Drug abuse, innate immunity and hepatitis C virus

2006 ◽  
Vol 16 (5) ◽  
pp. 311-327 ◽  
Author(s):  
Ting Zhang ◽  
Yuan Li ◽  
Wen-Zhe Ho
Keyword(s):  
Innate Immunity ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Drug Abuse

scholarly journals Innate immunity and hepatitis C virus infection: a microarray's view

2012 ◽  
Vol 7 (1) ◽  
Author(s):  
Luigi Buonaguro ◽  
Annacarmen Petrizzo ◽  
Maria Lina Tornesello ◽  
Franco M Buonaguro
Keyword(s):  
Innate Immunity ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Hepatitis C Virus Infection

scholarly journals Insights into antiviral innate immunity revealed by studying hepatitis C virus

Cytokine ◽  
2015 ◽  
Vol 74 (2) ◽  
pp. 190-197 ◽  
Author(s):  
Stacy M. Horner
Keyword(s):  
Innate Immunity ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Antiviral Innate Immunity

Innate immunity and hepatitis C virus: eluding the host cell defense

10.2741/3579 ◽  
2009 ◽  
Vol 14 (1) ◽  
pp. 4950 ◽  
Author(s):  
Deborah, R. Taylor
Keyword(s):  
Innate Immunity ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Host Cell ◽  
Cell Defense

HIV/hepatitis C virus co-infection: basic, behavioral and clinical research in mental health and drug abuse

AIDS ◽  
2005 ◽  
Vol 19 (Suppl 3) ◽  
pp. S3-S7 ◽  
Author(s):  
Jeymohan Joseph ◽  
David M Stoff ◽  
Charles van der Horst
Keyword(s):  
Mental Health ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Drug Abuse ◽  
Clinical Research

scholarly journals Hepatitis C treatment uptake and response among human immunodeficiency virus/hepatitis C virus-coinfected patients in a large integrated healthcare system

2019 ◽  
Vol 30 (7) ◽  
pp. 689-695 ◽  
Author(s):  
Jennifer O Lam ◽  
Leo B Hurley ◽  
Scott Chamberland ◽  
Jamila H Champsi ◽  
Laura C Gittleman ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Drug Abuse ◽  
Cell Count ◽  
Hcv Treatment ◽  
Cd4 Cell Count ◽  
Treatment Uptake ◽  
Immunodeficiency Virus ◽  
Cd4 Cell

U.S. guidelines recommend that patients coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) be prioritized for HCV treatment with direct-acting antiviral agents (DAAs), but the high cost of DAAs may contribute to disparities in treatment uptake and outcomes. We evaluated DAA initiation and effectiveness in HIV/HCV-coinfected patients in a U.S.-based healthcare system during October 2014–December 2017. Of 462 HIV/HCV-coinfected patients, 276 initiated DAAs (70% cumulative proportion treated over three years). Lower likelihood of DAA initiation was observed among patients with Medicare (government-sponsored insurance) versus commercial insurance (adjusted rate ratio [aRR] = 0.62, 95% CI = 0.46–0.84), patients with drug abuse diagnoses (aRR = 0.72, 95% CI = 0.54–0.97), patients with CD4 cell count <200 cells/µl versus ≥500 (aRR = 0.45, 95% CI = 0.23–0.91), and patients without prior HCV treatment (aRR = 0.68, 95% CI = 0.48–0.97). There were no significant differences in DAA initiation by age, gender, race/ethnicity, socioeconomic status, HIV transmission risk, alcohol use, smoking, fibrosis level, HIV RNA levels, antiretroviral therapy use, hepatitis B infection, or number of outpatient visits. Ninety-five percent of patients achieved sustained virologic response (SVR). We found little evidence of sociodemographic disparities in DAA initiation among HIV/HCV-coinfected patients, and SVR rates were high. Efforts are needed to increase DAA uptake among coinfected Medicare enrollees, patients with drug abuse diagnoses, patients with low CD4 cell count, and patients receiving first-time HCV treatment.

scholarly journals Innate Immune Response against Hepatitis C Virus: Targets for Vaccine Adjuvants

Vaccines ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 313
Author(s):  
Daniel Sepulveda-Crespo ◽  
Salvador Resino ◽  
Isidoro Martinez
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Innate Immune Response ◽  
Vaccine Development ◽  
Innate Immune ◽  
World Health ◽  
Cell Immune Response ◽  
Vaccine Adjuvants

Despite successful treatments, hepatitis C virus (HCV) infections continue to be a significant world health problem. High treatment costs, the high number of undiagnosed individuals, and the difficulty to access to treatment, particularly in marginalized susceptible populations, make it improbable to achieve the global control of the virus in the absence of an effective preventive vaccine. Current vaccine development is mostly focused on weakly immunogenic subunits, such as surface glycoproteins or non-structural proteins, in the case of HCV. Adjuvants are critical components of vaccine formulations that increase immunogenic performance. As we learn more information about how adjuvants work, it is becoming clear that proper stimulation of innate immunity is crucial to achieving a successful immunization. Several hepatic cell types participate in the early innate immune response and the subsequent inflammation and activation of the adaptive response, principally hepatocytes, and antigen-presenting cells (Kupffer cells, and dendritic cells). Innate pattern recognition receptors on these cells, mainly toll-like receptors, are targets for new promising adjuvants. Moreover, complex adjuvants that stimulate different components of the innate immunity are showing encouraging results and are being incorporated in current vaccines. Recent studies on HCV-vaccine adjuvants have shown that the induction of a strong T- and B-cell immune response might be enhanced by choosing the right adjuvant.

scholarly journals ISG12a Restricts Hepatitis C Virus Infection through the Ubiquitination-Dependent Degradation Pathway

2016 ◽  
Vol 90 (15) ◽  
pp. 6832-6845 ◽  
Author(s):  
Binbin Xue ◽  
Darong Yang ◽  
Jingjing Wang ◽  
Yan Xu ◽  
Xiaohong Wang ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Viral Infection ◽  
Viral Protein ◽  
E3 Ligase ◽  
Antiviral Effect ◽  
Degradation Pathway ◽  
Viral Spread ◽  
Ubiquitin E3 Ligase

ABSTRACTInterferons (IFNs) restrict various kinds of viral infection via induction of hundreds of IFN-stimulated genes (ISGs), while the functions of the majority of ISGs are broadly unclear. Here, we show that a high-IFN-inducible gene, ISG12a (also known as IFI27), exhibits a nonapoptotic antiviral effect on hepatitis C virus (HCV) infection. Viral NS5A protein is targeted specifically by ISG12a, which mediates NS5A degradation via a ubiquitination-dependent proteasomal pathway. K374R mutation in NS5A domain III abrogates ISG12a-induced ubiquitination and degradation of NS5A. S-phase kinase-associated protein 2 (SKP2) is identified as an ubiquitin E3 ligase for NS5A. ISG12a functions as a crucial adaptor that promotes SKP2 to interact with and degrade viral protein. Moreover, the antiviral effect of ISG12a is dependent on the E3 ligase activity of SKP2. These findings uncover an intriguing mechanism by which ISG12a restricts viral infection and provide clues for understanding the actions of innate immunity.IMPORTANCEUpon virus invasion, IFNs induce numerous ISGs to control viral spread, while the functions of the majority of ISGs are broadly unclear. The present study shows a novel antiviral mechanism of ISGs and elucidated that ISG12a recruits an E3 ligase, SKP2, for ubiquitination and degradation of viral protein and restricts viral infection. These findings provide important insights into exploring the working principles of innate immunity.

PS1-125 A robust induction of type III interferons and chemokines defines a unique pattern of hepatic innate immunity in response to hepatitis C virus infection

Cytokine ◽  
2011 ◽  
Vol 56 (1) ◽  
pp. 49 ◽  
Author(s):  
Emmanuel Thomas ◽  
Veronica D. Gonzalez ◽  
Qisheng Li ◽  
Ankit A. Modi ◽  
Lorenzo Uccellini ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Hepatitis C Virus Infection ◽  
Unique Pattern ◽  
Type Iii ◽  
Hepatic Innate Immunity
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