Blockade of interferon Beta, but not interferon alpha, signaling controls persistent viral infection.
Cell Host Microbe
; 17(5): 653-61, 2015 May 13.
Article
en En
| MEDLINE
| ID: mdl-25974304
ABSTRACT
Although type I interferon (IFN-I) is thought to be beneficial against microbial infections, persistent viral infections are characterized by high interferon signatures suggesting that IFN-I signaling may promote disease pathogenesis. During persistent lymphocytic choriomeningitis virus (LCMV) infection, IFNα and IFNß are highly induced early after infection, and blocking IFN-I receptor (IFNAR) signaling promotes virus clearance. We assessed the specific roles of IFNß versus IFNα in controlling LCMV infection. While blockade of IFNß alone does not alter early viral dissemination, it is important in determining lymphoid structure, lymphocyte migration, and anti-viral T cell responses that lead to accelerated virus clearance, approximating what occurs during attenuation of IFNAR signaling. Comparatively, blockade of IFNα was not associated with improved viral control, but with early dissemination of virus. Thus, despite their use of the same receptor, IFNß and IFNα have unique and distinguishable biologic functions, with IFNß being mainly responsible for promoting viral persistence.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Transducción de Señal
/
Interferón beta
/
Interferón-alfa
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Coriomeningitis Linfocítica
/
Virus de la Coriomeningitis Linfocítica
Límite:
Animals
Idioma:
En
Revista:
Cell Host Microbe
Asunto de la revista:
MICROBIOLOGIA
Año:
2015
Tipo del documento:
Article
País de afiliación:
Estados Unidos