|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
We examined three key mediators of the innate immune response: NF-KB, STAT1 and STAT2 during HCV infection in order to investigate the paradoxical induction of an innate immune response by HCV despite a multitude of mechanisms combating the host response.
|
31374104 |
2019 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
MxA-mediated inhibition of HCV replication was found to involve the JAK-STAT pathway: STAT1 phosphorylation and the expression of IFN-stimulated genes (ISGs) such as guanylate-binding protein 1 and 2'-5'-oligoadenylate synthetase 1 were augmented by MxA overexpression and reduced by endogenous MxA silencing.
|
29417241 |
2018 |
|
Hepatitis C
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
While both groups did not differ in the level of liver enzymes, HIV/HCV had higher T-cell activation/exhaustion, and constitutive STAT-1 phosphorylation compared to HCV.
|
28419653 |
2017 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
This was probably via inhibition of the STAT1 and STAT3 signaling pathways, which could suppress subsequent liver damage due to chronic hepatitis C. The current data suggested that IL-35 contributes to persistent HCV infection by inhibiting antiviral immune activity.
|
28644966 |
2017 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These findings suggest that IFN-α can inhibit HCV replication through a STAT2-dependent but STAT1-independent pathway, whereas IFN-λ induces ISG expression and inhibits HCV replication exclusively through a STAT1- and STAT2-dependent pathway.
|
27929099 |
2016 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Moreover, the decreased pSTAT1 and increased pSTAT6 were observed in PBMCs by HCV core/F protein stimulation with constant STAT1/6 expression.
|
25894282 |
2015 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The upregulation of miR-373 by HCV also inhibited STAT1 phosphorylation, which is involved in ISG factor 3 (ISGF3) complex formation and ISG expression.
|
25589644 |
2015 |
|
Hepatitis C
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We propose that IFN/ribavirin bitherapy‑induced mutations in the STAT1‑interacting domain of the HCV core protein may be responsible for the improved therapeutic response and viral clearance, thus amino acids 1-23 of the N-terminus of the core protein are an ideal antiviral target.
|
23799612 |
2013 |
|
Hepatitis C
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
These findings suggest that Tim-3 plays a crucial role in negative regulation of innate immune responses, through crosstalk with PD-1 and SOCS-1 and limiting STAT-1 phosphorylation, and may be a novel target for immunotherapy to HCV infection.
|
21637332 |
2011 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
Concomitant assessment of lower STAT1 nuclear-stain of hepatocytes and IL28B polymorphism is useful for prediction of SVR in HCV genotype 1 patients.
|
22174846 |
2011 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
Additionally, T cells isolated from chronically HCV-infected subjects exhibited increased PD-1 and SOCS-1 expression compared to healthy subjects, and SOCS-1 expression in T cells isolated from HCV-infected subjects was also inhibited by blocking PD-1 signaling; this in turn enhanced the phosphorylation of STAT-1, and improved the impaired T-cell proliferation observed in the setting of HCV infection.
|
20883163 |
2010 |
|
Hepatitis C
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In conclusion, our data show that genetic variants in the IRF-1 and Stat1 genes of the IFN pathway are associated with MS and HCV infection.
|
18338947 |
2008 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
P-STAT1 in the liver tissue prior to IFN therapy correlated with an increased BMI and increased insulin resistance, and might be a useful predictor of HCV clearance by IFN therapy.
|
19258717 |
2008 |
|
Hepatitis C
|
0.100 |
GeneticVariation
|
disease |
LHGDN |
In conclusion, our data show that genetic variants in the IRF-1 and Stat1 genes of the IFN pathway are associated with MS and HCV infection.
|
18338947 |
2008 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Expression and activation of STAT1 (a factor activated by both interferon (IFN)-alpha and IFN-gamma) were increased in HCV infected livers, particularly in those with high inflammatory activity.
|
16120756 |
2006 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, long-term IFN-gamma treatment inhibits IFN-alpha-activated signals most probably, at least in part, through the induction of STAT1 protein expression, which could partly contribute to IFN-alpha treatment failure in hepatitis C patients.
|
14690454 |
2004 |