Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Más filtros

Banco de datos
País/Región como asunto
Tipo del documento
País de afiliación
Intervalo de año de publicación
1.
Emerg Infect Dis ; 14(3): 487-90, 2008 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-18325269

RESUMEN

During the 2006-2007 winter season in South Korea, several outbreaks of highly pathogenic avian influenza virus (H5N1) were confirmed among domestic poultry and in migratory bird habitats. Phylogenetic analysis showed that all isolates were closely related and that all belong to the A/bar-headed goose/Qinghai/5/2005-like lineage rather than the A/chicken/Korea/ES/2003-like lineage.


Asunto(s)
Migración Animal , Pollos/virología , Patos/virología , Subtipo H5N1 del Virus de la Influenza A/aislamiento & purificación , Gripe Aviar/epidemiología , Codorniz/virología , Animales , Subtipo H5N1 del Virus de la Influenza A/genética , Gripe Aviar/virología , Corea (Geográfico)/epidemiología , Filogenia
2.
J Microbiol ; 53(8): 570-7, 2015 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-26224460

RESUMEN

Avian influenza A virus (AIV) is commonly isolated from domestic poultry and wild migratory birds, and the H9N2 subtype is the most prevalent and the major cause of severe disease in poultry in Korea. In addition to the veterinary concerns regarding the H9N2 subtype, it is also considered to be the next potential human pandemic strain due to its rapid evolution and interspecies transmission. In this study, we utilize serial lung-to-lung passage of a low pathogenic avian influenza virus (LPAI) H9N2 (A/Ck/Korea/163/04, WT163) (Y439-lineage) in mice to increase pathogenicity and investigate the potential virulence marker. Mouse-adapted H9N2 virus obtained high virulence (100% mortality) in mice after 98 serial passages. Sequence results show that the mouse adaptation (ma163) possesses several mutations within seven gene segments (PB2, PA, HA, NP, NA, M, and NS) relative to the wild-type strain. The HA gene showed the most mutations (at least 11) with one resulting in the loss of an N-glycosylation site (at amino acid 166). Moreover, reverse genetic studies established that an E627K substitution in PB2 and the loss of the N-glycosylation site in the HA protein (aa166) are critical virulence markers in the mouse-adapted H9N2 virus. Thus, these results add to the increasing body of mutational analysis data defining the function of the viral polymerase and HA genes and their roles in mammalian host adaptation. To our knowledge, this is first report of the generation of a mammalian-adapted Korea H9N2 virus (Y493-lineages). Therefore, this study offers valuable insights into the molecular evolution of the LPAI Korean H9N2 in a new host and adds to the current knowledge of the molecular markers associated with increased virulence.


Asunto(s)
Biomarcadores , Evolución Molecular , Genes Virales , Subtipo H9N2 del Virus de la Influenza A/patogenicidad , Infecciones por Orthomyxoviridae/virología , Animales , Subtipo H9N2 del Virus de la Influenza A/genética , Subtipo H9N2 del Virus de la Influenza A/fisiología , Pulmón/virología , Ratones , Mutación , República de Corea , Virulencia , Replicación Viral/genética
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA