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MP4: you may be interested in the following paper. It supports your idea that HBx interferes with the immune system (I still maintain the immune system is not damaged]
J Virol. 2010 Nov 10. [Epub ahead of print]
Hepatitis B virus regulatory HBx protein binds to adaptor protein IPS-1
and inhibits the activation of interferon-{beta}
Kumar M, Jung SY, Hodgson AJ, Madden CR, Qin J, Slagle BL.
Baylor College of Medicine, Houston, TX 77030; Departments of Molecular
Virology and Microbiology and Verna and Marrs McLean Department of
Biochemistry and Molecular Biology.
Abstract
The hepatitis B virus encodes the regulatory HBx protein that is required
for virus replication, although its specific role(s) in the replication
cycle remains under investigation. An immunoprecipitation/mass
spectrometry approach was used to identify four novel HBx binding proteins
from the cytoplasmic fraction of HBx transgenic mouse livers. One of these
HBx binding partners is interferon-β promoter stimulator 1 (IPS-1), an
adaptor protein that plays a critical role in mediating retinoic
acid-inducible gene I (RIG-I) signaling that leads to the activation of
interferon-β (IFN-β). The HBx-IPS-1 protein interaction was confirmed in
plasmid-transfected HepG2 cells by reciprocal co-immunoprecipitation and
Western Blot. We hypothesized that HBx might alter IPS-1 function since
proteins of the hepatitis C virus and hepatitis A virus similarly bind
IPS-1 and target it for inactivation. The effect of HBx on IPS-1-mediated
IFN-β signaling was tested in transfected 293T and HepG2 cells, and we
show that HBx inhibits dsDNA-mediated IFN-β activation in a
dose-dependent manner when expressed either alone or within the context of
HBV replication. However, HBx does not inhibit poly(I:C)-activated IFN-β
signaling. These results demonstrate that HBx interferes with the RIG-I
pathway of innate immunity. Hepatitis B virus now joins hepatitis C virus
and hepatitis A virus in targeting the same innate immune response
pathway, presumably as a shared strategy to benefit replication of these
viruses in the liver.
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