RESUMO
Características generales de la Fiebre Hemorrágica Argentina (FHA): Transmisión, presentación clínica, definición de caso sospechoso, tratamiento, medidas de prevención, y situación regional. Se describe el caso confirmado en la Ciudad de Buenos Aires.
Assuntos
Humanos , Feminino , Adulto , Febre Hemorrágica Americana/fisiopatologia , Febre Hemorrágica Americana/patologia , Febre Hemorrágica Americana/transmissão , Febre Hemorrágica Americana/epidemiologia , Notificação de Doenças , Monitoramento EpidemiológicoRESUMO
Analysis of data of the available literature on epidemiology of Bolivian hemorrhagic fever, manifestations of human disease, biological properties of the causative agent and development carried out abroad of means and methods of diagnostics, prophylaxis and therapy of this infection that presents a potential threat for the population and economy of the Russian Federation in case of introduction of the causative agent is presented.
Assuntos
Arenavirus do Novo Mundo/fisiologia , Febre Hemorrágica Americana/epidemiologia , Febre Hemorrágica Americana/fisiopatologia , Muridae/virologia , Vírion/fisiologia , Animais , Anticorpos Neutralizantes/sangue , Antivirais/uso terapêutico , Arenavirus do Novo Mundo/patogenicidade , Gerenciamento Clínico , Surtos de Doenças , Vetores de Doenças , Febre Hemorrágica Americana/terapia , Febre Hemorrágica Americana/virologia , Humanos , Federação Russa/epidemiologia , América do Sul/epidemiologia , Vírion/patogenicidade , Replicação ViralRESUMO
Junín virus of the Arenaviridae family is the etiological agent of Argentine hemorrhagic fever, a febrile syndrome causing hematological and neurological symptoms. We review historical perspectives of current knowledge on the disease, and update information related to the virion and its potential pathogenic mechanisms.
Assuntos
Febre Hemorrágica Americana/fisiopatologia , Vírus Junin/fisiologia , Vírus Junin/patogenicidade , Animais , Febre Hemorrágica Americana/virologia , Humanos , Vírus Junin/classificação , Vírus Junin/ultraestrutura , Modelos Animais , Replicação Viral/fisiologiaAssuntos
Doenças Transmissíveis Emergentes , Febre Hemorrágica Americana , Adulto , Arenavirus do Novo Mundo/classificação , Arenavirus do Novo Mundo/genética , Arenavirus do Novo Mundo/isolamento & purificação , Bolívia/epidemiologia , Doenças Transmissíveis Emergentes/epidemiologia , Doenças Transmissíveis Emergentes/mortalidade , Doenças Transmissíveis Emergentes/fisiopatologia , Doenças Transmissíveis Emergentes/virologia , Febre Hemorrágica Americana/epidemiologia , Febre Hemorrágica Americana/mortalidade , Febre Hemorrágica Americana/fisiopatologia , Febre Hemorrágica Americana/virologia , Humanos , Masculino , Dados de Sequência Molecular , Filogenia , RNA Viral/análise , RNA Viral/isolamento & purificação , Análise de Sequência de DNA , Adulto JovemRESUMO
RNA was purified from 39 strains of cell-cultured Junin virus (JUN) from central Argentina, which included both human- and rodent-derived isolates (a total of 26 and 13, respectively), as well as from 2 laboratory JUN strains, XJ Cl3 and XJ #44. JUN-specific primers were used to amplify a 511-nucleotide (nt) fragment of the nucleocapsid protein gene and a 495-nt fragment of the glycoprotein 1 (GP1) gene. Genetic diversity among JUN strains studied was up to 13% at the nt level and up to 9% at the amino acid (aa) level for the GP1 gene and up to 9% (nt) and 4% (aa) for the NP gene. Phylogenetic analyses of both genes revealed three distinct clades. The first clade was composed of the JUN strains from the center of the endemic area and included the majority of JUN strains analyzed in the current study. The second clade contained 4 JUN strains isolated between 1963 and 1971 from Cordoba Province, the western-most edge of the known endemic area. The third clade contained 4 JUN strains that originated from Calomys musculinus trapped in Zarate, the northeastern edge of the known endemic area. Certain JUN sequences, which were obtained from GenBank and identified as XJ, XJ #44, and Candid #1 strains, appeared to form a separate clade. Over 400 nt of the GP1 and GP2 genes were additionally sequenced for 7 JUN strains derived from patients with different clinical presentations and outcomes of Argentine hemorrhagic fever. Analysis of the corresponding aa sequences did not allow us to attribute any particular genetic marker to the changing severity or clinical form of the human disease.
Assuntos
Variação Genética/genética , Febre Hemorrágica Americana/epidemiologia , Febre Hemorrágica Americana/virologia , Vírus Junin/classificação , Vírus Junin/genética , Filogenia , Animais , Argentina/epidemiologia , Linhagem Celular , Análise Mutacional de DNA , Genes Virais/genética , Glicoproteínas/química , Glicoproteínas/genética , Febre Hemorrágica Americana/fisiopatologia , Humanos , Vírus Junin/química , Vírus Junin/patogenicidade , Camundongos , Dados de Sequência Molecular , Muridae/virologia , Mutação/genética , Nucleocapsídeo/química , Nucleocapsídeo/genética , RNA Viral/análise , RNA Viral/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Homologia de Sequência , Fatores de Tempo , Virulência/genéticaRESUMO
Chronic infections in specific rodents appear to be crucial to the long-term persistence of arenaviruses in nature. The cane mouse, Zygodontomys brevicauda, is a natural host of Guanarito virus (family Arenaviridae), the etiologic agent of Venezuelan hemorrhagic fever. The purpose of this study was to elucidate the natural history of Guanarito virus infection in Z. brevicauda. Thirty-nine laboratory-reared cane mice each were inoculated subcutaneously with 3.0 log10 plaque-forming units of the Guanarito virus prototype strain INH-95551. No lethality was associated with infection in any animal, regardless of age at inoculation. The 13 newborn, 14 weanling, and 8 of the 12 adult animals developed chronic viremic infections characterized by persistent shedding of infectious virus in oropharyngeal secretions and urine. These findings indicate that Guanarito virus infection in Z. brevicauda can be chronic and thus support the concept that this rodent species is the natural reservoir of Guanarito virus.
Assuntos
Arenaviridae/patogenicidade , Arenavirus do Novo Mundo/patogenicidade , Febre Hemorrágica Americana/fisiopatologia , Animais , Anticorpos Antivirais/sangue , Arenaviridae/isolamento & purificação , Arenavirus do Novo Mundo/isolamento & purificação , Febre Hemorrágica Americana/patologia , Febre Hemorrágica Americana/urina , Muridae , Orofaringe/virologia , Baço/virologia , VenezuelaRESUMO
Bolivian hemorrhagic fever (BHF) is a potentially severe febrile illness caused by Machupo virus (family Arenaviridae). Initial symptoms include headache, fever, arthralgia, and myalgia. In the later stages of this illness, patients may develop hemorrhagic manifestations including subconjunctival hemorrhage, epistaxis, hematemesis, melena, and hematuria, as well as neurological signs including tremor, seizures, and coma. During the BHF epidemics of the 1960s, convalescent-phase immune plasma from survivors of BHF was administered to selected patients infected with Machupo virus. However, there is currently a paucity of survivors of BHF who can donate immune plasma, and there is no active program for collection and storage of BHF immune plasma; therefore, we had the opportunity to offer intravenous ribavirin to two of three patients with this potentially life-threatening infection. One patient with laboratory-confirmed Machupo virus infection who received ribavirin recovered without sequelae, as did a second patient with suspected BHF whose epidemiological and clinical features were similar to those of the first patient. This report describes the first use of intravenous ribavirin therapy for BHF in humans, and the results suggest the need for more extensive clinical studies to assess the usefulness of ribavirin for treating BHF.
Assuntos
Antivirais/uso terapêutico , Febre Hemorrágica Americana/tratamento farmacológico , Ribavirina/uso terapêutico , Adulto , Antígenos Virais/análise , Arenavirus do Novo Mundo/imunologia , Arenavirus do Novo Mundo/isolamento & purificação , Evolução Fatal , Febre Hemorrágica Americana/fisiopatologia , Febre Hemorrágica Americana/virologia , Humanos , Injeções Intravenosas , Masculino , Pessoa de Meia-IdadeRESUMO
To determine whether phagocytic activity is affected by a viral infection known to induce astrocyte differentiation, a triple procedure (PAP labeling for GFAP, PAS reaction for added baker's yeast cells and hematoxylin for nuclear staining of the whole monolayer) was applied to Junin virus-inoculated cultures, as well as matched controls. The three-step staining simplified yeast cell count for subsequent statistical analysis, which discerned preferential uptake by differentiated rather than immature astrocytes. Accordingly, greater cell maturation induced by Junin virus was concomitant with early enhancement of phagocytic activity.
Assuntos
Astrócitos/fisiologia , Fagocitose/fisiologia , Fosfatase Ácida/análise , Animais , Arenavirus do Novo Mundo , Diferenciação Celular/fisiologia , Células Cultivadas , Febre Hemorrágica Americana/fisiopatologia , L-Lactato Desidrogenase/metabolismo , Ratos , Saccharomyces cerevisiae/fisiologia , Coloração e RotulagemRESUMO
Junin virus, the etiological agent of Argentine hemorrhagic fever, produces in man a disease mainly characterized by hemorrhagic alterations, commonly accompanied by neurological symptoms, and leading to 10% mortality. Intracerebral inoculation in 10-day-old rats or intraperitoneal inoculation in 2-day-old rats leads to high mortality due to severe encephalitis. Here, the effect of Ribavirin on these experimental models was tested in order to evaluate the degree of protection achieved against neuropathological manifestations. In intracerebrally infected 10-day-old rats the drug was administered 2 hr before virus inoculation. Doses ranged from 30 to 90 mg/kg body weight. Protection reached 40% for the 60 and 90 mg doses. Intraperitoneally infected 2-day-old rats received the drug in five 30-mg daily doses, starting the same day as virus inoculation. Survival was 73%. Viral replication within peritoneal macrophages dropped markedly, leading to much lower CNS viral titres. Together with results reported in primates, our findings support further studies on Ribavirin, with a view to eventual trials in humans.