|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
This study was conducted to determine whether polymorphisms near or in interferon-lambda (IFN-λs) genes and their receptor genes such as interleukin 28 receptor, alpha (IL28RA) and interleukin 10 receptor, beta (IL10RB) as well as p21-activated kinases 4 (PAK4) and iron/zinc purple acid phosphatase-like protein (PAPL), which are locate upstream of IFN-λs, and lastly the DEPDC5 gene are associated with hepatitis B virus-related liver disease in Han Chinese.
|
25032264 |
2014 |
|
Hepatitis B
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
A total of 39 single nucleotide polymorphism loci in 23 genes of the TLR-IFN pathway and four HLA polymorphism loci associated with chronic HBV infection identified by GWAS were selected for genotyping.
|
25469587 |
2015 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
Impaired expression and function of TLR8 in chronic HBV infection and its association with treatment responses during peg-IFN-α-2a antiviral therapy.
|
28236535 |
2017 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
The aim of this study was to assess the influence of hepatitis B virus (HBV) genotypes on serum hepatitis B surface antigen (HBsAg) kinetics in hepatitis B e antigen (HBeAg)-negative patients treated with pegylated interferon-alpha2a (PEG-IFN-alpha2a).
|
20032548 |
2009 |
|
Hepatitis B
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In vitro IFN-λ1 treatment of Hep3B and Huh7 human hepatoma cell lines increased MHC class I expression, activated JAK-STAT signaling pathways, induced IFN-stimulated gene expression, and inhibited hepatitis B surface antigen (HBsAg) expression.
|
24769671 |
2014 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
The aim of the study is to investigate whether SNPs in JAK1 were associated with outcomes of HBV infection and response to IFNα therapy.
|
22901011 |
2012 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
The main advantages of IFN-α over nucleoside analogues are the absence of resistance and the possibility of immune-mediated clearance of hepatitis B.
|
23286858 |
2013 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
Extended treatment with PEG IFNα-2a with lamivudine or adefovir for 96 weeks is a promising strategy to achieve high rates of sustainable HBeAg and HBsAg seroconversion and HBV DNA suppression in patients with HBeAg-positive CHB.
|
23615131 |
2013 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
By multifactor dimensionality reduction analysis, we found the interaction between IFNA5 (-2529) and IFNA1 (-1823) genes that gave the risk to chronic HBV infection, with the OR (95% CI) of the high-risk to low-risk group was 2.79 (1.77-4.40), P < 0.0001.
|
23566196 |
2013 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
In conclusion, a 24-month course of treatment with 6 MU IFN-alpha2b was well tolerated by most patients, led to sustained suppression of HBV in one third, and attenuated hepatitis in 81% of patients.
|
9398007 |
1997 |
|
Hepatitis B
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
We confirmed in two independent studies that the combination of HBsAg and HBV DNA levels at week 12 identifies HBeAg-negative patients with a very low chance of SR to either 48 or 96 weeks of PEG-IFN therapy.
|
22245886 |
2012 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
A total of 210 patients with chronic hepatitis C genotype 1 of high viral load (baseline serum hepatitis C virus RNA > 5.0 log10 IU/mL) were divided into two groups by type of treatment: triple therapy with telaprevir, pegylated-interferon-α (PEG-IFNα), and ribavirin (RBV) for 24 wk (n = 88), or dual therapy with PEG-IFNα and RBV for 48 wk (n = 122).
|
25914481 |
2015 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
Type I IFN (IFN-I) therapy is an important therapeutic option for HBV patients.
|
30150992 |
2018 |
|
Hepatitis B
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
For HBeAg-positive patients and HBeAg-negative patients with genotype D infection, PEG-IFN therapy could be terminated early at week 12 or 24 in primary non-responders defined by the Hepatitis B surface antigen stopping rules.
|
24738850 |
2014 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our study was intended to evaluate HBV expression in liver biopsies taken an average of two years after completion of IFN-a therapy in 10 children with serological markers of persistent HBV infection.
|
11782686 |
2002 |
|
Hepatitis B
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Vitamin D serum levels and receptor genetic polymorphisms are associated with hepatitis B virus and HIV infections and IFN-λ levels.
|
29493287 |
2017 |
|
Hepatitis B
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Knockdown of FN expression significantly inhibited HBV DNA replication and protein synthesis through activating endogenous IFN-α production.
|
27023403 |
2016 |
|
Hepatitis B
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Since hepatitis B virus (HBV) genotype is an important predictor of response to PEG-IFN, determination of HBV genotype is essential in patients in whom sustained off-treatment response is pursued.
|
19187869 |
2008 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
To explore the predictive role of serum quantitative HBsAg in predicting treatment response towards IFNα-1b in hepatitis B e antigen-positive chronic hepatitis B patients.
|
23411867 |
2013 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
We investigated whether HBV infection reduced IFN-α-mediated induction of antiviral defense mechanisms in human hepatocytes.
|
21376046 |
2011 |
|
Hepatitis B
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
These IFN-alphas have an activity profile that may result in an improved therapeutic index and, consequently, better clinical efficacy for the treatment of chronic viral diseases such as hepatitis B virus, human papilloma virus, HIV, or chronic hepatitis C.
|
17494769 |
2007 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
Intrahepatic mRNA levels of type-I interferon (IFN) receptor genes have been shown to correlate with the clinical efficacy of IFN therapy in patients with chronic hepatitis C. Recently, co-infection by serologically-silent hepatitis B virus (HBV) has been assumed to be associated with the poor IFN response in patients with chronic hepatitis C. The aim of this study was to investigate the relationship between the co-infection of serologically-silent HBV and type-I IFN receptor gene expression in the liver of patients with chronic hepatitis C. The intrahepatic mRNA levels of IFNAR2, one of the two subunits of the type-I IFN receptor, were quantified and compared with both the prevalence of HBV DNA and the hepatitis C virus (HCV) genotype in 45 patients with chronic hepatitis C, who were negative for hepatitis B surface antigen.
|
11170061 |
2001 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
Conclusion: These findings highlight a host gene, UBE2L3, contributing to the susceptibility to persistent HBV infection; UBE2L3 may be involved in IFN-mediated viral suppression and serve as a potential target in the prevention and treatment of HBV infection.
|
30614547 |
2019 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
The use of IFNs for the treatment of viral infectious diseases on their antiviral activity may become an important therapeutic option, for example, IFN-α is well known for the successful treatment of hepatitis B and C virus infections, and interest is increasing in the antiviral efficacy of other novel IFN classes and their potential applications.
|
30537741 |
2018 |
|
Hepatitis B
|
0.400 |
Biomarker
|
disease |
BEFREE |
In lamivudine-naive patients, abatement of HBV DNA<10(3) copies/ml by pretreatment with PEG-IFN-alpha2a completely prevents the emergence of YMDD mutants after 24 months of lamivudine monotherapy.
|
20032538 |
2009 |