RESUMO
Recent data in a nonhuman primate model showed that infants postnatally infected with Zika virus (ZIKV) were acutely susceptible to high viremia and neurological damage, suggesting the window of vulnerability extends beyond gestation. In this pilot study, we addressed the susceptibility of two infant rhesus macaques born healthy to dams infected with Zika virus during pregnancy. Passively acquired neutralizing antibody titers dropped below detection limits between 2 and 3 months of age, while binding antibodies remained detectable until viral infection at 5 months. Acute serum viremia was comparatively lower than adults infected with the same Brazilian isolate of ZIKV (n = 11 pregnant females, 4 males, and 4 non-pregnant females). Virus was never detected in cerebrospinal fluid nor in neural tissues at necropsy two weeks after infection. However, viral RNA was detected in lymph nodes, confirming some tissue dissemination. Though protection was not absolute and our study lacks an important comparison with postnatally infected infants born to naïve dams, our data suggest infants born healthy to infected mothers may harbor a modest but important level of protection from postnatally acquired ZIKV for several months after birth, an encouraging result given the potentially severe infection outcomes of this population.
Assuntos
Transmissão Vertical de Doenças Infecciosas , Macaca mulatta , Complicações Infecciosas na Gravidez/veterinária , Infecção por Zika virus/transmissão , Animais , Animais Recém-Nascidos/imunologia , Animais Recém-Nascidos/virologia , Anticorpos Neutralizantes/sangue , Anticorpos Antivirais/sangue , Feminino , Masculino , Projetos Piloto , Gravidez , Complicações Infecciosas na Gravidez/virologia , Zika virus , Infecção por Zika virus/imunologia , Infecção por Zika virus/virologiaRESUMO
We summarize and analyze historical and current data regarding the reemergence of St. Louis encephalitis virus (SLEV; genus Flavivirus) in the Americas. Historically, SLEV caused encephalitis outbreaks in the United States; however, it was not considered a public health concern in the rest of the Americas. After the introduction of West Nile virus in 1999, activity of SLEV decreased considerably in the United States. During 2014-2015, SLEV caused a human outbreak in Arizona and caused isolated human cases in California in 2016 and 2017. Phylogenetic analyses indicate that the emerging SLEV in the western United States is related to the epidemic strains isolated during a human encephalitis outbreak in Córdoba, Argentina, in 2005. Ecoepidemiologic studies suggest that the emergence of SLEV in Argentina was caused by the introduction of a more pathogenic strain and increasing populations of the eared dove (amplifying host).
Assuntos
Doenças Transmissíveis Emergentes/epidemiologia , Vírus da Encefalite de St. Louis/fisiologia , Encefalite de St. Louis/epidemiologia , Doenças Transmissíveis Emergentes/história , Doenças Transmissíveis Emergentes/transmissão , Doenças Transmissíveis Emergentes/virologia , Surtos de Doenças , Vírus da Encefalite de St. Louis/classificação , Vírus da Encefalite de St. Louis/genética , Encefalite de St. Louis/história , Encefalite de St. Louis/transmissão , Encefalite de St. Louis/virologia , Geografia Médica , História do Século XX , História do Século XXI , Humanos , Filogenia , América do Sul/epidemiologia , Estados Unidos/epidemiologiaRESUMO
Venezuelan equine encephalitis virus (VEEV) is an emerging pathogen of equids and humans, but infection of its rodent reservoir hosts has received little study. To determine whether responses to infection vary among geographic populations, we inoculated 3 populations of cotton rats with 2 enzootic VEEV strains (Co97-0054 [enzootic ID subtype] and 68U201 [enzootic IE subtype]). The 3 populations were offspring from wild-caught cotton rats collected in a VEE-enzootic area of south Florida, USA; wild-caught cotton rats from a non-VEE-enzootic area of Texas, USA; and commercially available (Harlan) colony-reared cotton rats from a non-VEE-enzootic region. Although each population had similar early viremia titers, no detectable disease developed in the VEE-sympatric Florida animals, but severe disease and death affected the Texas and Harlan animals. Our findings suggest that the geographic origins of cotton rats are important determinants of the outcome of VEE infection and reservoir potential of these rodents.
Assuntos
Vírus da Encefalite Equina Venezuelana/crescimento & desenvolvimento , Encefalomielite Equina Venezuelana/veterinária , Encefalomielite Equina Venezuelana/virologia , Doenças dos Roedores/virologia , Sigmodontinae/virologia , Animais , Reservatórios de Doenças/virologia , Encefalomielite Equina Venezuelana/epidemiologia , Encefalomielite Equina Venezuelana/imunologia , Feminino , Florida/epidemiologia , Masculino , Ratos , Doenças dos Roedores/epidemiologia , Doenças dos Roedores/imunologia , Sigmodontinae/imunologia , Texas/epidemiologia , Viremia/epidemiologia , Viremia/imunologia , Viremia/virologiaRESUMO
Quantifying the dose of an arbovirus transmitted by mosquitoes is essential for designing pathogenesis studies simulating natural infection of vertebrates. Titration of saliva collected in vitro from infected mosquitoes may not accurately estimate titers transmitted during blood feeding, and infection by needle injection may affect vertebrate pathogenesis. We compared the amount of Venezuelan equine encephalitis virus collected from the saliva of Aedes taeniorhynchus to the amount injected into a mouse during blood feeding. Less virus was transmitted by mosquitoes in vivo (geometric mean 11 PFU) than was found for comparable times of salivation in vitro (mean saliva titer 74 PFU). We also observed slightly lower early and late viremia titers in mice that were needle injected with 8 PFU, which represents the low end of the in vivo transmission range. No differences in survival were detected, regardless of the dose or infection route.
Assuntos
Vírus da Encefalite Equina Venezuelana/patogenicidade , Encefalomielite Equina Venezuelana/transmissão , Aedes/virologia , Animais , Encefalomielite Equina Venezuelana/mortalidade , Encefalomielite Equina Venezuelana/fisiopatologia , Encefalomielite Equina Venezuelana/virologia , Humanos , Insetos Vetores/virologia , Camundongos , Saliva/virologia , Viremia/fisiopatologia , Viremia/transmissão , Viremia/virologiaRESUMO
An epitope-blocking enzyme-linked immunosorbent assay was developed for the rapid differentiation of serologic responses to enzootic variety IE and ID versus epizootic variety IAB and IC strains of Venezuelan equine encephalitis (VEE) virus. Two monoclonal antibodies that differentially recognize epizootic versus enzootic VEE virus epitopes were used to measure the serotype-specific blocking abilities of antibodies in sera of naturally infected humans, equines, and bovines, as well as in experimentally infected equines. The assay is simple, species-independent, rapid, and sensitive, and will improve surveillance for VEE emergence. It could also be used to determine the epidemic potential of a VEE virus following an intentional introduction for bioterrorism.
Assuntos
Anticorpos Antivirais/sangue , Vírus da Encefalite Equina Venezuelana/isolamento & purificação , Animais , Bovinos , Linhagem Celular , Cricetinae , Vírus da Encefalite Equina Venezuelana/classificação , Vírus da Encefalite Equina Venezuelana/imunologia , Encefalomielite Equina Venezuelana/epidemiologia , Ensaio de Imunoadsorção Enzimática , Cavalos/sangue , Humanos , Sensibilidade e Especificidade , Especificidade da EspécieRESUMO
Five years after the apparent end of the major 1995 Venezuelan equine encephalitis (VEE) epizootic/epidemic, focal outbreaks of equine encephalitis occurred in Carabobo and Barinas States of western Venezuela. Virus isolates from horses in each location were nearly identical in sequence to 1995 isolates, which suggests natural persistence of subtype IC VEE virus (VEEV) strains in a genetically stable mode. Serologic evidence indicated that additional outbreaks occurred in Barinas State in 2003. Field studies identified known Culex (Melanoconion) spp. vectors and reservoir hosts of enzootic VEEV but a dearth of typical epidemic vectors. Cattle serosurveys indicated the recent circulation of enzootic VEEV strains, and possibly of epizootic strains. Persistence of VEEV subtype IC strains and infection of horses at the end of the rainy season suggest the possibility of an alternative, cryptic transmission cycle involving survival through the dry season of infected vectors or persistently infected vertebrates.
Assuntos
Surtos de Doenças , Vírus da Encefalite Equina Venezuelana/isolamento & purificação , Encefalomielite Equina Venezuelana/epidemiologia , Encefalomielite Equina Venezuelana/virologia , Cavalos/virologia , Animais , Bovinos , Culicidae/virologia , Didelphis/virologia , Reservatórios de Doenças/virologia , Vírus da Encefalite Equina Venezuelana/genética , Encefalomielite Equina Venezuelana/sangue , Cavalos/sangue , Humanos , Murinae/virologia , Filogenia , Estações do Ano , Vigilância de Evento Sentinela , Venezuela/epidemiologiaRESUMO
Since Venezuelan equine encephalitis virus (VEEV) was isolated in Peru in 1942, >70 isolates have been obtained from mosquitoes, humans, and sylvatic mammals primarily in the Amazon region. To investigate genetic relationships among the Peru VEEV isolates and between the Peru isolates and other VEEV strains, a fragment of the PE2 gene was amplified and analyzed by single-stranded conformation polymorphism. Representatives of seven genotypes underwent sequencing and phylogenetic analysis. The results identified four VEE complex lineages that cocirculate in the Amazon region: subtypes ID (Panama and Colombia/Venezuela genotypes), IIIC, and a new, proposed subtype IIID, which was isolated from a febrile human, mosquitoes, and spiny rats. Both ID lineages and the IIID subtype are associated with febrile human illness. Most of the subtype ID isolates belonged to the Panama genotype, but the Colombia/Venezuela genotype, which is phylogenetically related to epizootic strains, also continues to circulate in the Amazon basin.
Assuntos
Vírus da Encefalite Equina Venezuelana/classificação , Vírus da Encefalite Equina Venezuelana/genética , Encefalomielite Equina Venezuelana/epidemiologia , Doenças Endêmicas , Animais , Culicidae/virologia , Vírus da Encefalite Equina Venezuelana/isolamento & purificação , Encefalomielite Equina Venezuelana/virologia , Genótipo , Humanos , Glicoproteínas de Membrana/genética , Peru/epidemiologia , Filogenia , Polimorfismo Conformacional de Fita Simples , Precursores de Proteínas , RNA Viral/análise , RNA Viral/isolamento & purificação , Doenças dos Roedores/virologia , Roedores/virologia , Análise de Sequência de DNA , Proteínas Virais/genéticaRESUMO
West Nile virus (WNV) antibodies were detected in horses from five Mexican states, and WNV was isolated from a Common Raven in the state of Tabasco. Phylogenetic studies indicate that this isolate, the first from Mexico, is related to strains from the central United States but has a relatively high degree of sequence divergence.