Silencing the shutoff protein of Epstein-Barr virus in productively infected B cells points to (innate) targets for immune evasion.
J Gen Virol
; 96(Pt 4): 858-865, 2015 Apr.
Article
en En
| MEDLINE
| ID: mdl-25502648
ABSTRACT
During productive infection with Epstein-Barr virus (EBV), a dramatic suppression of cellular protein expression is caused by the viral alkaline exonuclease BGLF5. Among the proteins downregulated by BGLF5 are multiple immune components. Here, we show that shutoff reduces expression of the innate EBV-sensing Toll-like receptor-2 and the lipid antigen-presenting CD1d molecule, thereby identifying these proteins as novel targets of BGLF5. To silence BGLF5 expression in B cells undergoing productive EBV infection, we employed an shRNA approach. Viral replication still occurred in these cells, albeit with reduced late gene expression. Surface levels of a group of proteins, including immunologically relevant molecules such as CD1d and HLA class I and class II, were only partly rescued by depletion of BGLF5, suggesting that additional viral gene products interfere with their expression. Our combined approach thus provides a means to unmask novel EBV (innate) immune evasion strategies that may operate in productively infected B cells.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Proteínas Virales
/
Linfocitos B
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Herpesvirus Humano 4
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Infecciones por Virus de Epstein-Barr
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Desoxirribonucleasas
Límite:
Humans
Idioma:
En
Revista:
J Gen Virol
Año:
2015
Tipo del documento:
Article
País de afiliación:
Países Bajos