|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
Taken together, these data reveal that the NS4A Y16 residue regulates a noncanonical Riplet-TBK1-IRF3-dependent, but RIG-I-MAVS-independent, signaling pathway that limits HCV infection.<b>IMPORTANCE</b> The HCV NS3-NS4A protease complex facilitates viral replication by cleaving and inactivating the antiviral innate immune signaling proteins MAVS and Riplet, which are essential for RIG-I activation.
|
31534039 |
2019 |
|
Hepatitis C
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The current study genotyped two selected SNPs (IFIH1 rs3747517 and DDX58 rs9695310) using TaqMan allelic discrimination assay to assess their association with the susceptibility and clinical outcome of HCV infection among 3065 participants (1545 non-HCV infection individuals, 568 spontaneous HCV clearance cases, and 952 persistent infection patients).
|
30633820 |
2019 |
|
Hepatitis C
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Induction of Selenoprotein P mRNA during Hepatitis C Virus Infection Inhibits RIG-I-Mediated Antiviral Immunity.
|
30974086 |
2019 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
Although RIG-I has been recognized as the leading cytoplasmic sensor against HCV for a long time, recent findings that MDA5 regulates the IFN response to HCV have emerged.
|
29899107 |
2018 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
RIG-I is an innate immune receptor that detects and responds to infection by deadly RNA viruses such as influenza, and Hepatitis C. In the cytoplasm, RIG-I is faced with a difficult challenge: it must sensitively detect viral RNA while ignoring the abundance of host RNA.
|
28180316 |
2017 |
|
Hepatitis C
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In fact, activation of pathogen sensors induces the expression of CSR32/EGOT RIG-I and the RNA-activated kinase PKR sense HCV RNA, activate NF-κB and upregulate EGOT EGOT is increased in the liver of patients infected with HCV and after infection with influenza or Semliki Forest virus (SFV).
|
27283940 |
2016 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
Unexpectedly, the interaction between HCV's 3'UTR and RIG-I seemed to play a minor role in this activation, while another helicase MDA5 played a more important role in sensing HCV infection to trigger interferon response.
|
25463548 |
2015 |
|
Hepatitis C
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Our study reveals an important role of NS5A D2 for suppression of the IFN response that is activated by HCV via RIG-I and MDA5 in a sequential manner.
|
25908268 |
2015 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
Pathogen-Associated Molecular Pattern Recognition of Hepatitis C Virus Transmitted/Founder Variants by RIG-I Is Dependent on U-Core Length.
|
26311867 |
2015 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our results indicate that HCV RNA activates the NLRP3 inflammasome in a ROS-dependent manner, and RIG-I is not required for this process.
|
24400125 |
2014 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
The data indicate that sensing of HCV infection by RIG-I and TLR3 leads to direct recruitment of NF-κB and IRF3 to the CXCL10 promoter.
|
24257594 |
2014 |
|
Hepatitis C
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Second, we demonstrated that type III IFN induced RIG-I but not TLR3 expression in CD8(+) DCs and augmented type III IFN production in response to cytoplasmic HCV RNA.
|
24532585 |
2014 |
|
Hepatitis C
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, the HCV RNA polymerase was able to induce transcription from the IL28B promoter in a RIG-I-dependent manner.
|
24116050 |
2013 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
HuH7 human hepatoma cells expressing both TLR3 and RIG-I produced maximal CXCL10 during early HCV infection.
|
23770038 |
2013 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
HCV-encoded NS3/4A protease plays an important role in HCV immune evasion by cleaving key adapter proteins VISA and TRIF of the RIG-I-like receptors and Toll-like receptors mediated interferon (IFN) induction pathways.
|
23137809 |
2013 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
Alanine substitution of individual hydrophobic amino acids in the NS3 helix α(0) impaired HCV RNA replication in cells with a functional RIG-I pathway, but viral RNA replication was rescued in cells lacking RIG-I signaling.
|
22238314 |
2012 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
In addition, we observed much less induction in the interferon stimulated gene 15 (ISG15) after Sendai virus (SenV) stimulation of CD19-positive cells from infected patients versus healthy controls, thereby suggesting an impairment of RIG-I downstream signaling in HCV-infected patients.
|
20034464 |
2010 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
CTD_human |
Increased susceptibility of Huh7 cells to HCV replication does not require mutations in RIG-I.
|
20170495 |
2010 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
This review describes the virus and host processes that regulate the RIG-I pathway during HCV infection.
|
19708811 |
2009 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
By specially cleaving VISA with hepatitis C virus (HCV) non-structural (NS)3/4A, the RIG-I pathway was blocked, with subsequent simultaneous inhibition of CD437-induced NF-kappaB activation and cell apoptosis in A375 cells.
|
18936944 |
2009 |
|
Hepatitis C
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Our results show that IFN-alpha, TLR3, TLR7 and RIG-I mRNA levels are significantly down-regulated in patients with chronic HCV infection when compared with healthy controls.
|
18021446 |
2007 |