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Evolución histórica de las terapias antivirales en hepatitis crónica C
Sánchez Rodríguez,Yoan Antonio; Arús Soler,Enrique;
Revista Cubana de Medicina , 2010,
Abstract: a bibliographic review on the more significant features of historical course experienced by the antiviral therapies used in treatment of chronic hepatitis c virus was carried out due to the increasing incidence and prevalence of this disease with infection estimates about 3% of the world population. a updating was carried out on this subject matter from its origins with special emphasis on future perspectives of this therapeutics, nowadays under consideration by the international scientific community. for the carrying out of present work 69 bibliographic references were reviewed including the meta-analyses available in medline from 1998 up to present time, as well as the publications of researches results performed in our country on this subject.
Antiviral drugs against hepatitis C virus
Rehman Sidra,Ashfaq Usman A,Javed Tariq
Genetic Vaccines and Therapy , 2011, DOI: 10.1186/1479-0556-9-11
Abstract: Hepatitis C virus (HCV) infection is a major worldwide problem causes acute and chronic HCV infection. Current treatment of HCV includes pegylated interferon-α (PEG IFN- α) plus ribavirin (RBV) which has significant side effects depending upon the type of genotype. Currently, there is a need to develop antiviral agents, both from synthetic chemistry and Herbal sources. In the last decade, various novel HCV replication, helicase and entry inhibitors have been synthesized and some of which have been entered in different phases of clinical trials. Successful results have been acquired by executing combinational therapy of compounds with standard regime in different HCV replicons. Even though, diverse groups of compounds have been described as antiviral targets against HCV via Specifically Targeted Antiviral Therapy for hepatitis C (STAT-C) approach (in which compounds are designed to directly block HCV or host proteins concerned in HCV replication), still there is a need to improve the properties of existing antiviral compounds. In this review, we sum up potent antiviral compounds against entry, unwinding and replication of HCV and discussed their activity in combination with standard therapy. Conclusively, further innovative research on chemical compounds will lead to consistent standard therapy with fewer side effects.
Glycyrrhizin as antiviral agent against Hepatitis C Virus
Usman A Ashfaq, Muhammad S Masoud, Zafar Nawaz, Sheikh Riazuddin
Journal of Translational Medicine , 2011, DOI: 10.1186/1479-5876-9-112
Abstract: The present study was design to study the antiviral effect of Glycyrrhizin (GL) against HCV. For this purpose, HCV infected liver cells were treated with GL at non toxic doses and HCV titer was measured by Quantitative real time RT-PCR.Our results demonstrated that GL inhibit HCV titer in a dose dependent manner and resulted in 50% reduction of HCV at a concentration of 14 ± 2 μg. Comparative studies were made with interferon alpha to investigate synergistic effects, if any, between antiviral compound and interferon alpha 2a. Our data showed that GL exhibited synergistic effect when combined with interferon. Moreover, these results were verified by transiently transfecting the liver cells with HCV 3a core plasmid. The results proved that GL dose dependently inhibit the expression of HCV 3a core gene both at mRNA and protein levels while the GAPDH remained constant.Our results suggest that GL inhibit HCV full length viral particles and HCV core gene expression or function in a dose dependent manner and had synergistic effect with interferon. In future, GL along with interferon will be better option to treat HCV infection.Hepatitis C virus (HCV) is a major cause of liver associated diseases all over the world. An estimated 3% of the world's populations, (more than 350 million people) are chronically infected by HCV, which is the main cause of liver fibrosis, cirrhosis and hepatocellular carcinoma (HCC) [1]. Like other RNA viruses, HCV possess a high degree of sequence variability that likely contributes to its ability to establish chronic infections after a mild acute phase. Current treatment of standard for HCV comprises a combination of high-dose pegylated interferon alpha (IFN-α) with the guanosine analogue ribavirin (Rib). About 75% of patients receive no therapeutic benefit from the current combination therapy with PEG-IFN α and the guanosine analog ribavirin because of adverse side effects and high cost [2]. Vaccine development is hindered by the lack of good in
Revisión sistemática de evaluaciones económicas de fármacos antivirales para el tratamiento de la hepatitis B crónica Economic evaluation of antiviral treatment for chronic hepatitis B: a systematic review  [cached]
Lely Solari,Gisely Hijar,Renzo Zavala,Juan Manuel Ureta
Revista Peruana de Medicina Experimental y Salud Pública , 2010,
Abstract: Objetivo. Revisar la evidencia disponible acerca de la costo-efectividad de los regímenes antivirales en el tratamiento de la hepatitis B crónica. Material y Métodos. Se realizó una revisión sistemática de las bases de datos de MEDLINE, LILACS, NICE guidelines y COCHRANE sobre evaluaciones económicas de regímenes antivirales para el tratamiento de hepatitis B crónica. Se incluyó los estudios originales, revisiones sistemáticas y guías de manejo conteniendo información acerca de la costo-efectividad de dicho tratamiento. Se registró las características y resultados de los documentos obtenidos. Resultados. Se obtuvo 29 artículos originales, cuatro artículos de revisión y cuatro guías de manejo clínico. La mayoría de las publicaciones fueron hechas en los cinco últimos a os. Los autores tenían conflicto de interés, por trabajar en la industria farmacéutica, en 73% de los artículos originales. El 93% de los artículos que evalúan costo-efectividad de brindar tratamiento para hepatitis B crónica frente a manejo de complicaciones, encuentran que es costo-efectivo el tratamiento antiviral; 3/6 estudios que evalúan lamivudina frente a otros esquemas la encuentran como estrategia dominante, 3/5 encuentran a entecavir como estrategia dominante, 1/1 a tenofovir como dominante, 1/4 a interferón convencional como dominante y ninguno encuentra a adefovir ni interferón pegilado como estrategia dominante. Conclusiones. Consideramos que la evidencia disponible sugiere que brindar tratamiento antiviral para hepatitis B crónica sea una intervención costo-efectiva para muchos sistemas de salud, incluyendo el nuestro, con índices variables de costo-efectividad de acuerdo con los esquemas evaluados. Idealmente, se debe realizar evaluaciones económicas locales en este aspecto. Objective. To revise the available evidence on the cost-effectiveness of antiviral regimens for treatment of chronic hepatitis B. Material and methods. We performed a systematic revision on MEDLINE, LILACS NICE and COCHRANE databases, searching for economic evaluations of antiviral regimens for treatment of chronic hepatitis B. We included original studies, systematic revisions and management guidelines including information on the cost-effectiveness of this treatment. We registered the characteristics and results of the retrieved documents. Results. We obtained 29 original papers, 4 revision articles and 4 management guidelines. Most of these publications have been done in the last 5 years. There was conflict of interest in 73% of original articles, due to authors working for the pharmaceutical industry
Iron Regulator Hepcidin Exhibits Antiviral Activity against Hepatitis C Virus  [PDF]
Hongyan Liu, Thu Le Trinh, Huijia Dong, Robertson Keith, David Nelson, Chen Liu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0046631
Abstract: Hepatitis C viral infection affects 170 million people worldwide. It causes serious chronic liver diseases. HCV infection has been implicated in iron accumulation in the liver and iron overload has been shown to be a potential cofactor for HCV associated hepatocellular carcinoma progression. The underlying mechanisms are not understood. Human hepcidin, a 25 amino acid peptide mainly produced by hepatocytes, is a key regulator of iron metabolism. Alteration of hepcidin expression levels has been reported in the setting of chronic HCV infection and hepatocellular carcinoma. In this study, we aim to examine the interactions between HCV infection and hepcidin expression in liver cells. We found that hepcidin expression was suppressed in HCV infected cells. The suppressive effect appears to be regulated by histone acetylation but not DNA methylation. Moreover, we found that hepcidin had a direct antiviral activity against HCV replication in cell culture. The antiviral effect is associated with STAT3 activation. In conclusion, hepcidin can induce intracellular antiviral state while HCV has a strategy to suppress hepcidin expression. This may be a novel mechanism by which HCV circumvents hepatic innate antiviral defense.
Antiviral therapy in hepatitis C virus cirrhotic patients in compensated and decompensated condition  [cached]
Angelo Iacobellis, Antonio Ippolito, Angelo Andriulli
World Journal of Gastroenterology , 2008,
Abstract: The main goals of treating cirrhotic patients with antiviral therapy are to attain sustained viral clearance (SVR), halt disease progression, and prevent re-infection of the liver graft. However, while the medical need is great, the use of interferon and ribavirin might expose these patients to severe treated-related side effects as a large proportion of them have pre-existing hematological cytopenias. We have reviewed potential benefits and risks associated with antiviral drugs in patients with liver cirrhosis, due to hepatitis C virus (HCV) infection. In cases presenting with bridging fibrosis or cirrhosis, current regimens of antiviral therapy have attained a 44%-48% rate of SVR. In cirrhotic patients with portal hypertension, the SVR rate was 22% overall, 12.5% in patients with genotype 1, and 66.7% in those with genotypes 2 and 3 following therapy with low doses of either Peg-IFN alpha-2b and of ribavirin. In patients with decompensated cirrhosis, full dosages of Peg-IFN alpha-2b and of ribavirin produced a SVR rate of 35% overall, 16% in patients with genotype 1 and 4, and 59% in those with genotype 2 and 3. Use of hematological cytokines will either ensure full course of treatment to be accomplished with and prevent development of treatment-associated side effects. Major benefits after HCV eradication were partial recovery of liver metabolic activity, prevention of hepatitis C recurrence after transplantation, and removal of some patients from the waiting list for liver transplant. Several observations highlighted that therapy is inadvisable for individuals with poor hepatic reserve (Child-Pugh-Turcotte score ≥ 10). Although SVR rates are low in decompensated cirrhotics due to hepatitis C, these patients have the most to gain as successful antiviral therapy is potentially lifesaving.
Oscillations in serum ferritin associated with antiviral therapy in chronic hepatitis C
Ladero,J. M.; López-Alonso,G.; Devesa,M. J.; Cuenca,F.; Ortega,L.; Agreda,M.; Suárez,A.; Ropero,P.; Díaz-Rubio,M.;
Revista Espa?ola de Enfermedades Digestivas , 2009, DOI: 10.4321/S1130-01082009000100004
Abstract: background: hyperferritinemia is often found in patients with chronic hepatitis c (chc) and is predictive of poorer response to antiviral therapy. objective: to investigate changes in ferritinemia during and after antiviral therapy. patients and methods: serum ferritin levels were measured in 262 chc patients (163 males, mean age 48.5 years ± 10.1) before and during antiviral therapy, and six months post-treatment in all 154 patients whit undetectable serum hcv-rna after therapy completion. results: baseline serum ferritin was higher in patients with primary therapeutic failure than in those reaching sustained viral response (330 ± 291 ng/ml vs. 211 ± 192 ng/ml, p = 0.002). serum ferritin transiently increased during therapy from baseline (257 ± 242 ng/ml vs. 875 ± 630 ng/ml, p < 0.001). six months after finishing therapy, serum ferritin decreased under baseline values both in sustained responders (117 ± 102 ng/ml vs. 211± 192 ng/ml, p < 0.001) and, to a lesser extent, in relapsers (217 ± 174 ng/ml vs. 257 ± 221 ng/ml, p = 0.047). conclusions: baseline serum ferritin may predict response to antiviral treatment in chronic hepatitis c. combined antiviral therapy induces a marked increase in serum ferritin that falls below baseline values after sustained viral response, suggesting that the cause of hyperferritinemia in many patients is hcv infection itself rather than iron overload.
Antiviral Therapy for Hepatitis C Virus: Beyond the Standard of Care  [PDF]
Leen Delang,Lotte Coelmont,Johan Neyts
Viruses , 2010, DOI: 10.3390/v2040826
Abstract: Hepatitis C virus (HCV) represents a major health burden, with an estimated 180 million chronically infected individuals worldwide. These patients are at increased risk of developing liver cirrhosis and hepatocellular carcinoma. Infection with HCV is the leading cause of liver transplantation in the Western world. Currently, the standard of care (SoC) consists of pegylated interferon alpha (pegIFN-α) and ribavirin (RBV). However this therapy has a limited efficacy and is associated with serious side effects. Therefore more tolerable, highly potent inhibitors of HCV replication are urgently needed. Both Specifically Targeted Antiviral Therapy for HCV (STAT-C) and inhibitors that are believed to interfere with the host-viral interaction are discussed.
Neopterin as a Marker of Response to Antiviral Therapy in Hepatitis C Virus Patients  [PDF]
Gregory F. Oxenkrug,Pura J. Requintina,Dennis L. Mikolich,Robin Ruthazer,Kathleen Viveiros,Hannah Lee,Paul Summergrad
Hepatitis Research and Treatment , 2012, DOI: 10.1155/2012/619609
Abstract: Predicting the efficacy of antiviral treatment of hepatitis C virus (HCV) is of importance for both patient well-being and health care expense. The expression of interferon-stimulated genes (IFN-SGs) in the liver was suggested as a marker of response to anti-viral therapy. IFN-SGs encode the guanosine triphosphate cyclohydrolase 1 (GTPCH), a rate-limiting enzyme of pteridines biosynthesis. Neopterin, a stable byproduct of GTPCH-catalyzed reaction, is used as a marker of interferon-induced GTPCH activation. We hypothesized that assessment of neopterin concentrations might predict the response to antiviral therapy. Neopterin concentrations were evaluated in 260 HCV patients treated by pegylated interferon combined with ribavirin. Mean and median pretreatment neopterin concentrations were lower in patients with sustained virological response than in nonresponders. The rate of response was twofold higher among patients with pretreatment neopterin levels <16?nmol/L than in patients with neopterin levels ≥16?nmol/L, even after controlling for HCV genotype status. Our study suggests that the pretreatment level of neopterin might be used in routine clinical practice as rapid and cost-effective marker to predict the response to antiviral therapy in HCV patients. 1. Introduction Hepatitis C virus (HCV) is the most common blood-borne infection and a major cause of chronic liver disease, cirrhosis, and primary hepatocellular carcinoma and one of the leading indications for liver transplant [1]. The current standard therapy for chronic HCV (pegylated-interferon- (pegIFN-) combined with ribavirin) has limited efficacy (about 50%), is costly, and involves severe medical and psychiatric side effects. Recently introduced protease inhibitors, Telaprevir and Boceprevir, are effective in HCV1 and HCV2 while their antiviral activity is limited in HCV3 and HCV4 [2]. Therefore, search for biological markers to predict the response to antiviral treatment is of importance for both patient well-being and health care expense. HCV genotypes predict more favorite response among HCV1 and HCV4 (in comparison with HCV2- and HCV3- infected patients [1, 2]). The value of currently used assessment of allelic variants of the IL28B gene encoding IFNλ3 predicts antiviral response in HCV1 and HCV4 and is attenuated, but relevant also in HCV2 and HCV3, especially in patients not achieving rapid virological response [3]. Assessment of expression of interferon-stimulated genes (IFN-SGs) in the liver (but not in plasma) predicted antiviral response independently from IL28B polymorphism [4, 5].
Chronic hepatitis C and no response to antiviral therapy:A perpetual problem
Papatheodoridis G.,E. Cholongitas
Annals of Gastroenterology , 2007,
Abstract: SUMMARY No-response to antiviral therapy was observed in the majority of chronic hepatitis C patients treated with interferon alpha (IFN-a) monotherapy, but continues to represent a frequent problem even after treatment with newer, more potent, combination regimens. Non-responding patients represent a fairly heterogeneous group. Subgroups of nonresponders with biochemical but without virological response, or with breakthrough phenomena during therapy probably have a relatively more favorable prognosis. Retreatment with consensus IFN may be relatively effective, while the combination of IFN-a in usual dosage and ribavirin (RIB) achieves sustained virological response in 13% and 21% of such patients treated for 6 and 12 months, respectively. Induction courses of IFN-a in combination with RIB have been found to achieve initial virological response in 36-40% and sustained virological response in 17-26%. Triple antiviral therapy with IFN-a, RIB and amantadine has also been used, but more trials are needed for firm conclusions. Recently, the combination of pegylated IFN-a plus ribavirin was reported to achieve initial virological response in 36-40% of patients non-responding to IFN-a monotherapy or to a combination of IFN-a plus ribavirin. Extensive data suggest that therapy with IFN-a may delay the progression of fibrosis and decrease the incidence of hepatocellular carcinoma even in non-responding chronic hepatitis C patients. Thus, the decision whether or not to discon-tinue the antiviral therapy in non-responders is related to whether therapy aims the clearance of the virus or just a histological benefit. Key words: Chronic hepatitis C, no-response, Interferon, Ribavirin, Amantadine, Induction therapy
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