Population ,Disease ,Macaque ,Article ,Pathology and Forensic Medicine ,Monkeypox ,Species Specificity ,biology.animal ,medicine ,Smallpox ,Animals ,Humans ,Orthopoxvirus ,education ,education.field_of_study ,General Veterinary ,biology ,Poxviridae ,virus diseases ,biology.organism_classification ,medicine.disease ,Virology ,Macaca mulatta ,Comparative Pathology ,Variola virus - Abstract
In the three decades since the eradication of smallpox and cessation of routine vaccination, the collective memory of the devastating epidemics caused by this orthopoxvirus has waned, and the human population has become increasingly susceptible to a disease that remains high on the list of possible bioterrorism agents. Research using surrogate orthopoxviruses in their natural hosts, as well as limited variola virus research in animal models, continues worldwide; however, interpretation of findings is often limited by our relative lack of knowledge about the naturally occurring disease. For modern comparative pathologists, many of whom have no first-hand knowledge of naturally occurring smallpox, this work provides a contemporary review of this historical disease, as well as discussion of how it compares with human monkeypox and the corresponding diseases in macaques.
- Published
- 2012
42. Genus-specific recruitment of filovirus ribonucleoprotein complexes into budding particles
- Author
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Larissa Kolesnikova, Victoria Wahl-Jensen, Thomas Hoenen, Stephan Becker, Larissa Spiegelberg, and Heinz Feldmann
- Subjects
Ebolavirus ,Budding ,Viral matrix protein ,Animal ,Virion ,Biology ,medicine.disease_cause ,Marburgvirus ,biology.organism_classification ,Virus Replication ,Virology ,Viral Matrix Proteins ,VP40 ,Viral replication ,Ribonucleoproteins ,Species Specificity ,Transcription (biology) ,medicine ,Ribonucleoprotein ,Glycoproteins - Abstract
The filoviral matrix protein VP40 orchestrates virus morphogenesis and budding. To do this it interacts with both the glycoprotein (GP1,2) and the ribonucleoprotein (RNP) complex components; however, these interactions are still not well understood. Here we show that for efficient VP40-driven formation of transcription and replication-competent virus-like particles (trVLPs), which contain both an RNP complex and GP1,2, the RNP components and VP40, but not GP1,2 and VP40, must be from the same genus. trVLP preparations contained both spherical and filamentous particles, but only the latter were able to infect target cells and to lead to genome replication and transcription. Interestingly, the genus specificity of the VP40–RNP interactions was specific to the formation of filamentous trVLPs, but not to spherical particles. These results not only further our understanding of VP40 interactions, but also suggest that special care is required when using trVLP or VLP systems to model virus morphogenesis.
- Published
- 2011
43. Evaluation of Perceived Threat Differences Posed by Filovirus Variants
- Author
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Sina Bavari, Lori E. Dodd, Jens H. Kuhn, Victoria Wahl-Jensen, Peter B. Jahrling, and Sheli R. Radoshitzky
- Subjects
medicine.medical_specialty ,Health (social science) ,Biomedical Research ,Isolation (health care) ,Filoviridae ,Genome, Viral ,Management, Monitoring, Policy and Law ,medicine.disease_cause ,Antiviral Agents ,Disease Outbreaks ,Marburg virus ,National Institute of Allergy and Infectious Diseases (U.S.) ,medicine ,Filoviridae Infections ,Animals ,Humans ,Government ,Biodefense ,Ebola virus ,biology ,business.industry ,Viral Vaccine ,Public Health, Environmental and Occupational Health ,Viral Vaccines ,General Medicine ,Original Articles ,biology.organism_classification ,Marburgvirus ,Virology ,Bioterrorism ,United States ,Disease Models, Animal ,Family medicine ,business - Abstract
In the United States, filoviruses (ebolaviruses and marburgviruses) are listed as National Institute of Allergy and Infectious Diseases (NIAID) Category A Priority Pathogens, Select Agents, and Centers for Disease Control and Prevention (CDC) Category A Bioterrorism Agents. In recent months, U.S. biodefense professionals and policy experts have initiated discussions on how to optimize filovirus research in regard to medical countermeasure (ie, diagnostics, antiviral, and vaccine) development. Standardized procedures and reagents could accelerate the independent verification of research results across government agencies and establish baselines for the development of animal models acceptable to regulatory entities, such as the Food and Drug Administration (FDA), while being fiscally responsible. At the root of standardization lies the question of which filovirus strains, variants, or isolates ought to be the prototypes for product development, evaluation, and validation. Here we discuss a rationale for their selection. We conclude that, based on currently available data, filovirus biodefense research ought to focus on the classical taxonomic filovirus prototypes: Marburg virus Musoke in the case of marburgviruses and Ebola virus Mayinga in the case of Zaire ebolaviruses. Arguments have been made in various committees in favor of other variants, such as Marburg virus Angola, Ci67 or Popp, or Ebola virus Kikwit, but these rationales seem to be largely based on anecdotal or unpublished and unverified data, or they may reflect a lack of awareness of important facts about the variants' isolation history and genomic properties.
- Published
- 2011
44. Filovirus Infections
- Author
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Peter B. Jahrling, C. J. Peters, Jens H. Kuhn, Victoria Wahl-Jensen, and Heinz Feldmann
- Subjects
business.industry ,Medicine ,business - Published
- 2011
45. Progression of pathogenic events in cynomolgus macaques infected with variola virus
- Author
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Peter B. Jahrling, Kathleen Rubins, Lisa E. Hensley, Jo Lynne Raymond, Robert W Fisher, Anthony J. Johnson, Victoria Wahl-Jensen, John W. Huggins, Fabian de Kok-Mercado, Thomas Larsen, and Jennifer A. Cann
- Subjects
Male ,viruses ,Population ,lcsh:Medicine ,Viremia ,Microbiology ,Macaque ,complex mixtures ,Virus ,Body Temperature ,Virology ,Zoonoses ,biology.animal ,Hemorrhagic smallpox ,medicine ,Animals ,Smallpox ,education ,lcsh:Science ,Biology ,education.field_of_study ,Hematologic Tests ,Multidisciplinary ,biology ,Viral Immune Evasion ,Body Weight ,lcsh:R ,virus diseases ,Variola virus ,medicine.disease ,Vaccination ,Animal Models of Infection ,Kinetics ,Macaca fascicularis ,Infectious Diseases ,Immunology ,Disease Progression ,Medicine ,Female ,lcsh:Q ,Research Article ,Neglected Tropical Diseases - Abstract
Smallpox, caused by variola virus (VARV), is a devastating human disease that affected millions worldwide until the virus was eradicated in the 1970 s. Subsequent cessation of vaccination has resulted in an immunologically naive human population that would be at risk should VARV be used as an agent of bioterrorism. The development of antivirals and improved vaccines to counter this threat would be facilitated by the development of animal models using authentic VARV. Towards this end, cynomolgus macaques were identified as adequate hosts for VARV, developing ordinary or hemorrhagic smallpox in a dose-dependent fashion. To further refine this model, we performed a serial sampling study on macaques exposed to doses of VARV strain Harper calibrated to induce ordinary or hemorrhagic disease. Several key differences were noted between these models. In the ordinary smallpox model, lymphoid and myeloid hyperplasias were consistently found whereas lymphocytolysis and hematopoietic necrosis developed in hemorrhagic smallpox. Viral antigen accumulation, as assessed immunohistochemically, was mild and transient in the ordinary smallpox model. In contrast, in the hemorrhagic model antigen distribution was widespread and included tissues and cells not involved in the ordinary model. Hemorrhagic smallpox developed only in the presence of secondary bacterial infections - an observation also commonly noted in historical reports of human smallpox. Together, our results support the macaque model as an excellent surrogate for human smallpox in terms of disease onset, acute disease course, and gross and histopathological lesions.
- Published
- 2011
46. Contributors
- Author
-
Saad H. Abdalla, Gustavo Olszanski Acrani, Rakesh Aggarwal, Ban Mishu Allos, Miriam J. Alter, Jon K. Andrus, Juana Angel, Gregory M. Anstead, Eduardo Arathoon, Eurico Arruda, Ray R. Arthur, Robert L. Atmar, Patrick Banura, Alan G. Barbour, Alan D.T. Barrett, Dan Bausch, Steven L. Berk, Pascal O. Bessong, Frank J. Bia, Tihana Bicanic, Robert E. Black, Thomas P. Bleck, Andrea K. Boggild, William Bonnez, Joseph S. Bresee, Corrie Brown, Lillian B. Brown, Enrico Brunetti, Fabrizio Bruschi, Amy E. Bryant, Carlos C. (Kent) Campbell, Carlos Castillo-Solorzano, Martin S. Cetron, Ding-Shinn Chen, Pei-Jer Chen, Xiang-Sheng Chen, Thomas Cherian, K.B. Chua, Myron S. Cohen, Graham S. Cooke, Chester R. Cooper, Edward S. Cooper, Christina M. Coyle, John H. Cross†, David A.B. Dance, Mustapha A. Danesi, Chandler R. Dawson, Catherine de Martel, Ciro A. De Quadros, Anastacio de Queiroz Sousa, Nilanthi R. de Silva, Alexandre Leite de Souza, Christoph Dehio, David J. Diemert, Rebecca Dillingham, John E. Donelson, J. Stephen Dumler, Joseph A. Duncan, Herbert L. DuPont, Marlene L. Durand, Mark L. Eberhard, Joshua C. Eby, Charles Edwards, Rachel B. Eidex, Jerrold J. Ellner, Delia A. Enría, Onder Ergonul, Mary K. Estes, Ahmed Hassan Fahal, Paul E. Farmer, A.S.G. Faruque, Charles Feldman, Heinz Feldmann, Kimberley K. Fox, Silvia Franceschi, Manuel A. Franco, Charles F. Fulhorst, Hector H. Garcia, Robert M. Genta, Robert H. Gilman, Roger I. Glass, Jerome Goddard, Eduardo Gotuzzo, John R. Graybill, Harry B. Greenberg, Paul D. Griffiths, Duane J. Gubler, Richard L. Guerrant, Yezid Gutierrez, Erik L. Hewlett, David L. Heymann, David R. Hill, Mei-Shang Ho, Achim M. Hoerauf, Paul S. Hoffman, Stephen L. Hoffman, Michael R. Holbrook, Thomas L. Holland, Donald R. Hopkins, Duane R. Hospenthal, Peter J. Hotez, S. David Hudnall, James M. Hughes, Kao-Pin Hwang, Raul E. Isturiz, Peter B. Jahrling, Shahid Jameel, Selma M.B. Jeronimo, Edward C. Jones-Lopez, Anna Kabanova, Gagandeep Kang, Christopher L. Karp, James W. Kazura, Peter Kern, Gerald T. Keusch, Jay S. Keystone, Mehnaaz S. Khuroo, Mohammad S. Khuroo, Ik-Sang Kim, Charles H. King, Louis V. Kirchhoff, Amy D. Klion, Keith P. Klugman, Dennis J. Kopecko, Margaret Kosek, Frederick T. Koster, Phyllis E. Kozarsky, Thomas G. Ksiazek, Jens H. Kuhn, Albert J. Lastovica, James W. LeDuc, Peter A. Leone, Paul N. Levett, Michael Levin, Myron M. Levine, Aldo A.M. Lima, Gerhard Lindeque, David L. Longworth, David Mabey, J. Dick Maclean†, Alan J. Magill, Ismael Maguilnik, Ciro Maguiña, James H. Maguire, Siddhartha Mahanty, Shinji Makino, Christian W. Mandl, Thomas J. Marrie, Barry J. Marshall, Gregory J. Martin, Tadahiko Matsumoto, Steven D. Mawhorter, James S. McCarthy, Michael R. McGinnis, Paul S. Mead, Wayne M. Meyers, Robert F. Miller, Samuel I. Miller, James N. Mills, Thomas P. Monath, Christopher C. Moore, Thomas A. Moore, J.C. Morrill, J. Glenn Morris, Megan Murray, K. Darwin Murrell, G. Balakrish Nair, Theodore E. Nash, Barnett R. Nathan, Ricardo Negroni, Anne Nicholson-Weller, Marcio Nucci, Thomas B. Nutman, Nigel O’Farrell, Juan P. Olano, Eng Eong Ooi, Luis S. Ortega, Ynés R. Ortega, Mark A. Pallansch, Jean W. Pape, Georgios Pappas, Julie Parsonnet, Geoffrey Pasvol, Sharon J. Peacock, Richard D. Pearson, Rosanna W. Peeling, David A. Pegues, Jacques Pépin, C.J. Peters, Kristine M. Peterson, William A. Petri, Françoise Portaels, José Luiz Proença-Módena, Thomas C. Quinn, G. Raghurama Rao, Didier Raoult, Rino Rappuoli, John H. Rex, Steven J. Reynolds, José M.C. Ribeiro, Emmanuel Roilides, Pierre E. Rollin, Allan R. Ronald, Paul A. Rota, Sharon L. Roy, Ernesto Ruiz-Tiben, Edward T. Ryan, Debasish Saha, Mohammed A. Salam, Amidou Samie, Julius Schachter, Peter M. Schantz, W. Michael Scheld, Elizabeth P. Schlaudecker, David A. Schwartz, Joseph D. Schwartzman, Arlene C. Seña, Daniel J. Sexton, Truman W. Sharp, Wun-Ju Shieh, Shmuel Shoham, Afzal A. Siddiqui, Upinder Singh, David W. Smith, Michael B. Smith, Bonnie L. Smoak, A. George Smulian, Cynthia B. Snider, Tom Solomon, Samba O. Sow, P. Frederick Sparling, Lisa A. Spencer, Lawrence R. Stanberry, J. Erin Staples, Robert Steffen, Theodore S. Steiner, Mark C. Steinhoff, Dennis L. Stevens, Kathryn N. Suh, Khuanchai Supparatpinyo, Paul J. Szaniszlo, Milagritos D. Tapia, Herbert B. Tanowitz, Sam R. Telford, Robert B. Tesh, Nathan M. Thielman, Fernando J. Torres-Vélez, Joseph D. Tucker, Luis M. Valdez, Jesus G. Valenzuela, Diederik van de Beek, Pedro F.C. Vasconcelos, Govinda S. Visvesvara, Victoria Wahl-Jensen, David H. Walker, Douglas S. Walsh, Thomas J. Walsh, David A. Walton, Peter D. Walzer, Cirle A. Warren, Scott C. Weaver, Louis M. Weiss, Peter F. Weller, A. Clinton White, Nicholas J. White, Robert J. Wilkinson, Mary E. Wilson, Murray Wittner, Anita K.M. Zaidi, and Sherif R. Zaki
- Published
- 2011
47. A proposal to change existing virus species names to non-Latinized binomials
- Author
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Brian W. J. Mahy, Robert B. Tesh, Michael R. Holbrook, Peter J. Walker, Edward P. Rybicki, Scott C. Weaver, Peter B. Jahrling, Ralf G. Dietzgen, Donald S. Burke, Tim Skern, Victoria Wahl-Jensen, Guenther M. Keil, Charles H. Calisher, Karl M. Johnson, Marc H V Van Regenmortel, Giovanni P. Martelli, Jens H. Kuhn, Craig R. Pringle, Claude M. Fauquet, Marian C. Horzinek, and Said A. Ghabrial
- Subjects
biology ,Species name ,viruses ,Measles morbillivirus ,General Medicine ,biology.organism_classification ,Virology ,Virus ,Plant Viruses ,Measles virus ,Terminology as Topic ,Taxonomy (biology) ,Nomenclature ,Virus classification - Abstract
A proposal has been posted on the ICTV website (2011.001aG.N.v1.binomial_sp_names) to replace virus species names by non-Latinized binomial names consisting of the current italicized species name with the terminal word "virus" replaced by the italicized and non-capitalized genus name to which the species belongs. If implemented, the current italicized species name Measles virus, for instance, would become Measles morbillivirus while the current virus name measles virus and its abbreviation MeV would remain unchanged. The rationale for the proposed change is presented.
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- 2010
48. Demonstration of cross-protective vaccine immunity against an emerging pathogenic Ebolavirus Species
- Author
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Michael Bailey, Anna N. Honko, Nancy J. Sullivan, Victoria Wahl-Jensen, Clement Asiedu, Stuart T. Nichol, Sabue Mulangu, Thomas G. Ksiazek, Lisa E. Hensley, Mario Roederer, Giulia Fabozzi, Richard A. Koup, Daphne A. Stanley, Peter B. Jahrling, Pierre E. Rollin, and Joshua C. Johnson
- Subjects
CD4-Positive T-Lymphocytes ,lcsh:Immunologic diseases. Allergy ,Cellular immunity ,Immunology ,Biology ,CD8-Positive T-Lymphocytes ,Cross Reactions ,medicine.disease_cause ,Microbiology ,Communicable Diseases, Emerging ,Epitopes ,Viral Proteins ,Immune system ,Species Specificity ,Immunity ,Virology ,Immunology/Immunity to Infections ,Infectious Diseases/Viral Infections ,Genetics ,medicine ,Animals ,Humans ,Uganda ,Ebola Vaccines ,Molecular Biology ,lcsh:QH301-705.5 ,Virology/Vaccines ,Glycoproteins ,Ebolavirus ,Ebola virus ,Ebola vaccine ,Viral Vaccine ,Vaccination ,Hemorrhagic Fever, Ebola ,Immunity, Humoral ,Macaca fascicularis ,Infectious Diseases ,lcsh:Biology (General) ,DNA, Viral ,Immunology/Immune Response ,Parasitology ,lcsh:RC581-607 ,Research Article - Abstract
A major challenge in developing vaccines for emerging pathogens is their continued evolution and ability to escape human immunity. Therefore, an important goal of vaccine research is to advance vaccine candidates with sufficient breadth to respond to new outbreaks of previously undetected viruses. Ebolavirus (EBOV) vaccines have demonstrated protection against EBOV infection in nonhuman primates (NHP) and show promise in human clinical trials but immune protection occurs only with vaccines whose antigens are matched to the infectious challenge species. A 2007 hemorrhagic fever outbreak in Uganda demonstrated the existence of a new EBOV species, Bundibugyo (BEBOV), that differed from viruses covered by current vaccine candidates by up to 43% in genome sequence. To address the question of whether cross-protective immunity can be generated against this novel species, cynomolgus macaques were immunized with DNA/rAd5 vaccines expressing ZEBOV and SEBOV glycoprotein (GP) prior to lethal challenge with BEBOV. Vaccinated subjects developed robust, antigen-specific humoral and cellular immune responses against the GP from ZEBOV as well as cellular immunity against BEBOV GP, and immunized macaques were uniformly protected against lethal challenge with BEBOV. This report provides the first demonstration of vaccine-induced protective immunity against challenge with a heterologous EBOV species, and shows that Ebola vaccines capable of eliciting potent cellular immunity may provide the best strategy for eliciting cross-protection against newly emerging heterologous EBOV species., Author Summary Ebola virus causes death, fear, and economic disruption during outbreaks. It is a concern worldwide as a natural pathogen and a bioterrorism agent, and has caused death to residents and tourists of Africa where the virus circulates. A vaccine strategy to protect against all circulating Ebola viruses is complicated by the fact that there are five different virus species, and individual vaccines provide protection only against those included in the vaccine. Making broad vaccines that contain multiple components is complicated, expensive, and poses challenges for regulatory approval. Therefore, in the present work, we examined whether a prime-boost immunization strategy with a vaccine targeted to one Ebola virus species could cross protect against a different species. We found that genetic immunization with vectors expressing the Ebola virus glycoprotein from Zaire blocked infection with a newly emerged virus species, Bundibugyo EBOV, not represented in the vaccine. Protection occurred in the absence of antibodies against the second species and was mediated instead by cellular immune responses. Therefore, single-component vaccines may be improved to protect against multiple Ebola viruses if they are designed to generate this type of immunity.
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- 2010
49. Identification of N-glycans from Ebola virus glycoproteins by matrix-assisted laser desorption/ionisation time-of-flight and negative ion electrospray tandem mass spectrometry
- Author
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Gayle E. Ritchie, Friederike Feldmann, Ute Stroeher, Pauline M. Rudd, Raymond A. Dwek, Heinz Feldmann, Louise Royle, Victoria Wahl-Jensen, and David Harvey
- Subjects
PNGase F ,Glycan ,Mass spectrometry ,Tandem mass spectrometry ,Fucose ,Article ,Analytical Chemistry ,Cell Line ,chemistry.chemical_compound ,Viral Envelope Proteins ,Exoglycosidase ,Polysaccharides ,Tandem Mass Spectrometry ,Humans ,Polyacrylamide gel electrophoresis ,Spectroscopy ,chemistry.chemical_classification ,Chromatography ,biology ,Organic Chemistry ,Galactose ,Ebolavirus ,carbohydrates (lipids) ,Hemagglutinins ,chemistry ,Biochemistry ,Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ,biology.protein ,Electrophoresis, Polyacrylamide Gel ,Glycoprotein ,Mannose - Abstract
The larger fragment of the transmembrane glycoprotein (GP1) and the soluble glycoprotein (sGP) of Ebola virus were expressed in human embryonic kidney cells and the secreted products were purified from the supernatant for carbohydrate analysis. The N-glycans were released with PNGase F from within sodium dodecyl sulphate/polyacrylamide gel electrophoresis (SDS-PAGE) gels. Identification of the glycans was made with normal-phase high-performance liquid chromatography (HPLC), matrix-assisted laser desorption/ionisation mass spectrometry, negative ion electrospray ionisation fragmentation mass spectrometry and exoglycosidase digestion. Most glycans were complex bi-, tri- and tetra-antennary compounds with reduced amounts of galactose. No bisected compounds were detected. Triantennary glycans were branched on the 6-antenna; fucose was attached to the core GlcNAc residue. Sialylated glycans were present on sGP but were largely absent from GP1, the larger fragment of the transmembrane glycoprotein. Consistent with this was the generally higher level of processing of carbohydrates found on sGP as evidenced by a higher percentage of galactose and lower levels of high-mannose glycans than were found on GP1. These results confirm and expand previous findings on partial characterisation of the Ebola virus transmembrane glycoprotein. They represent the first detailed data on carbohydrate structures of the Ebola virus sGP.
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- 2010
50. Viral hemorrhagic fevers
- Author
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Lisa E. Hensley, Kathleen Rubins, Victoria Wahl-Jensen, and Joseph B. McCormick
- Subjects
Hemorrhagic Fevers ,business.industry ,Immunology ,medicine ,Lassa fever ,medicine.disease ,business ,Virology - Published
- 2010
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