Taken together, the results demonstrated that CA could modulate Keap1/Nrf2 interaction via increasing p62 expression, leading to stabilization of Nrf2 and HO-1 induction, and elicit IFNα antiviral response to suppress HCV replication.
After adjustment, HCV+ kidneys were 3.7 times more likely to be discarded than HCV- kidneys in the DAA era (adjusted relative rate, 3.363.674.02; P < 0.001); an increase from the IFN era (adjusted relative rate, 2.783.023.27; P < 0.001).
This study aimed to evaluate the real-world cost-effectiveness of IFN-based therapy according to the current strategies with PegIFN/RBV for "easy-to-treat" to provide a reference for application of future DAA development for IFN-eligible, treatment naïve HCV patients.
Our results suggest that HCV G3a along with immune responses such as cytokines in HCV patients should be taken into account when interpreting clinical data and IFN-based therapeutic response.
Vitamin D supplementation in combination with Peg-IFN-α injection and oral RBV significantly increased the rate of viral response for hepatitis C at 24 weeks after treatment in a random-effects meta-analysis (relative risk = 1.30; 95% confidence interval = 1.04-1.62; I<sup>2</sup> = 75.9%).
The inclusion criteria for patients were as follows: (1) treatment-naive and treated with PEG IFN-α/RBV, (2) HCV RNA was present in serum for over 6 months before treatment, (3) negative for hepatitis B (HBV) or HIV infection and (4) lacked any other hepatic diseases.All participants in this study were Chinese Han population and infected with HCV genotype 1b and treated with subcutaneous PEG IFN-α at a dose of 180 µg once a week with the addition of 800-1000 mg/d RBV according to weight orally for 48 weeks.
In chronic hepatitis C virus (HCV) infections, where the IFNL variants were first identified to be associated with response to interferon-α-ribavirin therapy, the available data clearly suggests that the causal variant could be the dinucleotide polymorphism rs368234815 that causes an open reading frame-shift in the IFNL4 gene resulting in expression of a functional IFN-λ4, a new type III IFN.
Neutropenia is a haematologic disorder commonly reported in patients with chronic hepatitis C virus (HCV) infection treated with pegylated interferon alfa-2a (PEG-IFN α-2a).
In summary, intrahepatic expression of IFNL4 was associated with increased antiviral ISG expression and decreased suppressive ISG expression at baseline, resulting in poor responsiveness to IFNα-based therapy in HCV infection.
Therefore, IFN-free anti-HCV treatment appears to be safe and effective in MC patients from virological and clinical points of view, thus supporting the importance of HCV eradication in leading MC remission.
Deep-sequencing analyses revealed that in five of seven patients treated by IFN-α for a concomitant HCV infection in the absence of antiretroviral drugs, the dominant Vpu sequences differed before and during treatment.
We retrospectively reviewed records of treatment-naïve adult patients with ESRD and chronic HCV infection who had been treated with Peg-IFN and low-dose ribavirin using a RGT approach.
We demonstrate that the supernatant from IFN-<i>α</i>-treated cultured cells restricted HBV and HCV infection by inhibiting viral entry into hepatoma cells.
Importantly, the expression of CD100 on NK cells from HCV patients was inversely associated with the HCV-RNA levels in the early phase of IFN-α therapy, and the IFN-α upregulated CD100 led to an enhanced NK killing activity through ligations with its receptors plexin-B1/B2 on target cells.
Despite new treatments for hepatitis C virus (HCV) infection, IFNα-based regimens still have clinical relevance in special populations of patients and remain the only therapeutic option for many patients.
We investigated whether the hepatitis C virus (HCV) coinfection contributes to such alterations by impairing the plasmacytoid dendritic cell (pDC) IFNα/TLR7 pathway in a highly homogeneous group of ART-treated HIV-1-HCV-coinfected patients.
Our findings indicated that MxA over-expression inhibited HCV replication and potentiated the IFNα-mediated anti-HCV activity; MxA stimulated the production of IFNα, IFNβ, and enhanced IFNα-induced activation of Jak-STAT signaling pathway.