Species-specific antagonism of host ISGylation by the influenza B virus NS1 protein.
J Virol
; 84(10): 5423-30, 2010 May.
Article
en En
| MEDLINE
| ID: mdl-20219937
ABSTRACT
Interferon-stimulated expression and conjugation of the ubiquitin-like modifier ISG15 restricts replication of several viruses. Here, we established complete E1-activating, E2-conjugating, and E3 ligase-dependent expression systems for assaying both human and mouse ISGylation. We confirm that human HerC5, but not human HerC6, has ISG15 E3 ligase activity and identify mouse HerC6 as a bona fide ISG15 E3 ligase. Furthermore, we demonstrate that influenza B virus NS1 protein potently antagonizes human but not mouse ISGylation, a property dependent on B/NS1 binding the N-terminal domain of human but not mouse ISG15. Using chimeric human/mouse ISG15 constructs, we show that the B/NS1ISG15 interaction is both necessary and sufficient to inhibit ISGylation regardless of the ligation machinery used. Inability to block ISGylation in certain species may contribute to limiting influenza B virus host range.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Virus de la Influenza B
/
Ubiquitinas
/
Citocinas
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Proteínas no Estructurales Virales
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Factores de Virulencia
Tipo de estudio:
Prognostic_studies
Límite:
Animals
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Humans
Idioma:
En
Revista:
J Virol
Año:
2010
Tipo del documento:
Article
País de afiliación:
Estados Unidos