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











Base de dados
Intervalo de ano de publicação
1.
PLoS One ; 12(12): e0189073, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29216247

RESUMO

Vesicular stomatitis virus (VSV) release from infected cells is inhibited by the interferon (IFN)-inducible antiviral host cell factor tetherin (BST-2, CD317). However, several viruses encode tetherin antagonists and it is at present unknown whether residual VSV spread in tetherin-positive cells is also promoted by a virus-encoded tetherin antagonist. Here, we show that the viral glycoprotein (VSV-G) antagonizes tetherin in transfected cells, although with reduced efficiency as compared to the HIV-1 Vpu protein. Tetherin antagonism did not involve alteration of tetherin expression and was partially dependent on a GXXXG motif in the transmembrane domain of VSV-G. However, mutation of the GXXXG motif did not modulate tetherin sensitivity of infectious VSV. These results identify VSV-G as a tetherin antagonist in transfected cells but fail to provide evidence for a contribution of tetherin antagonism to viral spread.


Assuntos
Antígeno 2 do Estroma da Médula Óssea/metabolismo , Vesiculovirus/metabolismo , Proteínas Virais/fisiologia , Vírion/fisiologia , Animais , Antígeno 2 do Estroma da Médula Óssea/imunologia , Linhagem Celular , Proteínas de Ligação ao GTP/imunologia , Humanos , Suínos
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA