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Chronic hepatitis C.

Jang JY, Chung RT - Gut Liver (2011)

Bottom Line: Improved SVR can be achieved with new specific inhibitors that target the HCV NS3/4A protease and the NS5B polymerase.Several long-term follow-up studies have shown that SVR, when achieved, is associated with a very low risk of virologic relapse.Furthermore, antiviral therapy can reduce the morbidity and mortality rates associated with chronic hepatitis C by reducing fibrosis progression, the incidence of cirrhosis, and hepatocellular carcinoma.

View Article: PubMed Central - PubMed

Affiliation: Institute for Digestive Research, Digestive Disease Center, Department of Internal Medicine, Soonchunhyang University College of Medicine, Seoul, Korea.

ABSTRACT
The goal of antiviral therapy for patients with chronic hepatitis C virus (HCV) infection is to attain a sustained virologic response (SVR), which is defined as undetectable serum HCV-RNA levels at 6 months after the cessation of treatment. Major improvements in antiviral therapy for chronic hepatitis C have occurred in the past decade. The addition of ribavirin to interferon-alfa therapy and the introduction of pegylated interferon (PEG-IFN) have substantially improved SVR rates in patients with chronic hepatitis C. The optimization of HCV therapy with PEG-IFN and ribavirin continues to evolve. Studies are ongoing that use viral kinetics to tailor therapy to an individual's antiviral response and determine the ideal length of treatment to maximize the chance of SVR. Improved SVR can be achieved with new specific inhibitors that target the HCV NS3/4A protease and the NS5B polymerase. Several long-term follow-up studies have shown that SVR, when achieved, is associated with a very low risk of virologic relapse. Furthermore, antiviral therapy can reduce the morbidity and mortality rates associated with chronic hepatitis C by reducing fibrosis progression, the incidence of cirrhosis, and hepatocellular carcinoma.

No MeSH data available.


Related in: MedlinePlus

Telaprevir increases sustained virologic response rates in patients with hepatitis C virus genotype 1 infection (Data from McHutchison JG, et al. N Engl J Med 2009;360:1827-1838).79
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Figure 10: Telaprevir increases sustained virologic response rates in patients with hepatitis C virus genotype 1 infection (Data from McHutchison JG, et al. N Engl J Med 2009;360:1827-1838).79

Mentions: The depth of our understanding of the HCV life cycle has significantly expanded over the previous decade and has led to multiple new anti-HCV therapies now under investigation. Initially, such oral specifically targeted antiviral therapies for hepatitis C (STAT-C) drugs will most likely be added to current PEG-RBV therapies and could lead to improved response rates and shorter therapy durations. Improved SVR rates could be achieved with new HCV-specific inhibitors that target the NS3/4A and NS5B polymerases. Recent trials reported SVR rates on the order of 61% to 68% and 67% to 75% following combination treatments of standard of care (SOC) and the protease inhibitors telaprevir (Fig. 10)79 and boceprevir,137 respectively, in patients with HCV genotype 1 infection. Future trials will need to evaluate the use of "cocktails" of oral agents to determine whether viral resistance can be minimized with HCV as it has been with HIV and HBV. Resistance could be avoided by either combining two or more specific inhibitors with non-verlapping resistance profiles, such as protease inhibitors with nucleoside and/or non-nucleoside inhibitors, or combining HCV-specific inhibitors with non-HCV-specific inhibitors, such as cyclophilin inhibitors. Although these therapy options are not yet available, we now have the ability to adopt improved strategies to maximize response rates with available therapies and to tailor treatment durations based on individual viral kinetic responses.138


Chronic hepatitis C.

Jang JY, Chung RT - Gut Liver (2011)

Telaprevir increases sustained virologic response rates in patients with hepatitis C virus genotype 1 infection (Data from McHutchison JG, et al. N Engl J Med 2009;360:1827-1838).79
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3140655&req=5

Figure 10: Telaprevir increases sustained virologic response rates in patients with hepatitis C virus genotype 1 infection (Data from McHutchison JG, et al. N Engl J Med 2009;360:1827-1838).79
Mentions: The depth of our understanding of the HCV life cycle has significantly expanded over the previous decade and has led to multiple new anti-HCV therapies now under investigation. Initially, such oral specifically targeted antiviral therapies for hepatitis C (STAT-C) drugs will most likely be added to current PEG-RBV therapies and could lead to improved response rates and shorter therapy durations. Improved SVR rates could be achieved with new HCV-specific inhibitors that target the NS3/4A and NS5B polymerases. Recent trials reported SVR rates on the order of 61% to 68% and 67% to 75% following combination treatments of standard of care (SOC) and the protease inhibitors telaprevir (Fig. 10)79 and boceprevir,137 respectively, in patients with HCV genotype 1 infection. Future trials will need to evaluate the use of "cocktails" of oral agents to determine whether viral resistance can be minimized with HCV as it has been with HIV and HBV. Resistance could be avoided by either combining two or more specific inhibitors with non-verlapping resistance profiles, such as protease inhibitors with nucleoside and/or non-nucleoside inhibitors, or combining HCV-specific inhibitors with non-HCV-specific inhibitors, such as cyclophilin inhibitors. Although these therapy options are not yet available, we now have the ability to adopt improved strategies to maximize response rates with available therapies and to tailor treatment durations based on individual viral kinetic responses.138

Bottom Line: Improved SVR can be achieved with new specific inhibitors that target the HCV NS3/4A protease and the NS5B polymerase.Several long-term follow-up studies have shown that SVR, when achieved, is associated with a very low risk of virologic relapse.Furthermore, antiviral therapy can reduce the morbidity and mortality rates associated with chronic hepatitis C by reducing fibrosis progression, the incidence of cirrhosis, and hepatocellular carcinoma.

View Article: PubMed Central - PubMed

Affiliation: Institute for Digestive Research, Digestive Disease Center, Department of Internal Medicine, Soonchunhyang University College of Medicine, Seoul, Korea.

ABSTRACT
The goal of antiviral therapy for patients with chronic hepatitis C virus (HCV) infection is to attain a sustained virologic response (SVR), which is defined as undetectable serum HCV-RNA levels at 6 months after the cessation of treatment. Major improvements in antiviral therapy for chronic hepatitis C have occurred in the past decade. The addition of ribavirin to interferon-alfa therapy and the introduction of pegylated interferon (PEG-IFN) have substantially improved SVR rates in patients with chronic hepatitis C. The optimization of HCV therapy with PEG-IFN and ribavirin continues to evolve. Studies are ongoing that use viral kinetics to tailor therapy to an individual's antiviral response and determine the ideal length of treatment to maximize the chance of SVR. Improved SVR can be achieved with new specific inhibitors that target the HCV NS3/4A protease and the NS5B polymerase. Several long-term follow-up studies have shown that SVR, when achieved, is associated with a very low risk of virologic relapse. Furthermore, antiviral therapy can reduce the morbidity and mortality rates associated with chronic hepatitis C by reducing fibrosis progression, the incidence of cirrhosis, and hepatocellular carcinoma.

No MeSH data available.


Related in: MedlinePlus