RESUMEN
Paracoccidioidomycosis (PCM) is the most important systemic mycoses in Latin America. We describe a severe case of paracoccidioidomycosis in a 14-year-old boy, with a rapid disease progression. The fungal strain was isolated and inoculated into a T and/or B cell immunocompromised mice, which revealed a highly virulent strain. The case report presented herein emphasizes the importance of considering PCM in the differential diagnosis of patients with other infectious diseases in endemic areas and highlights a novel isolate.
Asunto(s)
Paracoccidioides/aislamiento & purificación , Paracoccidioidomicosis/diagnóstico , Paracoccidioidomicosis/patología , Adolescente , Experimentación Animal , Animales , Brasil , Histocitoquímica , Humanos , Huésped Inmunocomprometido , Ganglios Linfáticos/patología , Masculino , Ratones , Microscopía , Paracoccidioides/patogenicidad , Paracoccidioidomicosis/microbiología , Análisis de SupervivenciaRESUMEN
Newcastle disease (ND) is caused by the avian paramyxovirus type 1 (APMV-1) or Newcastle disease virus (NDV) that comprises a diverse group of viruses with a single-stranded, negative-sense RNA genome. ND is one of the most important diseases of chickens, because it severely affects poultry production worldwide. In the 1970s, outbreaks of virulent ND were recorded in Brazil, and the strain APMV-1/Chicken/Brazil/SJM/75 (SJM) of NDV was isolated. This strain was characterized as highly pathogenic for chickens but not pathogenic for other bird species. Here we present the complete genome of NDV strain SJM and investigate the phylogenetic relationships of this virus with other NDV strains in terms of genome and proteins composition, as well as characterizing its evolution process. The NDV strain SJM is categorized as a velogenic virus and the complete genome is 15,192 nucleotides in length, consisting of six genes in the order 3'-NP-P-M-F-HN-L-5'. The presence of the major pathogenic determinant of NDV strains ((112)R-R-Q-K-R↓F(117)) was identified in the Fusion protein of the NDV strain SJM. In addition, phylogenetic analysis classified the NDV strain SJM as a member of class II, genotype V, and indicates that this virus help us in the understanding of the evolutionary process of strains belonging to this genotype. This study contributes to the growing interest involving the characterization of NDV isolates to improve our current understanding about the epidemiology, surveillance and evolution of the pathogenic strains.
Asunto(s)
Pollos , Genoma Viral , Enfermedad de Newcastle/epidemiología , Enfermedad de Newcastle/virología , Virus de la Enfermedad de Newcastle/clasificación , Virus de la Enfermedad de Newcastle/genética , Animales , Brasil/epidemiología , Biología Computacional , Brotes de Enfermedades , Evolución Molecular , Genotipo , Historia del Siglo XX , Datos de Secuencia Molecular , Enfermedad de Newcastle/historia , Virus de la Enfermedad de Newcastle/aislamiento & purificación , Filogenia , Proteínas Virales/química , Proteínas Virales/genética , VirulenciaRESUMEN
Infectious bursal disease virus (IBDV) is classified according to the antigenicity and virulence into classical virulent (cv), very virulent (vv), and antigenic variant strains. The molecular basis for the IBDV antigenic variation is well established and is associated to the capsid protein, VP2 (gene VP2 of segment A), whereas both VP2 and the RNA-dependent RNA polymerase, VP1 (gene VP1 of segment B), have been correlated with the virulence. In this study, seventeen Brazilian IBDV samples previously characterized by the VP2 gene as cv (three) and vv (fourteen) strains were genetically and molecularly analyzed for their VP1 gene. All of the strains kept with the same cv or vv classification except one sample, Br/03/DR. This sample was classified as vv by its VP2 gene, but it was most closely related to the cv strains by its VP1 partial sequence and phylogeny. Studies on the phylogeny of VP1 have suggested a possible reassortment event that originated the vvVP1. In this case, the sample carrying vvVP2 and cvVP1 could be a descendant of IBDV ancestors prior to the reassortment of vvVP1; alternatively, it could be the result of a genetic exchange between the segments of different strains or with a live attenuated vaccine. Nevertheless, this is the first report of natural genetic reassortment of IBDV in Brazil.
Asunto(s)
Animales , Infecciones por Birnaviridae , Variación Genética , Técnicas In Vitro , Filogenia , Reacción en Cadena de la Polimerasa , Recombinación Genética , Virus de la Enfermedad Infecciosa de la Bolsa/genética , Virus de la Enfermedad Infecciosa de la Bolsa/patogenicidad , Genotipo , Métodos , VirulenciaRESUMEN
Infectious bursal disease virus (IBDV) is classified according to the antigenicity and virulence into classical virulent (cv), very virulent (vv), and antigenic variant strains. The molecular basis for the IBDV antigenic variation is well established and is associated to the capsid protein, VP2 (gene VP2 of segment A), whereas both VP2 and the RNA-dependent RNA polymerase, VP1 (gene VP1 of segment B), have been correlated with the virulence. In this study, seventeen Brazilian IBDV samples previously characterized by the VP2 gene as cv (three) and vv (fourteen) strains were genetically and molecularly analyzed for their VP1 gene. All of the strains kept with the same cv or vv classification except one sample, Br/03/DR. This sample was classified as vv by its VP2 gene, but it was most closely related to the cv strains by its VP1 partial sequence and phylogeny. Studies on the phylogeny of VP1 have suggested a possible reassortment event that originated the vvVP1. In this case, the sample carrying vvVP2 and cvVP1 could be a descendant of IBDV ancestors prior to the reassortment of vvVP1; alternatively, it could be the result of a genetic exchange between the segments of different strains or with a live attenuated vaccine. Nevertheless, this is the first report of natural genetic reassortment of IBDV in Brazil.
RESUMEN
Infectious bursal disease virus (IBDV) is classified according to the antigenicity and virulence into classical virulent (cv), very virulent (vv), and antigenic variant strains. The molecular basis for the IBDV antigenic variation is well established and is associated to the capsid protein, VP2 (gene VP2 of segment A), whereas both VP2 and the RNA-dependent RNA polymerase, VP1 (gene VP1 of segment B), have been correlated with the virulence. In this study, seventeen Brazilian IBDV samples previously characterized by the VP2 gene as cv (three) and vv (fourteen) strains were genetically and molecularly analyzed for their VP1 gene. All of the strains kept with the same cv or vv classification except one sample, Br/03/DR. This sample was classified as vv by its VP2 gene, but it was most closely related to the cv strains by its VP1 partial sequence and phylogeny. Studies on the phylogeny of VP1 have suggested a possible reassortment event that originated the vvVP1. In this case, the sample carrying vvVP2 and cvVP1 could be a descendant of IBDV ancestors prior to the reassortment of vvVP1; alternatively, it could be the result of a genetic exchange between the segments of different strains or with a live attenuated vaccine. Nevertheless, this is the first report of natural genetic reassortment of IBDV in Brazil.