Mechanism of inhibiting type I interferon induction by hepatitis B virus X protein
Protein & Cell
;
(12): 1106-1117, 2010.
Article
in English
| WPRIM
| ID: wpr-757676
ABSTRACT
Hepatitis B virus (HBV) is regarded as a stealth virus, invading and replicating efficiently in human liver undetected by host innate antiviral immunity. Here, we show that type I interferon (IFN) induction but not its downstream signaling is blocked by HBV replication in HepG2.2.15 cells. This effect may be partially due to HBV X protein (HBx), which impairs IFNβ promoter activation by both Sendai virus (SeV) and components implicated in signaling by viral sensors. As a deubiquitinating enzyme (DUB), HBx cleaves Lys63-linked polyubiquitin chains from many proteins except TANK-binding kinase 1 (TBK1). It binds and deconjugates retinoic acid-inducible gene I (RIG I) and TNF receptor-associated factor 3 (TRAF3), causing their dissociation from the downstream adaptor CARDIF or TBK1 kinase. In addition to RIG I and TRAF3, HBx also interacts with CARDIF, TRIF, NEMO, TBK1, inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase epsilon (IKKi) and interferon regulatory factor 3 (IRF3). Our data indicate that multiple points of signaling pathways can be targeted by HBx to negatively regulate production of type I IFN.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Protein Binding
/
B-Lymphocytes
/
Signal Transduction
/
Interferon Type I
/
Trans-Activators
/
Cell Line
/
Hepatitis B virus
/
Sendai virus
/
Polyubiquitin
/
TNF Receptor-Associated Factor 3
Limits:
Animals
/
Humans
Language:
English
Journal:
Protein & Cell
Year:
2010
Type:
Article
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