Vantage Point: Transplantation

Antiviral Therapy for HCV in Liver Transplant Candidates

The emergence of direct-acting antiviral therapy has transformed the management of chronic hepatitis C virus infection. The availability of telaprevir and boceprevir in 2012, followed recently by simeprevir (Olysio, Janssen Therapeutics) and sofosbuvir (Sovaldi, Gilead), has provided clinicians with more highly effective and well-tolerated treatment options. An important subgroup of patients who have historically experienced the greatest challenges in HCV therapy are those with cirrhosis awaiting liver transplantation. Although these individuals may have the most to gain by achieving viral eradication, they have also been faced with lower efficacy, poor tolerance and safety concerns while undergoing therapy.

Stevan A. Gonzalez

Chronic HCV remains the most common chronic blood-borne infection in the United States, with an estimated prevalence of 5 million individuals. It accounts for two-thirds of newly diagnosed chronic liver disease and is the leading indication for liver transplantation. Although the overall US prevalence of HCV infection is expected to decline, the proportion of individuals with cirrhosis is on the rise. Consequently, the proportion of liver transplants for hepatocellular carcinoma (HCC) attributed to chronic HCV has progressively increased over the last decade (see Figure 1). In light of these trends, HCV will continue to be a major source of liver-related mortality as the prevalence of clinical decompensation and HCV-associated HCC is projected to increase further over the next few decades.

Figure 1. 

Figure 1. The most common indications for liver transplantation in the United States in 2013.
*Approximately one-half of transplant recipients with HCC have underlying chronic hepatitis C virus.
Abbreviations: HCC, hepatocellular carcinoma; NAFLD, nonalcoholic fatty liver disease; PSC, primary sclerosing cholangitis; PBC, primary biliary cirrhosis.
Data obtained from the US Organ Procurement and Transplantation Network and the Scientific Registry of Transplant Recipients (optn.transplant.hrsa.gov/).

Source: Gonzalez SA

As recurrence of HCV is universal in liver transplant recipients with HCV infection at the time of transplantation, efforts to achieve viral eradication prior to transplant could significantly improve outcomes. Recurrent HCV infection can lead to allograft dysfunction, chronic hepatitis and progressive fibrosis, resulting in cirrhosis within 5 years in up to 30% of individuals. The development of cirrhosis in this setting is associated with rapid progression and a high risk for clinical decompensation. Although it occurs in less than 10% of patients, a rapidly progressive form of recurrent HCV known as fibrosing cholestatic hepatitis C can develop within the first 6 months following transplantation and may lead to allograft failure within 1 year. As a result, the presence of HCV infection has remained an independent risk factor for increased mortality in liver transplant recipients.

Challenges of Interferon-Based Therapy

Antiviral therapy involving interferon-alfa (IFN) has presented a major challenge to patients with advanced HCV-associated liver disease due to its poor tolerability and increased risk for adverse events, particularly in patients with cirrhosis awaiting liver transplantation. Prior to the advent of direct-acting antiviral (DAA) therapy, several small studies evaluated the potential role of IFN-based therapy in patients with advanced liver disease, including liver transplant candidates. These studies found that if HCV RNA clearance can be achieved immediately prior to undergoing liver transplantation, a post-transplant sustained virologic response can occur in 42% to 75% of patients (see Figure 2). However, these studies also demonstrated a significant increase in the risk for adverse events associated with IFN in this population, including bacterial infection and pancytopenia. As a result, dose reductions and treatment interruptions were common. Although clinical decompensation of liver disease was frequently reported in these studies, the incidence was similar between treated patients and controls.

Figure 2. 

Figure 2. Post-transplant SVR in patients achieving negative HCV RNA at the time of transplantation.
*In patients with at least 4 weeks of viral negativity prior to undergoing transplant, post-transplant SVR occurred in 96% (24/25).
Abbreviations: IFN, standard interferon-alfa; RBV, ribavirin; PEG, pegylated interferon-alfa; SOF, sofosbuvir.

Source: Gonzalez SA

The first prospective, randomized, controlled trial evaluating pre-transplant antiviral therapy in patients with chronic HCV involved a cohort of patients from the Adult-to-Adult Living Donor Liver Transplantation Cohort Study (A2ALL). Patients enrolled were randomized 2:1 to receive treatment with pegylated interferon-alfa (PEG) plus ribavirin (RBV) or no treatment. As potential living donor liver transplant recipients and patients with HCC who met criteria for model end-stage liver disease (MELD) exception points, participants in this trial were considered ideal for evaluating treatment efficacy based on a lower prevalence of clinical decompensation and a predictable or shortened waitlist time. Although this select group had a mean Child-Turcotte-Pugh (CTP) score of 7 and MELD score of 12, pre-transplant serious adverse events occurred in almost one-half of treated patients, with a significant increase in cytopenia and infection compared with controls. A key finding in this study was an association between duration of pre-transplant therapy and virologic response, in which SVR was achieved in 50% of patients who maintained therapy for greater than 16 weeks while SVR did not occur in any patient treated for less than 8 weeks.

Experience with Protease Inhibitors

Although not specifically targeting a pre-transplant population, the largest experience with protease inhibitors in patients with advanced HCV-associated liver disease has arisen from the French Compassionate Use of Protease Inhibitors in Viral C Cirrhosis (CUPIC) study group. This study involved a cohort of 674 patients with compensated cirrhosis who previously failed antiviral therapy. All were treated with combination PEG, RBV and telaprevir (Incivek, Vertex) or boceprevir (Victrelis, Merck). Safety and response data in 497 patients who completed at least 16 weeks of therapy were recently reported. Approximately 60% of patients received telaprevir, 98% had a CTP classification of A and the mean MELD score was 8. Similar to past experiences with IFN-based therapy in patients with advanced disease, this study noted a high rate of serious adverse events (40% overall), including significant anemia in 29%, requirement for erythropoietin stimulating agents in 51%, hepatic decompensation in 2.4% and six deaths (1.2%), mostly due to severe infections. Factors independently associated with an increased risk for on-treatment clinical decompensation or mortality included thrombocytopenia (platelets ≤100,000/mm3) and hypoalbuminemia (serum albumin <3.5 g/dL).

Telaprevir and boceprevir have not been extensively studied in patients with decompensated cirrhosis or liver transplant candidates in the form of a pre-transplant regimen of antiviral therapy.

Sofosbuvir and Beyond

Sofosbuvir, a nucleotide analogue with inhibitory activity against the HCV NS5B RNA-dependent RNA polymerase, has emerged as a potent DAA with favorable tolerability, efficacy in multiple HCV genotypes, and a high barrier to resistance. The high potency associated with sofosbuvir has led to the availability of effective IFN-free regimens, particularly in patients with genotypes 2 and 3. IFN-free therapy involving sofosbuvir may also be considered for genotype 1 infection in patients who are IFN-intolerant, IFN-ineligible or in those with advanced liver disease. Phase 3 clinical trials in patients treated with combination sofosbuvir and RBV only noted mild increases in fatigue, insomnia and anemia compared with placebo, while the incidence of adverse events did not appear to be increased in those with compensated cirrhosis compared with noncirrhotics. Results from phase 3 studies suggest that the potential for SVR may be slightly diminished in patients with cirrhosis; however, the overall SVR rates remain comparatively high in these patients (see Figure 3).

Figure 3. 

Figure 3. SVR in treatment-naive patients with compensated cirrhosis receiving sofosbuvir-based therapy.
Data shown are based on results from phase 3 clinical trials.
Abbreviations: PEG, pegylated interferon-alfa; RBV, ribavirin; SOF, sofosbuvir.
Sources: Lawitz E. N Engl J Med. 2013; Zeuzem S. The Liver Meeting 2013.

Source: Gonzalez SA

A phase 2, open-label, multicenter, prospective study recently established a role for sofosbuvir in the treatment of patients with chronic HCV awaiting liver transplantation. This study enrolled 61 patients of genotypes 1 through 4 with compensated cirrhosis and HCC awaiting deceased donor liver transplantation. All patients were within Milan criteria for HCC, most were infected with genotype 1 HCV (74%) and most had failed prior IFN-based therapy (75%). All patients received up to 48 weeks of sofosbuvir and RBV. Of 44 patients who received a liver transplant, 41 (93%) achieved viral clearance at the time of transplantation. In patients who had reached week 12 post-transplant, 25 of 39 (64%) achieved SVR (see Figure 2). Most importantly, the only independent predictor of post-transplant viral clearance was the duration of negative serum HCV RNA prior to transplantation, as 24 of 25 (95%) of patients with at least 4 weeks of undetectable HCV RNA achieved SVR.

Sofosbuvir has been studied in combination with other DAA agents in patients with compensated cirrhosis, including simeprevir; however, data are limited. Interim results from a phase 2 clinical trial of sofosbuvir and simeprevir with or without RBV in patients with genotype 1 infection suggest a favorable virologic response associated with this combination. This trial, known as the COSMOS study, included patients with advanced fibrosis who received 12 weeks of therapy. Eighteen patients with compensated cirrhosis were included. Although one-half were prior treatment failures, overall SVR 4 in cirrhotics, defined by negative HCV RNA at 4 weeks following completion of therapy, was observed in 17 of 18 (94%) patients. In light of the small numbers of patients with cirrhosis included in this cohort, it is difficult to ascertain the safety profile associated with this regimen in patients with advanced liver disease.

As antiviral therapy for chronic HCV evolves and promising new DAA agents become available in the near future, our ability to achieve rapid viral clearance with minimal risk for adverse events will continue to improve. This has major implications for special populations including those with advanced cirrhosis, HCC and liver transplant candidates. Achievement of viral eradication at the time of transplantation may significantly improve post-transplant outcomes. Although initiation of antiviral therapy at an early phase following transplantation may also be an option, other factors must be considered including the need for immunosuppressive therapy, risk for allograft dysfunction in the setting of HCV recurrence and the potential for other post-transplant complications. A regimen of sofosbuvir and RBV has now been approved in the treatment of individuals with HCC and compensated cirrhosis secondary to HCV who currently await liver transplantation. Although safety concerns will likely continue to present a challenge in high-risk groups with advanced liver disease, efforts to optimize virologic response and ensure an adequate duration of viral negativity prior to undergoing transplantation may significantly enhance our ability to prevent post-transplant recurrence of HCV.

References:
American Association for the Study of Liver Diseases and Infectious Diseases Society of America. Recommendations for testing, managing and treating hepatitis C. www.hcvguidelines.org. Accessed April 1, 2014.
Bell BP. Am J Gastroenterol. 2008;103:2727-2736.
Carrion JA. J Hepatol. 2009;50:719-728.
Chak E. Liver Int. 2011;8:1090-1101.
Curry MP. Abstract #213. Pretransplant sofosbuvir and ribavirin to prevent recurrence of HCV infection after liver transplantation. Presented at: the 64th Annual Meeting of the American Association for the Study of Liver Diseases; Nov. 1-5, 2013; Washington, D.C.
Davis GL. Gastroenterology. 2010;138:513-521.
Everson GT. Hepatology. 2005;42:255-262.
Everson GT. Hepatology. 2013;57:1752-1762.
Forns X. J Hepatol. 2003;39:389-396.
Hezode C. J Hepatol. 2013;59:434-441.
Jacobson IM. N Engl J Med. 2013;368:1867-1877.
Jacobson IM. Abstract #LB3. SVR results of a once-daily regimen of simeprevir (TMC435) plus sofosbuvir (GS-7977) with or without ribavirin in cirrhotic and non-cirrhotic HCV genotype 1 treatment-naive and prior null responder patients: The COSMOS study. Presented at: the 64th Annual Meeting of the American Association for the Study of Liver Diseases; Nov. 1-5, 2013; Washington, D.C.
Kershenobich D. Liver Int. 2011;31(Suppl 2):4-17.
Lawitz E. N Engl J Med. 2013;368:1878-1887.
Patel K. Abstract #1093. Efficacy and safety of sofosbuvir in patients according to fibrosis stage: An analysis of phase 3 data. Presented at: the 64th Annual Meeting of the American Association for the Study of Liver Diseases; Nov. 1-5, 2013; Washington, D.C.
Watt KD. Am J Transplant. 2010;10:1420-1427.
Wong RJ. Hepatology. 2013;Epub
Zeuzem S. Abstract #1085. Sofosbuvir + ribavirin for 12 or 24 weeks for patients with HCV genotype 2 or 3: The VALENCE trial. Presented at: the 64th Annual Meeting of the American Association for the Study of Liver Diseases; Nov. 1-5, 2013; Washington, D.C.
For more information:
Stevan A. Gonzalez, MD, MS, is an HCV Next Editorial Board Member and attending physician in the division of hepatology at the Annette C. and Harold C. Simmons Transplant Institute, Baylor All Saints Medical Center, Baylor University Medical Center, Dallas. He can be reached at 1250 8th Ave., Suite 515, Fort Worth, TX 76104; email: stevan.gonzalez@baylorhealth.edu.
Disclosure: Gonzalez reports serving on speaker’s bureaus and advisory boards for Gilead.

The emergence of direct-acting antiviral therapy has transformed the management of chronic hepatitis C virus infection. The availability of telaprevir and boceprevir in 2012, followed recently by simeprevir (Olysio, Janssen Therapeutics) and sofosbuvir (Sovaldi, Gilead), has provided clinicians with more highly effective and well-tolerated treatment options. An important subgroup of patients who have historically experienced the greatest challenges in HCV therapy are those with cirrhosis awaiting liver transplantation. Although these individuals may have the most to gain by achieving viral eradication, they have also been faced with lower efficacy, poor tolerance and safety concerns while undergoing therapy.

Stevan A. Gonzalez

Chronic HCV remains the most common chronic blood-borne infection in the United States, with an estimated prevalence of 5 million individuals. It accounts for two-thirds of newly diagnosed chronic liver disease and is the leading indication for liver transplantation. Although the overall US prevalence of HCV infection is expected to decline, the proportion of individuals with cirrhosis is on the rise. Consequently, the proportion of liver transplants for hepatocellular carcinoma (HCC) attributed to chronic HCV has progressively increased over the last decade (see Figure 1). In light of these trends, HCV will continue to be a major source of liver-related mortality as the prevalence of clinical decompensation and HCV-associated HCC is projected to increase further over the next few decades.

Figure 1. 

Figure 1. The most common indications for liver transplantation in the United States in 2013.
*Approximately one-half of transplant recipients with HCC have underlying chronic hepatitis C virus.
Abbreviations: HCC, hepatocellular carcinoma; NAFLD, nonalcoholic fatty liver disease; PSC, primary sclerosing cholangitis; PBC, primary biliary cirrhosis.
Data obtained from the US Organ Procurement and Transplantation Network and the Scientific Registry of Transplant Recipients (optn.transplant.hrsa.gov/).

Source: Gonzalez SA

As recurrence of HCV is universal in liver transplant recipients with HCV infection at the time of transplantation, efforts to achieve viral eradication prior to transplant could significantly improve outcomes. Recurrent HCV infection can lead to allograft dysfunction, chronic hepatitis and progressive fibrosis, resulting in cirrhosis within 5 years in up to 30% of individuals. The development of cirrhosis in this setting is associated with rapid progression and a high risk for clinical decompensation. Although it occurs in less than 10% of patients, a rapidly progressive form of recurrent HCV known as fibrosing cholestatic hepatitis C can develop within the first 6 months following transplantation and may lead to allograft failure within 1 year. As a result, the presence of HCV infection has remained an independent risk factor for increased mortality in liver transplant recipients.

Challenges of Interferon-Based Therapy

Antiviral therapy involving interferon-alfa (IFN) has presented a major challenge to patients with advanced HCV-associated liver disease due to its poor tolerability and increased risk for adverse events, particularly in patients with cirrhosis awaiting liver transplantation. Prior to the advent of direct-acting antiviral (DAA) therapy, several small studies evaluated the potential role of IFN-based therapy in patients with advanced liver disease, including liver transplant candidates. These studies found that if HCV RNA clearance can be achieved immediately prior to undergoing liver transplantation, a post-transplant sustained virologic response can occur in 42% to 75% of patients (see Figure 2). However, these studies also demonstrated a significant increase in the risk for adverse events associated with IFN in this population, including bacterial infection and pancytopenia. As a result, dose reductions and treatment interruptions were common. Although clinical decompensation of liver disease was frequently reported in these studies, the incidence was similar between treated patients and controls.

Figure 2. 

Figure 2. Post-transplant SVR in patients achieving negative HCV RNA at the time of transplantation.
*In patients with at least 4 weeks of viral negativity prior to undergoing transplant, post-transplant SVR occurred in 96% (24/25).
Abbreviations: IFN, standard interferon-alfa; RBV, ribavirin; PEG, pegylated interferon-alfa; SOF, sofosbuvir.

Source: Gonzalez SA

The first prospective, randomized, controlled trial evaluating pre-transplant antiviral therapy in patients with chronic HCV involved a cohort of patients from the Adult-to-Adult Living Donor Liver Transplantation Cohort Study (A2ALL). Patients enrolled were randomized 2:1 to receive treatment with pegylated interferon-alfa (PEG) plus ribavirin (RBV) or no treatment. As potential living donor liver transplant recipients and patients with HCC who met criteria for model end-stage liver disease (MELD) exception points, participants in this trial were considered ideal for evaluating treatment efficacy based on a lower prevalence of clinical decompensation and a predictable or shortened waitlist time. Although this select group had a mean Child-Turcotte-Pugh (CTP) score of 7 and MELD score of 12, pre-transplant serious adverse events occurred in almost one-half of treated patients, with a significant increase in cytopenia and infection compared with controls. A key finding in this study was an association between duration of pre-transplant therapy and virologic response, in which SVR was achieved in 50% of patients who maintained therapy for greater than 16 weeks while SVR did not occur in any patient treated for less than 8 weeks.

PAGE BREAK

Experience with Protease Inhibitors

Although not specifically targeting a pre-transplant population, the largest experience with protease inhibitors in patients with advanced HCV-associated liver disease has arisen from the French Compassionate Use of Protease Inhibitors in Viral C Cirrhosis (CUPIC) study group. This study involved a cohort of 674 patients with compensated cirrhosis who previously failed antiviral therapy. All were treated with combination PEG, RBV and telaprevir (Incivek, Vertex) or boceprevir (Victrelis, Merck). Safety and response data in 497 patients who completed at least 16 weeks of therapy were recently reported. Approximately 60% of patients received telaprevir, 98% had a CTP classification of A and the mean MELD score was 8. Similar to past experiences with IFN-based therapy in patients with advanced disease, this study noted a high rate of serious adverse events (40% overall), including significant anemia in 29%, requirement for erythropoietin stimulating agents in 51%, hepatic decompensation in 2.4% and six deaths (1.2%), mostly due to severe infections. Factors independently associated with an increased risk for on-treatment clinical decompensation or mortality included thrombocytopenia (platelets ≤100,000/mm3) and hypoalbuminemia (serum albumin <3.5 g/dL).

Telaprevir and boceprevir have not been extensively studied in patients with decompensated cirrhosis or liver transplant candidates in the form of a pre-transplant regimen of antiviral therapy.

Sofosbuvir and Beyond

Sofosbuvir, a nucleotide analogue with inhibitory activity against the HCV NS5B RNA-dependent RNA polymerase, has emerged as a potent DAA with favorable tolerability, efficacy in multiple HCV genotypes, and a high barrier to resistance. The high potency associated with sofosbuvir has led to the availability of effective IFN-free regimens, particularly in patients with genotypes 2 and 3. IFN-free therapy involving sofosbuvir may also be considered for genotype 1 infection in patients who are IFN-intolerant, IFN-ineligible or in those with advanced liver disease. Phase 3 clinical trials in patients treated with combination sofosbuvir and RBV only noted mild increases in fatigue, insomnia and anemia compared with placebo, while the incidence of adverse events did not appear to be increased in those with compensated cirrhosis compared with noncirrhotics. Results from phase 3 studies suggest that the potential for SVR may be slightly diminished in patients with cirrhosis; however, the overall SVR rates remain comparatively high in these patients (see Figure 3).

Figure 3. 

Figure 3. SVR in treatment-naive patients with compensated cirrhosis receiving sofosbuvir-based therapy.
Data shown are based on results from phase 3 clinical trials.
Abbreviations: PEG, pegylated interferon-alfa; RBV, ribavirin; SOF, sofosbuvir.
Sources: Lawitz E. N Engl J Med. 2013; Zeuzem S. The Liver Meeting 2013.

Source: Gonzalez SA

A phase 2, open-label, multicenter, prospective study recently established a role for sofosbuvir in the treatment of patients with chronic HCV awaiting liver transplantation. This study enrolled 61 patients of genotypes 1 through 4 with compensated cirrhosis and HCC awaiting deceased donor liver transplantation. All patients were within Milan criteria for HCC, most were infected with genotype 1 HCV (74%) and most had failed prior IFN-based therapy (75%). All patients received up to 48 weeks of sofosbuvir and RBV. Of 44 patients who received a liver transplant, 41 (93%) achieved viral clearance at the time of transplantation. In patients who had reached week 12 post-transplant, 25 of 39 (64%) achieved SVR (see Figure 2). Most importantly, the only independent predictor of post-transplant viral clearance was the duration of negative serum HCV RNA prior to transplantation, as 24 of 25 (95%) of patients with at least 4 weeks of undetectable HCV RNA achieved SVR.

PAGE BREAK

Sofosbuvir has been studied in combination with other DAA agents in patients with compensated cirrhosis, including simeprevir; however, data are limited. Interim results from a phase 2 clinical trial of sofosbuvir and simeprevir with or without RBV in patients with genotype 1 infection suggest a favorable virologic response associated with this combination. This trial, known as the COSMOS study, included patients with advanced fibrosis who received 12 weeks of therapy. Eighteen patients with compensated cirrhosis were included. Although one-half were prior treatment failures, overall SVR 4 in cirrhotics, defined by negative HCV RNA at 4 weeks following completion of therapy, was observed in 17 of 18 (94%) patients. In light of the small numbers of patients with cirrhosis included in this cohort, it is difficult to ascertain the safety profile associated with this regimen in patients with advanced liver disease.

As antiviral therapy for chronic HCV evolves and promising new DAA agents become available in the near future, our ability to achieve rapid viral clearance with minimal risk for adverse events will continue to improve. This has major implications for special populations including those with advanced cirrhosis, HCC and liver transplant candidates. Achievement of viral eradication at the time of transplantation may significantly improve post-transplant outcomes. Although initiation of antiviral therapy at an early phase following transplantation may also be an option, other factors must be considered including the need for immunosuppressive therapy, risk for allograft dysfunction in the setting of HCV recurrence and the potential for other post-transplant complications. A regimen of sofosbuvir and RBV has now been approved in the treatment of individuals with HCC and compensated cirrhosis secondary to HCV who currently await liver transplantation. Although safety concerns will likely continue to present a challenge in high-risk groups with advanced liver disease, efforts to optimize virologic response and ensure an adequate duration of viral negativity prior to undergoing transplantation may significantly enhance our ability to prevent post-transplant recurrence of HCV.

References:
American Association for the Study of Liver Diseases and Infectious Diseases Society of America. Recommendations for testing, managing and treating hepatitis C. www.hcvguidelines.org. Accessed April 1, 2014.
Bell BP. Am J Gastroenterol. 2008;103:2727-2736.
Carrion JA. J Hepatol. 2009;50:719-728.
Chak E. Liver Int. 2011;8:1090-1101.
Curry MP. Abstract #213. Pretransplant sofosbuvir and ribavirin to prevent recurrence of HCV infection after liver transplantation. Presented at: the 64th Annual Meeting of the American Association for the Study of Liver Diseases; Nov. 1-5, 2013; Washington, D.C.
Davis GL. Gastroenterology. 2010;138:513-521.
Everson GT. Hepatology. 2005;42:255-262.
Everson GT. Hepatology. 2013;57:1752-1762.
Forns X. J Hepatol. 2003;39:389-396.
Hezode C. J Hepatol. 2013;59:434-441.
Jacobson IM. N Engl J Med. 2013;368:1867-1877.
Jacobson IM. Abstract #LB3. SVR results of a once-daily regimen of simeprevir (TMC435) plus sofosbuvir (GS-7977) with or without ribavirin in cirrhotic and non-cirrhotic HCV genotype 1 treatment-naive and prior null responder patients: The COSMOS study. Presented at: the 64th Annual Meeting of the American Association for the Study of Liver Diseases; Nov. 1-5, 2013; Washington, D.C.
Kershenobich D. Liver Int. 2011;31(Suppl 2):4-17.
Lawitz E. N Engl J Med. 2013;368:1878-1887.
Patel K. Abstract #1093. Efficacy and safety of sofosbuvir in patients according to fibrosis stage: An analysis of phase 3 data. Presented at: the 64th Annual Meeting of the American Association for the Study of Liver Diseases; Nov. 1-5, 2013; Washington, D.C.
Watt KD. Am J Transplant. 2010;10:1420-1427.
Wong RJ. Hepatology. 2013;Epub
Zeuzem S. Abstract #1085. Sofosbuvir + ribavirin for 12 or 24 weeks for patients with HCV genotype 2 or 3: The VALENCE trial. Presented at: the 64th Annual Meeting of the American Association for the Study of Liver Diseases; Nov. 1-5, 2013; Washington, D.C.
For more information:
Stevan A. Gonzalez, MD, MS, is an HCV Next Editorial Board Member and attending physician in the division of hepatology at the Annette C. and Harold C. Simmons Transplant Institute, Baylor All Saints Medical Center, Baylor University Medical Center, Dallas. He can be reached at 1250 8th Ave., Suite 515, Fort Worth, TX 76104; email: stevan.gonzalez@baylorhealth.edu.
Disclosure: Gonzalez reports serving on speaker’s bureaus and advisory boards for Gilead.