Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
Conclusion: Overall, our results indicate that NS5A contributes to the inhibition of innate immune pathways during HCV infection by exploiting the ability of LRPPRC to inhibit MAVS-regulated antiviral signaling.
|
30070380 |
2019 |
Hepatitis C
|
0.100 |
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 |
Virus Diseases
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Relatively weak inducible IFN-β production in HBV infected patients with IPS-1 rs7269320 SNP or wild-type may contribute to chronic virus infection.
|
30930359 |
2019 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
RNF34 binds to MAVS in the mitochondrial compartment after viral infection and negatively regulates RIG-I-like receptor (RLR)-mediated antiviral immunity.
|
31304625 |
2019 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
GoMAVS inhibited Newcastle disease virus replication by activating type I IFN pathways, especially at the early stages of infection.
|
30557581 |
2019 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
Their active forms activate mitochondrial antiviral signaling protein (MAVS) and trigger downstream immune responses against viral infection.
|
30569868 |
2019 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
NAC1 was able to interact with MAVS and TBK1 upon viral infection.
|
31235549 |
2019 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
Induction of OTUD4 by viral infection promotes antiviral responses through deubiquitinating and stabilizing MAVS.
|
30410068 |
2019 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we show that NLK inhibits the antiviral immune response during viral infection by targeting MAVS for degradation.
|
31324787 |
2019 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
Viral infection causes the aggregation of VISA, which is important for its recruitment of downstream signaling components.
|
31511639 |
2019 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
YOD1 was recruited to mitochondria to interact with MAVS through its UBX and Znf domains after viral infection.
|
30952814 |
2019 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
The interaction of FKBP8 with VISA, retinoic acid inducible protein 1 (RIG-I), and IFN regulatory factor 3 (IRF3) was confirmed during viral infection in mammalian cells by coimmunoprecipitation.
|
30267576 |
2019 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
In this study, we found that Newcastle disease virus (NDV) infection induced MAVS degradation.
|
31270229 |
2019 |
MRSA - Methicillin resistant Staphylococcus aureus infection
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In addition, agar dilution (MTT) helps to investigate outbreaks of methicillin-resistant Staphylococcus aureus (MRSA), VISA or VRSA.
|
31206950 |
2019 |
MRSA - Methicillin resistant Staphylococcus aureus infection
|
0.100 |
Biomarker
|
disease |
BEFREE |
The identification of a high percentage of MRSA and presence of VRSA and VISA isolates is a serious warning about the treatment of future MRSA infections and reveals the need for new and effective therapeutic agents.
|
30811005 |
2019 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
FAF1 Regulates Antiviral Immunity by Inhibiting MAVS but Is Antagonized by Phosphorylation upon Viral Infection.
|
30472208 |
2018 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we describe a novel method of visualizing and quantifying the aggregation of MAVS in response to dsRNA stimulation or viral infection in vitro using confocal microscopy.
|
29177867 |
2018 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
The collective results of this study suggest a novel regulation mechanism of MAVS-mediated immunity during RNA viral infection by miR-3570.
|
29093090 |
2018 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
The mitochondrial adaptor molecule MAVS plays a critical role in innate immune response to viral infection.
|
29743353 |
2018 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
MAVS forms prion-like aggregates on the mitochondria after virus infection.
|
29245018 |
2018 |
Virus Diseases
|
0.100 |
Biomarker
|
group |
BEFREE |
Taken together, these results suggest that ASC, as a negative regulator of the MAVS-mediated innate immunity, may play an important role in host protection upon virus infection.
|
29280086 |
2018 |
MRSA - Methicillin resistant Staphylococcus aureus infection
|
0.100 |
Biomarker
|
disease |
BEFREE |
Both compounds were active against clinical isolates of methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-intermediate and vancomycin-resistant S. aureus (VISA and VRSA respectively) and vancomycin-resistant Enterococcus faecalis (VRE).
|
29957525 |
2018 |
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
Detailed studies revealed that HCV infection activates MAVS that in turn recruits TRAF6 via TRAF-interacting-motifs (TIMs), and TRAF6 subsequently directly recruits GP73 to MAVS via coiled-coil domain.
|
28394926 |
2017 |
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
The activity of asunaprevir-regulated innate immunity signal pathway was assessed with IFN-β promoter or IFN-stimulated responsive element (ISRE) reporter assays and immunoblotting of key signal proteins. siRNA-mediated MAVS and TRIF knockdown of cells was performed to assess the effect of asunaprevir-regulated innate immunity against HCV and DENV.
|
28473813 |
2017 |
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The down regulation of TRIF, TLR3, and MAVS expressions in CHC correlates with the disease severity and the outcome of HCV infection.
|
28480979 |
2017 |