A novel T cell evasion mechanism in persistent RNA virus infection.
Trans Am Clin Climatol Assoc
; 125: 14-24; discussion 24-6, 2014.
Article
en En
| MEDLINE
| ID: mdl-25125715
ABSTRACT
Hepatitis C virus (HCV) and GB virus type C (GBV-C) are associated with impaired T cell function despite the fact that HCV replicates in hepatocytes and GBV-C in a small proportion of lymphocytes. Recently, we showed that HCV and GBV-C E2-envelope proteins reduce T cell activation via the T cell receptor (TCR) by competing for phosphorylation with a critical kinase in the TCR signaling cascade (Lck). E2 interfered with TCR signaling in E2 expressing cells and in bystander cells. The bystander effect was mediated by virus particles and extracellular microvesicular particles (exosomes). Multiple kinase substrate sites are predicted to reside on viral structural proteins and based on bioinformatic predictions, many RNA virus pathogens may interfere with TCR signaling via a similar mechanism. Identification of T cell inhibitory effects of virus structural proteins may provide novel approaches to enhance the immunogenicity and memory of viral vaccines.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Activación de Linfocitos
/
Linfocitos T
/
Proteínas del Envoltorio Viral
/
Hepacivirus
/
Virus GB-C
/
Evasión Inmune
/
Hepatitis
Tipo de estudio:
Prognostic_studies
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Trans Am Clin Climatol Assoc
Año:
2014
Tipo del documento:
Article