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  1 / 396 MEDLINE  
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[PMID]:28327796
[Au] Autor:Ellwanger JH; Chies JA
[Ad] Endereço:Laboratório de Imunogenética, Programa de Pós-Graduação em Genética e Biologia Molecular, Departamento de Genética, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brasil.
[Ti] Título:Keeping track of hidden dangers - The short history of the Sabiá virus.
[So] Source:Rev Soc Bras Med Trop;50(1):3-8, 2017 Jan-Feb.
[Is] ISSN:1678-9849
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Emerging infectious diseases are a global threat. In countries like Brazil, where biodiversity is high and public health conditions in terms of infrastructure and medical care are often precarious, emerging diseases are particularly worrisome. The lack of monitoring strategies to identify pathogens with the potential to cause outbreaks or epidemics is another problem in Brazil and other developing countries. In this article, we present the history of the Sabiá virus (SABV), a pathogen that was described in the 1990s in Brazil. Several aspects of the biology and ecology of the SABV remain unknown. The SABV has the potential to cause hemorrhagic fever in humans. To date, four cases of human infections have been reported worldwide; two were naturally acquired (both in Brazil), whereas the other two were linked to occupational exposure in the laboratory environment (one in Brazil and one in the USA). In this review, we summarize the basic biological and ecological characteristics of the SABV. This is the first work to gather all available data on the historical aspects involving the cases of SABV infection along with an update on its characteristic features.
[Mh] Termos MeSH primário: Acidentes de Trabalho
Arenavirus do Novo Mundo
Febre Hemorrágica Americana/virologia
[Mh] Termos MeSH secundário: Adulto
Brasil
Seres Humanos
Pessoal de Laboratório
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170503
[Lr] Data última revisão:
170503
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE


  2 / 396 MEDLINE  
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[PMID]:28220142
[Au] Autor:Manning JT; Seregin AV; Yun NE; Koma T; Huang C; Barral J; de la Torre JC; Paessler S
[Ad] Endereço:Department of Pathology, University of Texas Medical Branch Galveston, TX, USA.
[Ti] Título:Absence of an N-Linked Glycosylation Motif in the Glycoprotein of the Live-Attenuated Argentine Hemorrhagic Fever Vaccine, Candid #1, Results in Its Improper Processing, and Reduced Surface Expression.
[So] Source:Front Cell Infect Microbiol;7:20, 2017.
[Is] ISSN:2235-2988
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Junin virus (JUNV), a highly pathogenic New World arenavirus, is the causative agent of Argentine hemorrhagic fever (AHF). The live-attenuated Candid #1 (Can) strain currently serves as a vaccine for at-risk populations. We have previously shown that the Can glycoprotein (GPC) gene is the primary gene responsible for attenuation in a guinea pig model of AHF. However, the mechanisms through which the GPC contributes to the attenuation of the Can strain remain unknown. A more complete understanding of the mechanisms underlying the attenuation and immunogenicity of the Can strain will potentially allow for the rational design of additional safe and novel vaccines. Here, we provide a detailed comparison of both RNA and protein expression profiles between both inter- and intra-segment chimeric JUNV recombinant clones expressing combinations of genes from the Can strain and the pathogenic Romero (Rom) strain. The recombinant viruses that express Can GPC, which were shown to be attenuated in guinea pigs, displayed different RNA levels and GPC processing patterns as determined by Northern and Western blot analyses, respectively. Analysis of recombinant viruses containing amino acid substitutions selected at different mouse brain passages during the generation of Can revealed that altered Can GPC processing was primarily due to the T168A substitution within G1, which eliminates an N-linked glycosylation motif. Incorporation of the T168A substitution in the Rom GPC resulted in a Can-like processing pattern of Rom GPC. In addition, JUNV GPCs containing T168A substitution were retained within the endoplasmic reticulum (ER) and displayed significantly lower cell surface expression than wild-type Rom GPC. Interestingly, the reversion A168T in Can GPC significantly increased GPC expression at the cell surface. Our results demonstrate that recombinant JUNV (rJUNV) expressing Can GPC display markedly different protein expression and elevated genomic RNA expression when compared to viruses expressing Rom GPC. Additionally, our findings indicate that the N-linked glycosylation motif at amino acid positions 166-168 is important for trafficking of JUNV GPC to the cell surface, and the elimination of this motif interferes with the GPC release from the ER.
[Mh] Termos MeSH primário: Motivos de Aminoácidos
Arenavirus do Novo Mundo/imunologia
Glicoproteínas/genética
Glicoproteínas/metabolismo
Febre Hemorrágica Americana
Vacinas Virais
[Mh] Termos MeSH secundário: Animais
Arenavirus do Novo Mundo/genética
Linhagem Celular
Células Cultivadas
Cricetinae
Retículo Endoplasmático/metabolismo
Estresse do Retículo Endoplasmático
Expressão Gênica
Regulação Viral da Expressão Gênica
Glicoproteínas/química
Glicoproteínas/imunologia
Glicosilação
Febre Hemorrágica Americana/imunologia
Febre Hemorrágica Americana/metabolismo
Febre Hemorrágica Americana/prevenção & controle
Febre Hemorrágica Americana/virologia
Seres Humanos
Processamento de Proteína Pós-Traducional
Transporte Proteico
Transcrição Genética
Vacinas Virais/genética
Vacinas Virais/imunologia
Virulência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycoproteins); 0 (Viral Vaccines)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE
[do] DOI:10.3389/fcimb.2017.00020


  3 / 396 MEDLINE  
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[PMID]:27580122
[Au] Autor:Koma T; Huang C; Aronson JF; Walker AG; Miller M; Smith JN; Patterson M; Paessler S
[Ad] Endereço:Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America.
[Ti] Título:The Ectodomain of Glycoprotein from the Candid#1 Vaccine Strain of Junin Virus Rendered Machupo Virus Partially Attenuated in Mice Lacking IFN-αß/γ Receptor.
[So] Source:PLoS Negl Trop Dis;10(8):e0004969, 2016 Aug.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Machupo virus (MACV), a New World arenavirus, is the etiological agent of Bolivian hemorrhagic fever (BHF). Junin virus (JUNV), a close relative, causes Argentine hemorrhagic fever (AHF). Previously, we reported that a recombinant, chimeric MACV (rMACV/Cd#1-GPC) expressing glycoprotein from the Candid#1 (Cd#1) vaccine strain of JUNV is completely attenuated in a murine model and protects animals from lethal challenge with MACV. A rMACV with a single F438I substitution in the transmembrane domain (TMD) of GPC, which is equivalent to the F427I attenuating mutation in Cd#1 GPC, was attenuated in a murine model but genetically unstable. In addition, the TMD mutation alone was not sufficient to fully attenuate JUNV, indicating that other domains of the GPC may also contribute to the attenuation. To investigate the requirement of different domains of Cd#1 GPC for successful attenuation of MACV, we rescued several rMACVs expressing the ectodomain of GPC from Cd#1 either alone (MCg1), along with the TMD F438I substitution (MCg2), or with the TMD of Cd#1 (MCg3). All rMACVs exhibited similar growth curves in cultured cells. In mice, the MCg1 displayed significant reduction in lethality as compared with rMACV. The MCg1 was detected in brains and spleens of MCg1-infected mice and the infection was associated with tissue inflammation. On the other hand, all animals survived MCg2 and MCg3 infection without detectable levels of virus in various organs while producing neutralizing antibody against Cd#1. Overall our data suggest the indispensable role of each GPC domain in the full attenuation and immunogenicity of rMACV/Cd#1 GPC.
[Mh] Termos MeSH primário: Vírus Junin/imunologia
Glicoproteínas de Membrana/imunologia
Receptores de Interferon/deficiência
Proteínas do Envelope Viral/imunologia
Vacinas Virais/imunologia
[Mh] Termos MeSH secundário: Células A549
Animais
Anticorpos Neutralizantes/sangue
Anticorpos Antivirais/sangue
Cricetinae
Modelos Animais de Doenças
Haplorrinos
Febre Hemorrágica Americana/prevenção & controle
Vírus Junin/patogenicidade
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Testes de Neutralização
Receptores de Interferon/genética
Proteínas Recombinantes/imunologia
Vacinas Atenuadas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Antibodies, Viral); 0 (GPC protein, junin virus); 0 (Membrane Glycoproteins); 0 (Receptors, Interferon); 0 (Recombinant Proteins); 0 (Vaccines, Attenuated); 0 (Viral Envelope Proteins); 0 (Viral Vaccines)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170729
[Lr] Data última revisão:
170729
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0004969


  4 / 396 MEDLINE  
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[PMID]:27044104
[Au] Autor:Zeitlin L; Geisbert JB; Deer DJ; Fenton KA; Bohorov O; Bohorova N; Goodman C; Kim D; Hiatt A; Pauly MH; Velasco J; Whaley KJ; Altmann F; Gruber C; Steinkellner H; Honko AN; Kuehne AI; Aman MJ; Sahandi S; Enterlein S; Zhan X; Enria D; Geisbert TW
[Ad] Endereço:Mapp Biopharmaceutical, Inc., San Diego, CA 92121; larry.zeitlin@mappbio.com twgeisbe@UTMB.EDU.
[Ti] Título:Monoclonal antibody therapy for Junin virus infection.
[So] Source:Proc Natl Acad Sci U S A;113(16):4458-63, 2016 Apr 19.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Countermeasures against potential biothreat agents remain important to US Homeland Security, and many of these pharmaceuticals could have dual use in the improvement of global public health. Junin virus, the causative agent of Argentine hemorrhagic fever (AHF), is an arenavirus identified as a category A high-priority agent. There are no Food and Drug Administration (FDA) approved drugs available for preventing or treating AHF, and the current treatment option is limited to administration of immune plasma. Whereas immune plasma demonstrates the feasibility of passive immunotherapy, it is limited in quantity, variable in quality, and poses safety risks such as transmission of transfusion-borne diseases. In an effort to develop a monoclonal antibody (mAb)-based alternative to plasma, three previously described neutralizing murine mAbs were expressed as mouse-human chimeric antibodies and evaluated in the guinea pig model of AHF. These mAbs provided 100% protection against lethal challenge when administered 2 d after infection (dpi), and one of them (J199) was capable of providing 100% protection when treatment was initiated 6 dpi and 92% protection when initiated 7 dpi. The efficacy of J199 is superior to that previously described for all other evaluated drugs, and its high potency suggests that mAbs like J199 offer an economical alternative to immune plasma and an effective dual use (bioterrorism/public health) therapeutic.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Anticorpos Antivirais/farmacologia
Febre Hemorrágica Americana/tratamento farmacológico
Febre Hemorrágica Americana/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/genética
Anticorpos Monoclonais/imunologia
Anticorpos Antivirais/genética
Anticorpos Antivirais/imunologia
Modelos Animais de Doenças
Avaliação Pré-Clínica de Medicamentos
Cobaias
Seres Humanos
Vírus Junin
Camundongos
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/imunologia
Proteínas Recombinantes de Fusão/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Viral); 0 (Recombinant Fusion Proteins)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160405
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1600996113


  5 / 396 MEDLINE  
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[PMID]:26912630
[Au] Autor:Chou YY; Cuevas C; Carocci M; Stubbs SH; Ma M; Cureton DK; Chao L; Evesson F; He K; Yang PL; Whelan SP; Ross SR; Kirchhausen T; Gaudin R
[Ad] Endereço:Department of Cell Biology, Harvard Medical School, Boston, Massachusetts, USA Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, Massachusetts, USA.
[Ti] Título:Identification and Characterization of a Novel Broad-Spectrum Virus Entry Inhibitor.
[So] Source:J Virol;90(9):4494-510, 2016 May.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Virus entry into cells is a multistep process that often requires the subversion of subcellular machineries. A more complete understanding of these steps is necessary to develop new antiviral strategies. While studying the potential role of the actin network and one of its master regulators, the small GTPase Cdc42, during Junin virus (JUNV) entry, we serendipitously uncovered the small molecule ZCL278, reported to inhibit Cdc42 function as an entry inhibitor for JUNV and for vesicular stomatitis virus, lymphocytic choriomeningitis virus, and dengue virus but not for the nonenveloped poliovirus. Although ZCL278 did not interfere with JUNV attachment to the cell surface or virus particle internalization into host cells, it prevented the release of JUNV ribonucleoprotein cores into the cytosol and decreased pH-mediated viral fusion with host membranes. We also identified SVG-A astroglial cell-derived cells to be highly permissive for JUNV infection and generated new cell lines expressing fluorescently tagged Rab5c or Rab7a or lacking Cdc42 using clustered regularly interspaced short palindromic repeat (CRISPR)-caspase 9 (Cas9) gene-editing strategies. Aided by these tools, we uncovered that perturbations in the actin cytoskeleton or Cdc42 activity minimally affect JUNV entry, suggesting that the inhibitory effect of ZCL278 is not mediated by ZCL278 interfering with the activity of Cdc42. Instead, ZCL278 appears to redistribute viral particles from endosomal to lysosomal compartments. ZCL278 also inhibited JUNV replication in a mouse model, and no toxicity was detected. Together, our data suggest the unexpected antiviral activity of ZCL278 and highlight its potential for use in the development of valuable new tools to study the intracellular trafficking of pathogens. IMPORTANCE: The Junin virus is responsible for outbreaks of Argentine hemorrhagic fever in South America, where 5 million people are at risk. Limited options are currently available to treat infections by Junin virus or other viruses of the Arenaviridae, making the identification of additional tools, including small-molecule inhibitors, of great importance. How Junin virus enters cells is not yet fully understood. Here we describe new cell culture models in which the cells are susceptible to Junin virus infection and to which we applied CRISPR-Cas9 genome engineering strategies to help characterize early steps during virus entry. We also uncovered ZCL278 to be a new antiviral small molecule that potently inhibits the cellular entry of the Junin virus and other enveloped viruses. Moreover, we show that ZCL278 also functions in vivo, thereby preventing Junin virus replication in a mouse model, opening the possibility for the discovery of ZCL278 derivatives of therapeutic potential.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Benzamidas/farmacologia
Descoberta de Drogas
Tioureia/análogos & derivados
Internalização do Vírus/efeitos dos fármacos
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Linhagem Celular
Células Cultivadas
Clatrina/metabolismo
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Endocitose/efeitos dos fármacos
Endossomos/efeitos dos fármacos
Endossomos/virologia
Técnicas de Inativação de Genes
Febre Hemorrágica Americana/genética
Febre Hemorrágica Americana/metabolismo
Febre Hemorrágica Americana/virologia
Seres Humanos
Vírus Junin/efeitos dos fármacos
Vírus Junin/fisiologia
Camundongos
Ligação Proteica
Transporte Proteico
Proteólise
Ribonucleoproteínas/metabolismo
Tioureia/farmacologia
Carga Viral
Proteínas Virais/metabolismo
Ligação Viral/efeitos dos fármacos
Replicação Viral/efeitos dos fármacos
Proteína cdc42 de Ligação ao GTP/genética
Proteína cdc42 de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Actins); 0 (Antiviral Agents); 0 (Benzamides); 0 (Clathrin); 0 (Ribonucleoproteins); 0 (Viral Proteins); 0 (ZCL278); EC 3.6.5.2 (cdc42 GTP-Binding Protein); GYV9AM2QAG (Thiourea)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161228
[Lr] Data última revisão:
161228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160226
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.00103-16


  6 / 396 MEDLINE  
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[PMID]:26792737
[Au] Autor:Golden JW; Maes P; Kwilas SA; Ballantyne J; Hooper JW
[Ad] Endereço:Department of Molecular Virology, Virology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA.
[Ti] Título:Glycoprotein-Specific Antibodies Produced by DNA Vaccination Protect Guinea Pigs from Lethal Argentine and Venezuelan Hemorrhagic Fever.
[So] Source:J Virol;90(7):3515-29, 2016 Jan 20.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Several members of the Arenaviridae can cause acute febrile diseases in humans, often resulting in lethality. The use of convalescent-phase human plasma is an effective treatment in humans infected with arenaviruses, particularly species found in South America. Despite this, little work has focused on developing potent and defined immunotherapeutics against arenaviruses. In the present study, we produced arenavirus neutralizing antibodies by DNA vaccination of rabbits with plasmids encoding the full-length glycoprotein precursors of Junín virus (JUNV), Machupo virus (MACV), and Guanarito virus (GTOV). Geometric mean neutralizing antibody titers, as measured by the 50% plaque reduction neutralization test (PRNT(50)), exceeded 5,000 against homologous viruses. Antisera against each targeted virus exhibited limited cross-species binding and, to a lesser extent, cross-neutralization. Anti-JUNV glycoprotein rabbit antiserum protected Hartley guinea pigs from lethal intraperitoneal infection with JUNV strain Romero when the antiserum was administered 2 days after challenge and provided some protection (∼30%) when administered 4 days after challenge. Treatment starting on day 6 did not protect animals. We further formulated an IgG antibody cocktail by combining anti-JUNV, -MACV, and -GTOV antibodies produced in DNA-vaccinated rabbits. This cocktail protected 100% of guinea pigs against JUNV and GTOV lethal disease. We then expanded on this cocktail approach by simultaneously vaccinating rabbits with a combination of plasmids encoding glycoproteins from JUNV, MACV, GTOV, and Sabia virus (SABV). Sera collected from rabbits vaccinated with the combination vaccine neutralized all four targets. These findings support the concept of using a DNA vaccine approach to generate a potent pan-arenavirus immunotherapeutic. IMPORTANCE: Arenaviruses are an important family of emerging viruses. In infected humans, convalescent-phase plasma containing neutralizing antibodies can mitigate the severity of disease caused by arenaviruses, particularly species found in South America. Because of variations in potency of the human-derived product, limited availability, and safety concerns, this treatment option has essentially been abandoned. Accordingly, despite this approach being an effective postinfection treatment option, research on novel approaches to produce potent polyclonal antibody-based therapies have been deficient. Here we show that DNA-based vaccine technology can be used to make potently neutralizing antibodies in rabbits that exclusively target the glycoproteins of several human-pathogenic arenaviruses found in South America, including JUNV, MACV, GTOV, and SABV. These antibodies protected guinea pigs from lethal disease when given post-virus challenge. We also generated a purified antibody cocktail with antibodies targeting three arenaviruses and demonstrated protective efficacy against all three targets. Our findings demonstrate that use of the DNA vaccine technology could be used to produce candidate antiarenavirus neutralizing antibody-based products.
[Mh] Termos MeSH primário: Anticorpos Neutralizantes/administração & dosagem
Anticorpos Antivirais/administração & dosagem
Antígenos Virais/imunologia
Arenavirus do Novo Mundo/imunologia
Glicoproteínas/imunologia
Febre Hemorrágica Americana/prevenção & controle
Imunização Passiva/métodos
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/imunologia
Anticorpos Antivirais/imunologia
Modelos Animais de Doenças
Feminino
Cobaias
Imunoglobulina G/administração & dosagem
Imunoglobulina G/imunologia
Testes de Neutralização
Coelhos
Análise de Sobrevida
Resultado do Tratamento
Vacinas de DNA/administração & dosagem
Vacinas de DNA/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Antibodies, Viral); 0 (Antigens, Viral); 0 (Glycoproteins); 0 (Immunoglobulin G); 0 (Vaccines, DNA)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160911
[Lr] Data última revisão:
160911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160122
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.02969-15


  7 / 396 MEDLINE  
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[PMID]:26711718
[Au] Autor:Westover JB; Sefing EJ; Bailey KW; Van Wettere AJ; Jung KH; Dagley A; Wandersee L; Downs B; Smee DF; Furuta Y; Bray M; Gowen BB
[Ad] Endereço:Department of Animal, Dairy, and Veterinary Sciences, Utah State University, Logan, UT, USA.
[Ti] Título:Low-dose ribavirin potentiates the antiviral activity of favipiravir against hemorrhagic fever viruses.
[So] Source:Antiviral Res;126:62-8, 2016 Feb.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Favipiravir is approved in Japan to treat novel or re-emerging influenza viruses, and is active against a broad spectrum of RNA viruses, including Ebola. Ribavirin is the only other licensed drug with activity against multiple RNA viruses. Recent studies show that ribavirin and favipiravir act synergistically to inhibit bunyavirus infections in cultured cells and laboratory mice, likely due to their different mechanisms of action. Convalescent immune globulin is the only approved treatment for Argentine hemorrhagic fever caused by the rodent-borne Junin arenavirus. We previously reported that favipiravir is highly effective in a number of small animal models of Argentine hemorrhagic fever. We now report that addition of low dose of ribavirin synergistically potentiates the activity of favipiravir against Junin virus infection of guinea pigs and another arenavirus, Pichinde virus infection of hamsters. This suggests that the efficacy of favipiravir against hemorrhagic fever viruses can be further enhanced through the addition of low-dose ribavirin.
[Mh] Termos MeSH primário: Amidas/farmacologia
Antivirais/farmacologia
Febres Hemorrágicas Virais/tratamento farmacológico
Pirazinas/farmacologia
Vírus de RNA/efeitos dos fármacos
Ribavirina/farmacologia
[Mh] Termos MeSH secundário: Animais
Arenavirus/efeitos dos fármacos
Cercopithecus aethiops
Cricetinae
Vírus da Dengue/efeitos dos fármacos
Modelos Animais de Doenças
Sinergismo Farmacológico
Feminino
Cobaias
Hantavirus/efeitos dos fármacos
Vírus da Febre Hemorrágica da Crimeia-Congo/efeitos dos fármacos
Febre Hemorrágica Americana/tratamento farmacológico
Doença pelo Vírus Ebola/tratamento farmacológico
Febres Hemorrágicas Virais/sangue
Febres Hemorrágicas Virais/veterinária
Febres Hemorrágicas Virais/virologia
Vírus Junin/efeitos dos fármacos
Masculino
Mesocricetus
Camundongos
Células Vero
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Amides); 0 (Antiviral Agents); 0 (Pyrazines); 49717AWG6K (Ribavirin); EW5GL2X7E0 (favipiravir)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170201
[Lr] Data última revisão:
170201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151230
[St] Status:MEDLINE


  8 / 396 MEDLINE  
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[PMID]:26139838
[Au] Autor:Bell TM; Bunton TE; Shaia CI; Raymond JW; Honnold SP; Donnelly GC; Shamblin JD; Wilkinson ER; Cashman KA
[Ad] Endereço:US Army Medical Research Institute of Infectious Diseases, Frederick, MD, USA todd.m.bell.mil@mail.mil.
[Ti] Título:Pathogenesis of Bolivian Hemorrhagic Fever in Guinea Pigs.
[So] Source:Vet Pathol;53(1):190-9, 2016 Jan.
[Is] ISSN:1544-2217
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Machupo virus, the cause of Bolivian hemorrhagic fever, is a highly lethal viral hemorrhagic fever with no Food and Drug Administration-approved vaccines or therapeutics. This study evaluated the guinea pig as a model using the Machupo virus-Chicava strain administered via aerosol challenge. Guinea pigs (Cavia porcellus) were serially sampled to evaluate the temporal progression of infection, gross and histologic lesions, and sequential changes in serum chemistry and hematology. The incubation period was 5 to 12 days, and complete blood counts revealed leukopenia with lymphopenia and thrombocytopenia. Gross pathologic findings included congestion and hemorrhage of the gastrointestinal mucosa and serosa, noncollapsing lungs with fluid exudation, enlarged lymph nodes, and progressive pallor and friability of the liver. Histologic lesions consisted of foci of degeneration and cell death in the haired skin, liver, pancreas, adrenal glands, lymph nodes, tongue, esophagus, salivary glands, renal pelvis, small intestine, and large intestine. Lymphohistiocytic interstitial pneumonia was also present. Inflammation within the central nervous system, interpreted as nonsuppurative encephalitis, was histologically apparent approximately 16 days postexposure and was generally progressive. Macrophages in the tracheobronchial lymph node, on day 5 postexposure, were the first cells to demonstrate visible viral antigen. Viral antigen was detected throughout the lymphoid system by day 9 postexposure, followed by prominent spread within epithelial tissues and then brain. This study provides insight into the course of Machupo virus infection and supports the utility of guinea pigs as an additional animal model for vaccine and therapeutic development.
[Mh] Termos MeSH primário: Arenavirus do Novo Mundo/patogenicidade
Modelos Animais de Doenças
Cobaias
Febre Hemorrágica Americana/patologia
[Mh] Termos MeSH secundário: Glândulas Suprarrenais/patologia
Aerossóis
Animais
Epitélio/patologia
Feminino
Febre Hemorrágica Americana/virologia
Seres Humanos
Fígado/patologia
Pulmão/patologia
Linfonodos/patologia
Masculino
Pâncreas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Aerosols)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150704
[St] Status:MEDLINE
[do] DOI:10.1177/0300985815588609


  9 / 396 MEDLINE  
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[PMID]:26950993
[Au] Autor:Sizikova TE; Lebedev VN; Pantyukhov VB; Borisevich SV; Merkulov VA
[Ti] Título:[EXPERIENCE OF STUDY AND POSSIBLE WAYS OF ELIMINATION OF FALSE POSITIVE AND FALSE NEGATIVE RESULTS DURING EXECUTION OF POLYMERASE CHAIN REACTION ON AN EXAMPLE OF JUNIN VIRUS RNA DETECTION].
[So] Source:Zh Mikrobiol Epidemiol Immunobiol;(6):78-82, 2015 Nov-Dec.
[Is] ISSN:0372-9311
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:AIM: Experience of study and possible ways of elimination of false positive and false negative results during execution of polymerase chain reaction on an example of Junin virus RNA detection. MATERIALSS AND METHODS: Junin virus--causative agent of Argentine hemorrhagic fever (AHF) strain XJpR37/5787 was obtained from the State collection of pathogenicity group I causative agents of the 48th Central Research Institute. Reagent kit for detection of Junin virus RNA by RT-PCR was developed in the Institute and consists of 4 sets: for isolation of RNA, execution of reverse-transcription reaction, execution of PCR and electrophoretic detection of PCR products. RT-PCR was carried out by a standard technique. Continuous cell cultures of African green monkey Vero B, GMK-AH-1(D) were obtained from the museum of cell culture department of the Centre. RESULTS: An experimental study of the effect of various factors of impact on the sample under investigation ("thawing-freezing", presence of formaldehyde, heparin) on the obtaining of false negative results during Junin virus RNA detection by using RT-PCR was studied. Addition of 0.01% heparin to the samples was shown to completely inhibit PCR. Addition of 0.05% formaldehyde significantly reduces sensitivity of the method. A possibility of reduction of analysis timeframe from 15 to 5 days was shown during detection of the causative agent in samples with low concentration of the latter by growing the samples and subsequent analysis of the material obtained by using RT-PCR. CONCLUSION: During detection of causative agent by using RT-PCR false negative results could appear in the presence of formaldehyde and heparin in the sample. A possibility of elimination of false negative PCR results due to concentration of the causative agent in the sample under investigation at a level below sensitivity threshold was shown on the example of Junin virus RNA detection by using growing of the pathogen in appropriate accumulation system with subsequent analysis of the material obtained using PCR.
[Mh] Termos MeSH primário: Formaldeído/química
Febre Hemorrágica Americana/diagnóstico
Heparina/química
Vírus Junin/genética
RNA Viral/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa/normas
[Mh] Termos MeSH secundário: Animais
Cercopithecus aethiops
Reações Falso-Negativas
Reações Falso-Positivas
Febre Hemorrágica Americana/sangue
Febre Hemorrágica Americana/virologia
Seres Humanos
Vírus Junin/isolamento & purificação
RNA Viral/isolamento & purificação
Kit de Reagentes para Diagnóstico/normas
Células Vero
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Viral); 0 (Reagent Kits, Diagnostic); 1HG84L3525 (Formaldehyde); 9005-49-6 (Heparin)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:160308
[Lr] Data última revisão:
160308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160309
[St] Status:MEDLINE


  10 / 396 MEDLINE  
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[PMID]:26581982
[Au] Autor:Koma T; Patterson M; Huang C; Seregin AV; Maharaj PD; Miller M; Smith JN; Walker AG; Hallam S; Paessler S
[Ad] Endereço:Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
[Ti] Título:Machupo Virus Expressing GPC of the Candid#1 Vaccine Strain of Junin Virus Is Highly Attenuated and Immunogenic.
[So] Source:J Virol;90(3):1290-7, 2015 Nov 18.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Machupo virus (MACV) is the causative agent of Bolivian hemorrhagic fever. Our previous study demonstrated that a MACV strain with a single amino acid substitution (F438I) in the transmembrane domain of glycoprotein is attenuated but genetically unstable in mice. MACV is closely related to Junin virus (JUNV), the causative agent of Argentine hemorrhagic fever. Others and our group have identified the glycoprotein to be the major viral factor determining JUNV attenuation. In this study, we tested the compatibility of the glycoprotein of the Candid#1 live-attenuated vaccine strain of JUNV in MACV replication and its ability to attenuate MACV in vivo. Recombinant MACV with the Candid#1 glycoprotein (rMACV/Cd#1-GPC) exhibited growth properties similar to those of Candid#1 and was genetically stable in vitro. In a mouse model of lethal infection, rMACV/Cd#1-GPC was fully attenuated, more immunogenic than Candid#1, and fully protective against MACV infection. Therefore, the MACV strain expressing the glycoprotein of Candid#1 is safe, genetically stable, and highly protective against MACV infection in a mouse model. IMPORTANCE: Currently, there are no FDA-approved vaccines and/or treatments for Bolivian hemorrhagic fever, which is a fatal human disease caused by MACV. The development of antiviral strategies to combat viral hemorrhagic fevers, including Bolivian hemorrhagic fever, is one of the top priorities of the Implementation Plan of the U.S. Department of Health and Human Services Public Health Emergency Medical Countermeasures Enterprise. Here, we demonstrate for the first time that MACV expressing glycoprotein of Candid#1 is a safe, genetically stable, highly immunogenic, and protective vaccine candidate against Bolivian hemorrhagic fever.
[Mh] Termos MeSH primário: Arenavirus do Novo Mundo/genética
Arenavirus do Novo Mundo/imunologia
Glicoproteínas de Membrana/genética
Recombinação Genética
Proteínas do Envelope Viral/genética
Vacinas Virais/administração & dosagem
Vacinas Virais/imunologia
[Mh] Termos MeSH secundário: Estruturas Animais/patologia
Animais
Arenavirus do Novo Mundo/patogenicidade
Peso Corporal
Modelos Animais de Doenças
Instabilidade Genômica
Febre Hemorrágica Americana/patologia
Febre Hemorrágica Americana/prevenção & controle
Histocitoquímica
Camundongos Endogâmicos C57BL
Dados de Sequência Molecular
Análise de Sequência de DNA
Análise de Sobrevida
Temperatura Ambiente
Vacinas Atenuadas/administração & dosagem
Vacinas Atenuadas/genética
Vacinas Atenuadas/imunologia
Vacinas Virais/genética
Virulência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (GPC protein, junin virus); 0 (Membrane Glycoproteins); 0 (Vaccines, Attenuated); 0 (Viral Envelope Proteins); 0 (Viral Vaccines)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151120
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.02615-15



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