Hepatitis C New Drugs Review
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Hepatitis C New Drugs Review
FDA approved Incivek(telaprevir, Vertex) on Monday 23 May by its PDUFA deadline.A paradigm shift in the treatment of Hepatitis C virus infection. http://knol.google.com/k/krishan-maggon/boceprevir-merck-telaprevir-vertex/3fy5eowy8suq3/151#
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Created public version #121 of the knol: "Boceprevir (Merck) & Telaprevir (Vertex) Hepatitis C : FDA Review & Approval"

Created public version #121 of the knol: "Boceprevir (Merck) & Telaprevir (Vertex) Hepatitis C : FDA Review & Approval" | Hepatitis C New Drugs Review | Scoop.it
Krishan Maggon published version 121 of a knol titled: "Boceprevir (Merck) & Telaprevir (Vertex) Hepatitis C : FDA Review & Approval"...
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Molecular Liver Cancer Prevention in Cirrhosis by Organ Transcriptome Analysis and Lysophosphatidic Acid Pathway Inhibition

Molecular Liver Cancer Prevention in Cirrhosis by Organ Transcriptome Analysis and Lysophosphatidic Acid Pathway Inhibition | Hepatitis C New Drugs Review | Scoop.it

Summary Cirrhosis is a milieu that develops hepatocellular carcinoma (HCC), the second most lethal cancer worldwide. HCC prediction and prevention in cirrhosis are key unmet medical needs. Here we have established an HCC risk gene signature applicable to all major HCC etiologies: hepatitis B/C, alcohol, and non-alcoholic steatohepatitis. A transcriptome meta-analysis of >500 human cirrhotics revealed global regulatory gene modules driving HCC risk and the lysophosphatidic acid pathway as a central chemoprevention target. Pharmacological inhibition of the pathway in vivo reduced tumors and reversed the gene signature, which was verified in organotypic ex vivo culture of patient-derived fibrotic liver tissues. These results demonstrate the utility of clinical organ transcriptome to enable a strategy, namely, reverse-engineering precision cancer prevention. 


 Keywords: hepatocellular carcinoma, cancer chemoprevention, transcriptome, gene signature, prognostic prediction

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Cost-effectiveness of Early Treatment of Hepatitis C Virus Genotype 1 by Stage of Liver Fibrosis in a US Treatment-Naive Population

Cost-effectiveness of Early Treatment of Hepatitis C Virus Genotype 1 by Stage of Liver Fibrosis in a US Treatment-Naive Population | Hepatitis C New Drugs Review | Scoop.it
Novel treatments for hepatitis C virus (HCV) infection are highly efficacious but costly. Thus, many insurers cover therapy only in advanced fibrosis stages. The added health benefits and costs of early treatment are unknown.To assess the cost-effectivenes
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Viral Escape Hatch Could be Treatment Target for Hepatitis E, Study Finds

Viral Escape Hatch Could be Treatment Target for Hepatitis E, Study Finds | Hepatitis C New Drugs Review | Scoop.it
The technique that the hepatitis E virus -- an emerging liver virus historically found in developing countries but now on the rise in Europe -- uses to
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Hepatitis B and C in the Spotlight. A public health response in the Americas, 2016

Hepatitis B and C in the Spotlight. A public health response in the Americas, 2016 | Hepatitis C New Drugs Review | Scoop.it
RT @pahowho: New PAHO report: #Hepatitis B and C in the Spotlight. A public health response in the Americas. https://t.co/VEfNG4kGmM https:…
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European Commission Grants Marketing Authorization for Gilead’s Vemlidy® (Tenofovir Alafenamide, TAF) for the Treatment of Chronic Hepatitis B Virus Infection | Gilead

European Commission Grants Marketing Authorization for Gilead’s Vemlidy® (Tenofovir Alafenamide, TAF) for the Treatment of Chronic Hepatitis B Virus Infection | Gilead | Hepatitis C New Drugs Review | Scoop.it

FOSTER CITY, Calif.--(BUSINESS WIRE)--Jan. 11, 2017-- Gilead Sciences, Inc. (Nasdaq: GILD) today announced that the European Commission has granted marketing authorization for Vemlidy® (tenofovir alafenamide, TAF) 25 mg, a once-daily tablet for the treatment of chronic hepatitis B virus (HBV) infection in adults and adolescents (aged 12 years and older with body weight at least 35 kg).


TAF’s approval is supported by 48-week data from two international Phase 3 studies (Studies 108 and 110) in 1,298 adult chronic HBV patients. Study 108 randomized 425 HBeAg-negative patients to receive either TAF or TDF, and Study 110 randomized 873 HBeAg-positive patients to receive either TAF or TDF. Both studies met their primary endpoint of non-inferiority to TDF based on the percentage of patients with chronic hepatitis B with plasma HBV DNA levels below 29 IU/mL at 48 weeks of therapy. Patients in the TAF arm of the trials also experienced numerically higher rates of normalization of blood serum alanine aminotransferase (ALT) levels. Both studies showed TAF and TDF to be well-tolerated by patients and discontinuations due to adverse events were 1% and 1.2%, respectively. The most common reported adverse events with TAF were diarrhea, vomiting, nausea, abdominal pain, abdominal distension, flatulence, fatigue, headache, dizziness, rash, pruritus, increased ALT and arthralgia.


While the primary efficacy assessment was performed at week 48, data show that at week 72 viral suppression as well as biochemical responses were maintained with continued TAF treatment. The safety assessment includes analyses performed at both week 48 and week 72 of treatment (median duration of exposure of 88 weeks), and safety endpoints included changes from baseline in bone mineral density at the hip and spine, and changes from baseline in serum creatinine and in eGFR, key indicators of renal health. In both studies, at weeks 48 and 72, changes in renal and bone laboratory safety parameters favored the TAF treatment groups.

Krishan Maggon 's insight:
TAF is a novel, targeted prodrug of tenofovir that has demonstrated antiviral efficacy similar to Gilead’s Viread® (tenofovir disoproxil fumarate, TDF) 245 mg, but at one-tenth the dose. Data show that because TAF has greater plasma stability and more efficiently delivers tenofovir to hepatocytes (cells of the liver) compared to TDF, it can be given at a lower dose, which means there is less tenofovir in the bloodstream. By reducing exposure to tenofovir, TAF is associated with improved renal and bone laboratory safety parameters compared to TDF in clinical trials.

Vemlidy was approved by the U.S. Food and Drug Administration on November 10, 2016 for the treatment of chronic HBV infection in adults with compensated liver disease, and by the Japanese Ministry of Health, Labour and Welfare on December 19, 2016 for the suppression of viral replication in chronic hepatitis B patients with evidence of hepatitis B virus replication and abnormal liver function. 

 For important safety information for TAF in Europe, including posology and method of administration, special warnings, drug interactions and adverse drug reactions, please see the European Summary of Product Characteristics (SmPC) for Vemlidy, available from the EMA website at http://www.ema.europa.eu. The full prescribing information for TAF in the United States, including BOXED WARNING, is available at www.gilead.com.
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Krishan Maggon 's curator insight, January 13, 5:52 AM
TAF is a novel, targeted prodrug of tenofovir that has demonstrated antiviral efficacy similar to Gilead’s Viread® (tenofovir disoproxil fumarate, TDF) 245 mg, but at one-tenth the dose. Data show that because TAF has greater plasma stability and more efficiently delivers tenofovir to hepatocytes (cells of the liver) compared to TDF, it can be given at a lower dose, which means there is less tenofovir in the bloodstream. By reducing exposure to tenofovir, TAF is associated with improved renal and bone laboratory safety parameters compared to TDF in clinical trials. 

 Vemlidy was approved by the U.S. Food and Drug Administration on November 10, 2016 for the treatment of chronic HBV infection in adults with compensated liver disease, and by the Japanese Ministry of Health, Labour and Welfare on December 19, 2016 for the suppression of viral replication in chronic hepatitis B patients with evidence of hepatitis B virus replication and abnormal liver function. 

 For important safety information for TAF in Europe, including posology and method of administration, special warnings, drug interactions and adverse drug reactions, please see the European Summary of Product Characteristics (SmPC) for Vemlidy, available from the EMA website at http://www.ema.europa.eu. The full prescribing information for TAF in the United States, including BOXED WARNING, is available at www.gilead.com.
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Antiviral Drug Prevents Recurrence of HCV in Liver Transplant Patients

Antiviral Drug Prevents Recurrence of HCV in Liver Transplant Patients | Hepatitis C New Drugs Review | Scoop.it
"Antiviral Drug Prevents Recurrence of HCV in Liver Transplant Patients - Drug Discovery & Development" https://t.co/oBb5dyLolt
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Small-molecule inhibitors of hepatitis C virus (HCV) non-structural protein 5A (NS5A): a patent review (2010-2015)

Small-molecule inhibitors of hepatitis C virus (HCV) non-structural protein 5A (NS5A): a patent review (2010-2015) | Hepatitis C New Drugs Review | Scoop.it
(2017). Small-molecule inhibitors of hepatitis C virus (HCV) non-structural protein 5A (NS5A): a patent review (2010-2015). Expert Opinion on Therapeutic Patents. Ahead of Print. doi: 10.1080/13543776.2017.1272573

ABSTRACT 

Introduction: Non-structural 5A (NS5A) protein has achieved a considerable attention as an attractive target for the treatment of hepatitis C (HCV). A number of novel NS5A inhibitors have been reported to date. Several drugs having favorable ADME properties and mild side effects were launched into the pharmaceutical market. For instance, daclatasvir was launched in 2014, elbasvir is currently undergoing registration, ledipasvir was launched in 2014 as a fixed-dose combination with sofosbuvir (NS5B inhibitor). 

 Areas covered: Thomson integrity database and SciFinder database were used as a valuable source to collect the patents on small-molecule NS5A inhibitors. All the structures were ranked by the date of priority. Patent holder and antiviral activity for each scaffold claimed were summarized and presented in a convenient manner. A particular focus was placed on the best-in-class bis-pyrrolidine-containing NS5A inhibitors. 

 Expert opinion: Several first generation NS5A inhibitors have recently progressed into advanced clinical trials and showed superior efficacy in reducing viral load in infected subjects. Therapy schemes of using these agents in combination with other established antiviral drugs with complementary mechanisms of action can address the emergence of resistance and poor therapeutic outcome frequently attributed to antiviral drugs. 

 KEYWORDS: NS5A inhibitors, hepatitis C virus, HCV, drug design
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Antiviral drug prevents recurrence of hepatitis C in liver transplant patients

Antiviral drug prevents recurrence of hepatitis C in liver transplant patients | Hepatitis C New Drugs Review | Scoop.it
Patients with hepatitis C virus infection who received an antiviral drug around the time they underwent liver transplantation saw a high rate of sustained virologic response, according to a Northwestern Medicine phase I
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Hepatitis C virus has a genetically determined lymphotropism through co-receptor B7.2

Hepatitis C virus has a genetically determined lymphotropism through co-receptor B7.2 | Hepatitis C New Drugs Review | Scoop.it
Infection of B cells by hepatitis C virus (HCV) is poorly understood, but is thought to result in lymphoproliferative disorders.
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Prediction of Fibrosis Progression Rate in Patients with Chronic Hepatitis C Genotype 4: Role of Cirrhosis Risk Score and Host Factors. - PubMed - NCBI

Prediction of Fibrosis Progression Rate in Patients with Chronic Hepatitis C Genotype 4: Role of Cirrhosis Risk Score and Host Factors. - PubMed - NCBI | Hepatitis C New Drugs Review | Scoop.it
J Interferon Cytokine Res. 2017 Jan 9. doi: 10.1089/jir.2016.0111. [Epub ahead of print]

Abstract The rate of liver fibrosis progression in chronic hepatitis C (CHC) patients is highly variable and affected by different factors. This study aimed to assess the role of cirrhosis risk score (CRS) based on 7 genetic variants (7 single-nucleotide polymorphisms [SNPs]) and host factors (age and sex) in the prediction of the rate of fibrosis progression in CHC. Duration of infection was determined in 115 patients. The fibrosis progression rate (FPR) per year was calculated as the ratio between fibrosis stage and the duration of infection. SNP genotyping were performed and CRS was determined based on it. FPR was significantly elevated in patients who acquired infection at age >40 years versus those who acquired infection at 30-40 years and those who acquired infection at <30 years. Median FPR was significantly higher in males than females (0.17 vs. 0.15) with P = 0.001. CRS value ≥0.8 is predictive of patients with high risk for cirrhosis, and CRS value <0.5 is predictive of patients with low risk for cirrhosis. There was significant positive correlation between CRS and FPR (P ≤ 0.001). CRS based on 7 SNPs at cutoff value ≥0.8, age at infection >40 years, and male sex are predictors of higher FPR. 

KEYWORDS: CHC; cirrhosis risk score; fibrosis progression; host factors
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ASP5878, a Novel Inhibitor of FGFR1, 2, 3, and 4, Inhibits the Growth of FGF19-Expressing Hepatocellular Carcinoma

ASP5878, a Novel Inhibitor of FGFR1, 2, 3, and 4, Inhibits the Growth of FGF19-Expressing Hepatocellular Carcinoma | Hepatitis C New Drugs Review | Scoop.it
Hepatocellular carcinoma is an aggressive cancer with poor prognosis. Fibroblast growth factor 19, a member of the fibroblast growth factor family, is a ligand for fibroblast growth factor receptor 4. Moreover, it plays a crucial role in the progression of hepatocellular carcinoma. ASP5878 is a novel inhibitor of fibroblast growth factor receptors 1, 2, 3, and 4 that is under development. It inhibits fibroblast growth factor receptor 4 kinase activity with an IC50 of 3.5 nmol/L. ASP5878 potently suppressed the growth of the fibroblast growth factor 19–expressing hepatocellular carcinoma cell lines Hep3B2.1-7, HuH-7, and JHH-7. In the Hep3B2.1-7 cell line, ASP5878 inhibited the phosphorylation of fibroblast growth factor receptor 4 and its downstream signaling molecules as well as induced apoptosis. Oral administration of ASP5878 at 3 mg/kg induced sustained tumor regression in a subcutaneous xenograft mouse model using Hep3B2.1-7. In HuH-7, an orthotopic xenograft mouse model, ASP5878 induced complete tumor regression and dramatically extended the survival of the mice. These results suggest that ASP5878 is a potentially effective therapeutic agent for hepatocellular carcinoma patients with tumors expressing fibroblast growth factor 19. Mol Cancer Ther; 16(1); 68–75. ©2016 AACR .
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TRPV4 activation of endothelial nitric oxide synthase resists nonalcoholic fatty liver disease by blocking CYP2E1-mediated redox toxicity

TRPV4 activation of endothelial nitric oxide synthase resists nonalcoholic fatty liver disease by blocking CYP2E1-mediated redox toxicity | Hepatitis C New Drugs Review | Scoop.it
RT @medicosergio: Actualización en hígado graso no alcohólico
REF: https://t.co/9R0wlc8ZW0
REV: https://t.co/DVGDGSSjbR
#obesidad #medicin…

Highlights • TRPV4 loss of function leads to uninterrupted CYP2E1 activity and protein levels. • Blocking CYP2E1-induced redox toxicity improves outcome in NAFLD pathology. • TRPV4 blocks CYP2E1 activity by activating NOS3 and NO release. • Mechanistically, Kupffer cell induced NO blocks CYP2E1 in a paracrine manner. • TRPV4-CYP2E1 axis is a novel pathway in NAFLD pathology.
Krishan Maggon 's insight:
Free Radical Biology and Medicine Volume 102, January 2017, Pages 260–273
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The clinically approved antiviral drug sofosbuvir inhibits Zika virus replication

The clinically approved antiviral drug sofosbuvir inhibits Zika virus replication | Hepatitis C New Drugs Review | Scoop.it

Abstract Zika virus (ZIKV) is a member of the Flaviviridae family, along with other agents of clinical significance such as dengue (DENV) and hepatitis C (HCV) viruses. Since ZIKV causes neurological disorders during fetal development and in adulthood, antiviral drugs are necessary. Sofosbuvir is clinically approved for use against HCV and targets the protein that is most conserved among the members of the Flaviviridae family, the viral RNA polymerase. Indeed, we found that sofosbuvir inhibits ZIKV RNA polymerase, targeting conserved amino acid residues. Sofosbuvir inhibited ZIKV replication in different cellular systems, such as hepatoma (Huh-7) cells, neuroblastoma (SH-Sy5y) cells, neural stem cells (NSC) and brain organoids. In addition to the direct inhibition of the viral RNA polymerase, we observed that sofosbuvir also induced an increase in A-to-G mutations in the viral genome. Together, our data highlight a potential secondary use of sofosbuvir, an anti-HCV drug, against ZIKV.

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Scientific Reports 7, Article number: 40920 (2017) doi:10.1038/srep40920
Published online: 18 January 2017
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Crystal Structure of a Full-Length Human Tetraspanin Reveals a Cholesterol-Binding Pocket

Crystal Structure of a Full-Length Human Tetraspanin Reveals a Cholesterol-Binding Pocket | Hepatitis C New Drugs Review | Scoop.it

Summary Tetraspanins comprise a diverse family of four-pass transmembrane proteins that play critical roles in the immune, reproductive, genitourinary, and auditory systems. Despite their pervasive roles in human physiology, little is known about the structure of tetraspanins or the molecular mechanisms underlying their various functions. Here, we report the crystal structure of human CD81, a full-length tetraspanin. The transmembrane segments of CD81 pack as two largely separated pairs of helices, capped by the large extracellular loop (EC2) at the outer membrane leaflet. The two pairs of helices converge at the inner leaflet to create an intramembrane pocket with additional electron density corresponding to a bound cholesterol molecule within the cavity. Molecular dynamics simulations identify an additional conformation in which EC2 separates substantially from the transmembrane domain. Cholesterol binding appears to modulate CD81 activity in cells, suggesting a potential mechanism for regulation of tetraspanin function. 


 Keywords: CD81, CD19, membrane protein, X-ray crystallography, protein structure, protein trafficking

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Differential hepatitis C virus RNA target site selection and host factor activities of naturally occurring miR-122 3΄ variants | Nucleic Acids Research | Oxford Academic

Differential hepatitis C virus RNA target site selection and host factor activities of naturally occurring miR-122 3΄ variants | Nucleic Acids Research | Oxford Academic | Hepatitis C New Drugs Review | Scoop.it
Differential HCV RNA target site selection and host factor activities of naturally occurring miR-122 3΄ variants https://t.co/tsZWQX0c8H
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Bile acids and nonalcoholic fatty liver disease: Molecular insights and therapeutic perspectives

Bile acids and nonalcoholic fatty liver disease: Molecular insights and therapeutic perspectives | Hepatitis C New Drugs Review | Scoop.it

Abstract Nonalcoholic fatty liver disease (NAFLD) is a burgeoning health problem worldwide and an important risk factor for both hepatic and cardiometabolic mortality. The rapidly increasing prevalence of this disease and of its aggressive form nonalcoholic steatohepatitis (NASH) will require novel therapeutic approaches to prevent disease progression to advanced fibrosis or cirrhosis and cancer. In recent years, bile acids have emerged as relevant signaling molecules that act at both hepatic and extrahepatic tissues to regulate lipid and carbohydrate metabolic pathways as well as energy homeostasis. Activation or modulation of bile acid receptors, such as the farnesoid X receptor and TGR5, and transporters, such as the ileal apical sodium-dependent bile acid transporter, appear to affect both insulin sensitivity and NAFLD/NASH pathogenesis at multiple levels, and these approaches hold promise as novel therapies. In the present review, we summarize current available data on the relationships of bile acids to NAFLD and the potential for therapeutically targeting bile-acid-related pathways to address this growing world-wide disease. (Hepatology 2017;65:350-362)

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Experimental & Molecular Medicine - Gene-metabolite network analysis in different nonalcoholic fatty liver disease phenotypes

Experimental & Molecular Medicine - Gene-metabolite network analysis in different nonalcoholic fatty liver disease phenotypes | Hepatitis C New Drugs Review | Scoop.it
Experimental & Molecular Medicine is an open access journal that publishes the highest quality articles in translational research and biomedical studies.
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Oncotarget | Immune cells in liver regeneration

Oncotarget | Immune cells in liver regeneration | Hepatitis C New Drugs Review | Scoop.it
Immune cells in liver regeneration
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Effect of Sorafenib in Patients With Advanced Hepatocellular Carcinoma May Depend on Hepatitis Status - The ASCO Post

Effect of Sorafenib in Patients With Advanced Hepatocellular Carcinoma May Depend on Hepatitis Status - The ASCO Post | Hepatitis C New Drugs Review | Scoop.it
Effect of Sorafenib in Patients With Advanced Hepatocellular Carcinoma May Depend on Hepatitis Status By Matthew Stenger Posted: 1/11/2017 11:27:53 AM Last Updated: 1/11/2017 11:27:53 AM Tweet this page Key Points Sorafenib was associated with a survival benefit among HBV-negative/HCV-positive...
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High Frequency of Tregs After Curing Hepatitis C Could Enhance Liver Cancer Risk

High Frequency of Tregs After Curing Hepatitis C Could Enhance Liver Cancer Risk | Hepatitis C New Drugs Review | Scoop.it
Even after eradicating hepatitis C with direct-acting antivirals, high frequency of Tregs could pose complications.
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Cell Research - Immunotherapy against cancer-related viruses

Cell Research - Immunotherapy against cancer-related viruses | Hepatitis C New Drugs Review | Scoop.it
Cell Research (2017) 27:59–73. doi:10.1038/cr.2016.153; published online 23 December 2016 Immunotherapy against cancer-related viruses Haruko Tashiro1 and Malcolm K Brenner1

Abstract Approximately 12% of all cancers worldwide are associated with viral infections. To date, eight viruses have been shown to contribute to the development of human cancers, including Epstein-Barr virus (EBV), Hepatitis B and C viruses, and Human papilloma virus, among others. These DNA and RNA viruses produce oncogenic effects through distinct mechanisms. First, viruses may induce sustained disorders of host cell growth and survival through the genes they express, or may induce DNA damage response in host cells, which in turn increases host genome instability. Second, they may induce chronic inflammation and secondary tissue damage favoring the development of oncogenic processes in host cells. Viruses like HIV can create a more permissive environment for cancer development through immune inhibition, but we will focus on the previous two mechanisms in this review. Unlike traditional cancer therapies that cannot distinguish infected cells from non-infected cells, immunotherapies are uniquely equipped to target virus-associated malignancies. The targeting and functioning mechanisms associated with the immune response can be exploited to prevent viral infections by vaccination, and can also be used to treat infection before cancer establishment. Successes in using the immune system to eradicate established malignancy by selective recognition of virus-associated tumor cells are currently being reported. For example, numerous clinical trials of adoptive transfer of ex vivo generated virus-specific T cells have shown benefit even for established tumors in patients with EBV-associated malignancies. Additional studies in other virus-associated tumors have also been initiated and in this review we describe the current status of immunotherapy for virus-associated malignancies and discuss future prospects. 

 Keywords: virus-associated malignancies; immunotherapy; Epstein-Barr virus; HPV; HBV; HCV
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Hepatic fibrosis and factors associated with liver stiffness in HIV mono-infected individuals

Hepatic fibrosis and factors associated with liver stiffness in HIV mono-infected individuals | Hepatitis C New Drugs Review | Scoop.it
Background Liver disease has become an important cause of morbidity and mortality even in those HIV-infected individuals who are devoid of hepatitis virus co-infection. The aim of this study was to evaluate the degree of hepatic fibrosis and the role of associated factors using liver stiffness measurement in HIV mono-infected patients without significant alcohol intake. Methods We performed a cross-sectional study of 101 HIV mono-infected patients recruited prospectively from March 1, 2014 to October 30, 2014 at the Center for HIV, St István and St László Hospital, Budapest, Hungary. To determine hepatic fibrosis, liver stiffness was measured with transient elastography. Demographic, immunologic and other clinical parameters were collected to establish a multivariate model. Bayesian Model Averaging (BMA) was performed to identify predictors of liver stiffness. Results Liver stiffness ranged from 3.0–34.3 kPa, with a median value of 5.1 kPa (IQR 1.7). BMA provided a very high support for age (Posterior Effect Probability-PEP: 84.5%), moderate for BMI (PEP: 49.3%), CD4/8 ratio (PEP: 44.2%) and lipodystrophy (PEP: 44.0%). For all remaining variables, the model rather provides evidence against their effect. These results overall suggest that age and BMI have a positive association with LS, while CD4/8 ratio and lipodystrophy are negatively associated. Discussion Our findings shed light on the possible importance of ageing, overweight and HIV-induced immune dysregulation in the development of liver fibrosis in the HIV-infected population. Nonetheless, further controlled studies are warranted to clarify causal relations.
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Hepatitis Education Canada | Programme canadien d’éducation sur l’hépatite

Hepatitis Education Canada | Programme canadien d’éducation sur l’hépatite | Hepatitis C New Drugs Review | Scoop.it
Hepatitis C Resources Adapted for Urd
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Access and elimination: the future of DAAs in hepatitis C - Pharmaphorum

Access and elimination: the future of DAAs in hepatitis C - Pharmaphorum | Hepatitis C New Drugs Review | Scoop.it
How direct-acting antivirals are transforming treatment of hepatitis C.
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ICYMI - 2016 Study Compared Hepatitis C Treatment Costs

ICYMI - 2016 Study Compared Hepatitis C Treatment Costs | Hepatitis C New Drugs Review | Scoop.it
A study, “Comparison of Hepatitis C Treatment Costs, Estimates of Net Prices and Usage in the U.S. and Other Major Markets,” was published by the IMS Institute for Healthcare Informatics.
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