IFITM1 is a tight junction protein that inhibits hepatitis C virus entry.
Hepatology
; 57(2): 461-9, 2013 Feb.
Article
en En
| MEDLINE
| ID: mdl-22996292
ABSTRACT
UNLABELLED Type 1 interferon (IFN) continues to be the foundation for the current standard of care combination therapy for chronic hepatitis C virus (HCV) infection, yet the component interferon-stimulated genes (ISGs) that mediate the antiviral actions of IFN are not fully defined. Interferon-induced transmembrane protein 1 (IFITM1) is an ISG product that suppresses early stage infection by a number of viruses through an unknown mechanism of action. Moreover, the actions of IFITM1 on HCV infection are not fully elucidated. Here we identify IFITM1 as a hepatocyte tight junction protein and a potent anti-HCV effector molecule. IFITM1 expression is induced early during IFN treatment of hepatocytes and accumulates at hepatic tight junctions in HCV-infected human patient liver during IFN therapy. Additionally, we found that IFITM1 interacts with HCV coreceptors, including CD81 and occludin, to disrupt the process of viral entry. Thus, IFITM1 is an anti-HCV ISG whose actions impart control of HCV infection through interruption of viral coreceptor function. CONCLUSION:
This study defines IFITM1 as an ISG effector with action against HCV entry. Design of therapy regimens to enhance IFITM1 expression should improve the virologic response among HCV patients undergoing treatment with type I IFN.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Antivirales
/
Receptores Virales
/
Antígenos de Diferenciación
/
Interferón Tipo I
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Hepatitis C
/
Proteínas de Uniones Estrechas
Tipo de estudio:
Prognostic_studies
Límite:
Humans
Idioma:
En
Revista:
Hepatology
Año:
2013
Tipo del documento:
Article
País de afiliación:
Estados Unidos