Recommended
2018
HCV Genotypes/Treatment
Offered on this page is current research with a focus on treating HCV according to genotype using FDA approved medicines. Information is extracted from news articles, peer-reviewed journals, as well as liver meetings/conferences, research manuscripts and interactive learning activities.
2018
Research Articles
Current full text articles covering every aspect of hepatitis C.
This article is now archived and will no longer be updated.
Conference Coverage
The Liver Meeting® 2017
Friday, October 20, 2017 - Tuesday, October 24, 2017
Liver Meeting 2017: I'm A HCV Patient - Show Me What I Need To Know!
I highly suggest you follow Henry E. Chang on Twitter if you are interested in reading full text articles about hepatitis C.
Hepatitis C Treatment: What to Expect in 2017
*Article; Hepatitis C Treatment: What to Expect in 2017 - is located further down this page following current updates with key data on the treatment and management of the hepatitis C virus.Hepatitis C Treatment: What to Expect in 2017
Research Articles
Dec 1, 2017
2017 December
Summary from AASLD 2017 for Hepatitis C HCV: Game over?
November 17, 2017
October 2017
The changing HCV treatment cascade Although the IDSA/AASLD guidelines provide the map to managing HCV, they do not identify the ideal interferon-free regimen to begin with, nor have they given a clear path to treating genotype 3 and those with decompensated cirrhosis. This ever-changing field will require collaboration among health care providers, including those specializing in infectious diseases, hepatology and gastroenterology, as well as pharmacists, to optimize treatment strategies. As the landscape of HCV continues to update with new literature and new medications, this subspecialty continues to be dynamic.
High sustained virological response rates using imported generic direct acting antiviral treatment for hepatitis C
This analysis assessed the efficacy of generic imported DAAs.
Oct 5, 2017
September 2017
AASLD IDSA
HCV Guidance Updates
Recommendations Reflecting Vosevi and Mavyret.
Stay current with all guideline updates, "click here."
Updated - Geno 1 & 3 Treatment-Naïve & Treatment-Experienced
Read more click here.....
September 22, 2017
“Sofosbuvir-Velpatasvir-Voxilaprevir for Chronic Hepatitis C – A Review”
Gastroenterology & Hepatology.AASLD IDSA
HCV Guidance Updates
Recommendations Reflecting Vosevi and Mavyret.
Stay current with all guideline updates, "click here."
Updated - Geno 1 & 3 Treatment-Naïve & Treatment-Experienced
Read more click here.....
September 22, 2017
“Sofosbuvir-Velpatasvir-Voxilaprevir for Chronic Hepatitis C – A Review”
Chronic hepatitis C virus infection: Everyone should be treated
Authors Steven Flamm
First Published: 29 September 2017
Abstract
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References
Watch a video presentation of this article
Watch the interview with the author
Abstract
Full Text (HTML)
PDF (91.3KB)
PDF (91.3KB)
References
Watch a video presentation of this article
Watch the interview with the author
Aug 26, 2017
The new paradigm in the treatment of chronic hepatitis C disease: Faster, Higher and Stronger
Systematic review: cost-effectiveness of DAAs for treatment of HCV genotypes 2-6
Aug 17, 2917
Which Hepatitis C Treatment to Start in 2017 - Are All Treatments Created Equal?
FDA Update
Aug 3, 2107
FDA Approved - MAVYRET AbbVie Receives U.S. FDA Approval of MAVYRET™ (glecaprevir/pibrentasvir) Aug 1, 2017
FDA Approves Expanded Labeling for Epclusa® for Hepatitis C in Patients Co-Infected with HIV
FDA Update
July 18, 2017
FDA Approved Gilead's VoseviTM
Sofosbuvir/Velpatasvir/Voxilaprevir
Genotype 1, 2, 3, 4, 5 or 6 - Re-treatment of chronic hepatitis C virus
Research Articles
Aug 1, 2017
Viral Hepatitis: The Search for a Cure
Liver International
SOF/VEL in patients with HCV GT 1-6 & compensated cirrhosis or advanced fibrosis
Curr Hepatology Rep
Next-generation direct-acting antiviral drug-based regimens for HCV
Link to PDF full text articles provided by @HenryEChang via Twitter
In chronic HCV infection, oral DAAs have high sustained virologic response
In patients with chronic hepatitis C virus (HCV) infection, what are the efficacy and safety of oral direct-acting antiviral (DAA) regimens?
All patients with chronic HCV infection should undergo a thorough renal survey at diagnosis and receive regular follow-up.
July/August 2017
Understanding HCV drug resistance: Clinical implications for current & future regimens
IAS–USA Topics in Antiviral Medicine
July - 2017
Hepatitis C Therapies Perform Well in Challenging PatientsWilliam F. Balistreri, MD
At this year's Digestive Disease Week, several studies looked into the nuances of treating hepatitis C virus (HCV)infection. Of particular interest were new data regarding difficult-to-treat groups and the validation of shorter, simpler regimens
2017 - June
June 30
Clinical Liver Disease (CLD) just launched; Pangenotypic regimens and the next generation hepatitis C virus therapy a multimedia overview of: Three new antiviral therapies for viral hepatitis C anticipated in the next several months: GP, glecaprevir (protease inhibitor [PI])/pibrentasvir (NS5A inhibitor); SOF/VEL/VOX, sofosbuvir (NS5B inhibitor)/velpatasvir (NS5A)/voxilaprevir (NS3); and MK3, grazoprevir (NS3) + MK-3682 (NS5B) + NS5A inhibitor (elbasvir or Ruzasvir).
June 27
Impact of DAA therapy for treatment of HCV genotypes 1,3 & 4: A real life experience from IndiaJune 22
Listen Or Watch: Mark Sulkowski, MD discuss current treatment options for all HCV genotypes
Listen to Mark Sulkowski, MD discuss HCV screening, diagnosis, noninvasive tests for assessing liver fibrosis and current treatment options for all HCV genotypes (1-6).
June 13, 2017
Digestive Disease Week (DDW) 2017
Nancy S. Reau, MD
Despite the incredible evolution in hepatitis C (HCV) therapeutics, much remains to be done to affect the incidence, prevalence, and morbidity caused by this silent but curable disease. Several presentations at the recent Digestive Disease Week (DDW) meeting offer new perspectives in screening, reinfection, and therapy.
Nancy S. Reau, MD
Despite the incredible evolution in hepatitis C (HCV) therapeutics, much remains to be done to affect the incidence, prevalence, and morbidity caused by this silent but curable disease. Several presentations at the recent Digestive Disease Week (DDW) meeting offer new perspectives in screening, reinfection, and therapy.
2017 - May Updates
May 27May 2017 - Hepatitis C in a New Era: A Review of Current Therapies
Review of recommended HCV regimens according to genotype or comorbid patient conditions
Oral direct-acting agent therapy for HCV infection: A systematic review
May 26
Current therapy for chronic hepatitis C: The role of direct-acting antivirals.
Antiviral Res. 2017 Jun;142:83-122. doi: 10.1016/j.antiviral.2017.02.014. Epub 2017 Feb 24.
Highlights
• HCV genotype-specific drugs evolve to pan-genotypic drugs.
• Drug potency increases from moderate (∼60%) to high (>90%) levels of sustained virologic response.
• Treatment durations are shortened from a 48-week to 12-week or 8-week period.
• HCV therapies based upon multiple pills per day are simplified to a single pill per day.
• HCV therapies are administered orally regardless of prior treatment history and cirrhotic status.
May 18
The Changing HCV Landscape: Pangenotypic Regimens
Conference Updates
The International Liver CongressTM 2017April 19-23, 2017
Investigational Regimen of Glecaprevir/Pibrentasvir
April 2017
Direct-acting antivirals: the endgame for hepatitis C? March 2017
Review FDA Approved Therapies
2017 / Hepatitis C: Down but Not Out - Oral Direct-Acting Agent Therapy for HCV
Of Interest - Mar 2017
Care of Patients Who Have Achieved a Sustained Virologic Response (SVR) Following Antiviral Therapy for Chronic Hepatitis C Infection
Clinical efficacy and tolerability of direct-acting antivirals in elderly patients with chronic hepatitis C
Delaying HCV treatment regardless of fibrosis stage may be detrimental given increased risk of mortality
November 2016
Summary for AASLD 2016 for Hepatitis C - New HCV two and three drug regimens on their way: what do they promise? And what do clinicians need to look out for under DAA combination therapy and beyond SVR?
Abbvie dual combination Glecaprevir /Pibrentasvir
Gilead fixed dose combination SOF/VEL/VOX
Merck fixed-dose combination tablet MK3 (MK-3682/grazoprevir/ruzasvir)
_______________________________________________
ARC Journal of Hepatology and Gastroenterology
Volume-1 Issue-1, 2016, Page No: 9-16 ARC Journal of Hepatology and Gastroenterology
Hepatitis C Treatment: What to Expect in 2017
Andreia Gi1, Ana Miguel Matos1,2, Cristina Luxo1,2
Abstract
Hepatitis C virus infection is a substantial health problem on a global scale [1] It is estimated that approximately 185 million people live with hepatitis C worldwide, with 350,000–500,000 patients dying each year from liver disease associated with hepatitis C[2]. However, something is about to change. In the latest years, there has been a shift in treatment paradigm due to the discovery and approval of direct-acting antiviral agents [3]. Nevertheless, these regimens still included ribavirin, which increased side effects, cost, and inconvenience of treatment. Moreover, improved treatment options for patients who did not respond to prior direct-acting antiviral agents (and may have drug-resistant virus) and for hepatitis C virus genotype 3 infection, with or without cirrhosis, were desirable. Thus, three new promising direct-acting antiviral agents were developed to fulfill these significant unmet medical needs [4,5]
In many countries, sustainability has been the buzzword across all stakeholders. Still, direct-acting antiviral agents have demonstrated a favorable cost-effectiveness profile [6] and their exceptional cure rates have already helped establish the concept that chronic hepatitis C virus infection can be cured in most, if not all, affected individuals.
This review summarizes the clinical potential of velpatasvir-sofosbuvir, velpatasvir-voxilaprevir-sofosbuvir and glecaprevir-pibrentasvir, discussing key results and future directions. Its aim is to highlight the significance of a future free from hepatitis C.
Keywords: Hepatitis C Virus, Direct-Acting Antiviral Agents, Sustained Virologic Response, Cure, Difficult-To- Treat Populations
In many countries, sustainability has been the buzzword across all stakeholders. Still, direct-acting antiviral agents have demonstrated a favorable cost-effectiveness profile [6] and their exceptional cure rates have already helped establish the concept that chronic hepatitis C virus infection can be cured in most, if not all, affected individuals.
This review summarizes the clinical potential of velpatasvir-sofosbuvir, velpatasvir-voxilaprevir-sofosbuvir and glecaprevir-pibrentasvir, discussing key results and future directions. Its aim is to highlight the significance of a future free from hepatitis C.
Keywords: Hepatitis C Virus, Direct-Acting Antiviral Agents, Sustained Virologic Response, Cure, Difficult-To- Treat Populations
Abbreviations
HCV - Hepatitis C virus
HCC - Hepatocellular carcinoma
SVR - Sustained Virologic Response
IFN - Interferon
RBV - Ribavirin
DAAs - Direct-acting antiviral agents
SOF – Sofosbuvir
VEL – Velpatasvir
VOX - Voxilaprevir
HCV - Hepatitis C virus
HCC - Hepatocellular carcinoma
SVR - Sustained Virologic Response
IFN - Interferon
RBV - Ribavirin
DAAs - Direct-acting antiviral agents
SOF – Sofosbuvir
VEL – Velpatasvir
VOX - Voxilaprevir
Introduction
The Hepatitis C virus (HCV) is a small-enveloped virus of the Flaviridae family and genus Hepacivirus, [7] with a single-stranded positive RNA molecule of approximately 9.6 kb [8]. Prior to the discovery of the viral agent, HCV was mainly transmitted via blood products. Since then, injection drug use has arisen as the major mode of transmission in developed countries [2]
The main problem is that, following exposure to HCV, only a minority of patients clears the acute infection, whereas 80% persist with life-long chronic viremia[9] Chronic HCV infection is a serious, progressive, and potentially life-threatening disease [10,11] If left untreated, over time it can cause liver damage or failure due to the development of cirrhosis. This liver complication can lead patients at substantial risk of decompensated disease and hepatocellular carcinoma (HCC), [12] which impose a considerable burden on affected people, healthcare systems and society [13,14] Early diagnosis could help prevent these consequences, but HCV infection is often undiagnosed because it is usually asymptomatic during decades and so, the majority of HCV-infected individuals are unaware of their infection [15].
The goal of treatment in all infected individuals, regardless of which of the six major genotypes are present, remains the achievement of a sustained virologic response (SVR) in which circulating HCV RNA is undetectable (with the use of a highly sensitive assay) following treatment. When a SVR is achieved, there is a 99% chance that the hepatitis C infection is cured [13,16]. Historically, SVR was defined as HCV RNA levels below a designated threshold of quantification 24 weeks after completion of treatment (SVR24)[17]. However, more recent data shows that viral clearance 12 weeks post-treatment (and sometimes, even 8 weeks) correlates closely to SVR24[18]. Therefore, an undetectable HCV RNA at 12 weeks after treatment (SVR12) is considered an appropriate primary efficacy endpoint [19] and translates into “cure” for nearly all patients[13]
The main problem is that, following exposure to HCV, only a minority of patients clears the acute infection, whereas 80% persist with life-long chronic viremia[9] Chronic HCV infection is a serious, progressive, and potentially life-threatening disease [10,11] If left untreated, over time it can cause liver damage or failure due to the development of cirrhosis. This liver complication can lead patients at substantial risk of decompensated disease and hepatocellular carcinoma (HCC), [12] which impose a considerable burden on affected people, healthcare systems and society [13,14] Early diagnosis could help prevent these consequences, but HCV infection is often undiagnosed because it is usually asymptomatic during decades and so, the majority of HCV-infected individuals are unaware of their infection [15].
The goal of treatment in all infected individuals, regardless of which of the six major genotypes are present, remains the achievement of a sustained virologic response (SVR) in which circulating HCV RNA is undetectable (with the use of a highly sensitive assay) following treatment. When a SVR is achieved, there is a 99% chance that the hepatitis C infection is cured [13,16]. Historically, SVR was defined as HCV RNA levels below a designated threshold of quantification 24 weeks after completion of treatment (SVR24)[17]. However, more recent data shows that viral clearance 12 weeks post-treatment (and sometimes, even 8 weeks) correlates closely to SVR24[18]. Therefore, an undetectable HCV RNA at 12 weeks after treatment (SVR12) is considered an appropriate primary efficacy endpoint [19] and translates into “cure” for nearly all patients[13]
2. Direct-Acting Antiviral Agents Versus Interferon-Based Therapies
The new regimens for HCV mean a breakthrough novelty in the history of anti-HCV treatment. Previous treatments for HCV were often long and difficult. Many lasted from 24 to 48 weeks and showed suboptimal efficacy in viral response with a range of commonly occurring significant side effects, which impaired therapeutic compliance[20]. Nowadays, HCV patients can benefit from a less complex administration schedule and expect interferon (IFN) and even ribavirin (RBV)-free combinations. This results in a reduction of the incidence and severity of adverse events, optimizing quality of life during therapy and improving adherence to direct-acting antiviral agents (DAAs).
3. Sofosbuvir-Velpatasvir
Sofosbuvir-velpatasvir (EPCLUSA®) is a prescription medicine used to treat adults with chronic (lasting a long time) hepatitis C genotype 1, 2, 3, 4, 5, or 6 infection with or without cirrhosis (compensated). In clinical studies, sofosbuvir-velpatasvir (SOF-VEL) had high overall cure rates. (Table 1) The most common side effects were headache and tiredness [21].
| Clinical Study (Reference) | Number of patients (% cirrhosis) | HCV genotype (%) | Treatment History | SVR12 by Genotype, Cirrhosis and Treatment Experience | ||
| ASTRAL-1 (22) | 740 (19%) | 1 2 4 5 6 | Treatment-naïve and treatment- experienced | SOF - VEL, 12 weeks | Genotype 1a | 98% (206/210) |
| Genotype 1b | 99% (117/118) | |||||
| Genotype 2 | 100% (104/104) | |||||
| Genotype 4 | 100% (116/116) | |||||
| Genotype 5 | 97% (34/35) | |||||
| Genotype 6 | 100% (41/41) | |||||
| Without Cirrhosis | 99% (496/501) | |||||
| With Cirrhosis | 99% (120/121) | |||||
| Treatment- naïve | 99% (418/423) | |||||
| Treatment- experienced | 99% (200/201) | |||||
| ASTRAL-2 (23) | 266(14%) | 2(100%) | Treatment-naïve and treatment- experienced | SOF - VEL, 12weeks | Treatment- naïve without cirrhosis | 99% (99/100) |
| SOF + RBV, 12 weeks | Treatment- naïve without cirrhosis | 96% (92/96) | ||||
| SOF - VEL, 12 weeks | Treatment- naïve with cirrhosis | 100% (15/15) | ||||
| SOF + RBV, 12 weeks | Treatment- naïve with cirrhosis | 93% (14/15) | ||||
| SOF - VEL, 12 weeks | Treatment- experienced without cirrhosis | 100% (15/15) | ||||
| SOF + RBV, 12 weeks | Treatment- experienced without cirrhosis | 81% (13/16) | ||||
| SOF - VEL, 12 weeks | Treatment- experienced with cirrhosis | 100% (4/4) | ||||
| SOF + RBV, 12 weeks | Treatment- experienced with cirrhosis | 100% (4/4) | ||||
| ASTRAL-3 (23) | 552(30%) | 3(100%) | Treatment-naïve and treatment- experienced | SOF - VEL, 12 weeks | Treatment- naïve without cirrhosis | 98% (160/163) |
| SOF + RBV, 24 weeks | Treatment- naïve without cirrhosis | 90% (141/156) | ||||
| SOF - VEL, 12 weeks | Treatment- naïve with cirrhosis | 93% (40/43) | ||||
| SOF + RBV, 24 weeks | Treatment- naïve with cirrhosis | 73% (33/45) | ||||
| SOF - VEL, 12 weeks | Treatment- experienced without cirrhosis | 91% (31/34) | ||||
| SOF + RBV, 24 weeks | Treatment- experienced without cirrhosis | 71% (22/31) | ||||
| SOF - VEL, 12 weeks | Treatment- experienced with cirrhosis | 89% (33/37) | ||||
| SOF + RBV, 24 weeks | Treatment- experienced with cirrhosis | |||||
4. Sofosbuvir-Velpatasvir-Voxilaprevir
Four Phase 3 clinical studies (POLARIS-1, POLARIS-2, POLARIS-3 and POLARIS-4) evaluated a once-daily, fixed-dose combination of sofosbuvir (SOF), a nucleotide analog NS5B polymerase inhibitor; velpatasvir (VEL), a pangenotypic NS5A inhibitor; and voxilaprevir (VOX; GS-9857), an investigational pangenotypic NS3/4A protease inhibitor, for the treatment of genotype 1,2,3,4,5 and 6 chronic HCV infection. (Table 3)
The most common adverse events among patients who received SOF-VEL-VOX were headache, fatigue, diarrhea and nausea. The overall incidence of adverse events was similar to placebo or SOF- VEL. Among the 1,056 patients who received SOF-VEL-VOX in the four studies, only a patient receiving SOF-VEL-VOX for 12 weeks discontinued due to an adverse event[26]. These results show that this new three-drug co-formulation with different mechanisms of action and high barrier to resistance can provide high cure rates for patients who had previously failed treatment with other DAAs.
Table 2. Summary of clinical studies of sofosbuvir-velpatasvir in special populations
| Clinical Study (Reference) | Number of patients (% cirrhosis) | HCV genotype (%) | Treatment History | SVR12 by Genotype, Cirrhosis status and Treatment history | ||
| ASTRAL-4 (24) | 267 | 1 2 4 5 6 | Treatment- naïve and treatment- experienced | SOF - VEL, 12 weeks | Genotype 1 | 88% (60/68) |
| Genotype 3 | 50% (7/14) | |||||
| Genotypes 2,4 and 6 | 100% (8/8) | |||||
| SOF - VEL + RBV, 12 weeks | Genotype 1 | 96% (65/68) | ||||
| Genotype 3 | 85% (11/13) | |||||
| Genotypes 2,4 and 6 | 100% (6/6) | |||||
| SOF - VEL, 24 weeks | Genotype 1 | 92% (65/71) | ||||
| Genotype 3 | 50% (6/12) | |||||
| Genotypes 2,4 and 6 | 86% (6/7) | |||||
| ASTRAL-5 (25) | 106(18%) | 1 (74%) 2 (10%) 3 (11%) 4 (5%) | Treatment- naïve and treatment- experienced | SOF - VEL, 12 weeks | Genotype 1a | 95% (62/65) |
| Genotype 1b | 92% (11/12) | |||||
| Genotype 2 | 100% (11/11) | |||||
| Genotype 3 | 92% (11/12) | |||||
| Genotype 4 | 100% (4/4) | |||||
| Without Cirrhosis | 94% (80/85) | |||||
| With Cirrhosis | 100% (19/19) | |||||
| Treatment-naïve | 93% (71/75) | |||||
| Treatment-experienced | 97% (28/29) | |||||
3. Summary of clinical studies of sofosbuvir-velpatasvir-voxilaprevir
| Clinical Study (Reference) | Population | Number of patients (% cirrhosis) | HCV Genotype | Treatment | Duration | SVR12 Rates |
| POLARIS- 1 | Patients who failed prior treatment with an NS5A inhibitor. The most common prior NS5A inhibitors were ledipasvir (55%) and daclatasvir (23%). | 415 (41% hadcirrhosis) | 1 2 4 5 6 | SOF- VEL- VOX | 12 weeks | 96% (253/263) |
| Placebo | 12 weeks | 0% (0/152) | ||||
| POLARIS- 2(26) | DAA-naïve 23% hadpreviouslyfailedtreatmentwithan IFN-basedregimen. | 941 (18% had cirrhosis) | 1 2 4 5 6 | SOF- VEL- VOX | 8 weeks | 95% (476/501) |
| SOF-VEL | 12 weeks | 98% (432/440) | ||||
| POLARIS- 3 (26) | DAA-naïve 31% hadpreviouslyfailedtreatmentwithan IFN-basedregimen. | 219 (100% had cirrhosis) | 3 | SOF- VEL- VOX | 8 weeks | 96% (106/110) |
| SOF-VEL | 12 weeks | 96% (105/109) | ||||
| POLARIS- 4 (26) | Patients with prior DAA experience that did not include an NS5A inhibitor. Mostpatients (85%) had prior DAA experiencewith SOF. | 333 (46% hadcirrhosis) | 1 2 3 4 | SOF- VEL- VOX | 12 weeks | 97% (177/182) |
5. Glecaprevir-Pibrentasvir
Glecaprevir-pibrentasvir is an investigational, pan-genotypic regimen that is being evaluated (table 4) not only as a potential cure in 8 weeks for HCV patients without cirrhosis and who are new to treatment, but also in patients with specific treatment challenges, such as genotype 3, patients who were not cured with previous DAA treatment and those with chronic kidney disease, including patients on dialysis.
This investigational, pan-genotypic regimen of glecaprevir-pibrentasvir is showing to be well tolerated with a favorable safety profile in these difficult-to-treat populations. The most commonly reported adverse events included fatigue and nausea.
Table 4. Summary of clinical studies of glecaprevir-pibrentasvir
| Clinical Study (Reference) | Patient Population | Treatment | Duration | SVR12 Rates |
| ENDURANCE-1 (27) | Genotype 1 without cirrhosis, naïve or not cured with previous IFN- based treatments (pegIFN +/- RBV or SOF/RBV +/- pegIFN), and patients co-infected with HIV-1. | glecaprevir- pibrentasvir | 8 weeks | 99% (348/351) |
| ENDURANCE-3 (27) | Genotype 3 withoutcirrhosis, naïve. | glecaprevir- pibrentasvir | 8 weeks | 95% (149/157) |
| SURVEYOR-II, part 3 (28) | Genotype 3 with compensated cirrhosis and/or prior treatment experience. | glecaprevir- pibrentasvir | 8 weeks | 96% |
| SURVEYOR-II, part 4 (27) | Genotypes 2, 4, 5, 6 without cirrhosis, naïve or not cured with previous IFN-based treatments (pegIFN, SOF/RBV or pegIFN/SOF). | glecaprevir- pibrentasvir | 8 weeks | 97% (196/203) |
| EXPEDITION-4 (29) | Patients with genotypes 1 to 6 chronic HCV infection and stage 4 and 5 CKD, with an eGFR< 30 mL/min/1.73 m2), including 85 patients (82%) who were receiving dialysis at enrollment and 20 patients (19%) who had compensated cirrhosis. It also included patients who were not cured with previous SOF with RBV or IFN with RBV; with or without SOF (44 patients, 42%). | glecaprevir- pibrentasvir | 12 weeks | 98% (102/104) |
6. Discussion
Although the post-marketing phase always requires a careful evaluation of data from the “everyday” clinical practice experience, clinical trials have showed that these new DAA combinations have resolved most issues related to HCV treatment compared with the past regimens. Despite the approval of the first DAAs which have provided high cure rates and simplified treatment for most HCV patients, HCV genotype 3-infected patients with cirrhosis, patients with chronic kidney disease and those who have failed previous treatment with DAAs continued to represent an unmet medical need. In the era of velpatasvir-sofosbuvir, velpatasvir-voxilaprevir-sofosbuvir and glecaprevir- pibrentasvir, DAA therapy provides a new way to manage these difficult-to-treat HCV-infected patients, who are at a high risk of serious conditions[30]. They are now contemplated and are therefore expected to have a much better prognosis than they have had until very recently. Perhaps, soon, we may no longer have difficult-to-treat populations.
The advent of new generation oral antiviral therapy has led to major improvements in efficacy and tolerability but has also resulted in an explosion of data with increased treatment choice complexity [31].
Thus, clinicians need more detailed, accurate and timely information in order to choose the right regimen for individual patients and educate them. When they counsel and guide their patients, these ones are less likely to be anxious or resistant about taking steps toward possible cure. However, cure does not prevent reinfection and so, it is crucial to advise patients on measures that will reduce their risk (avoid alcohol intake and sexual and injection risk behaviors, eat a balanced diet and take exercise are some examples).
7. Conclusion
DAAs have shown that it is possible to minimize the spread of HCV and the morbidity and mortality associated with HCV infection[32].
Despite the financial controversy around their high costs, which have served as a major barrier for more widespread use, many stakeholders recognize now their long-term cost-benefits and the advantages of a future free from hepatitis C are manifest.
It is true that patients undergoing treatment need systematic monitoring before, during and after therapy, but these new treatment options have offered them hope and re-awakening. It is a clear evolution compared with the previous IFN-based therapies.
8. Future Directions
At a future time, treatment failure and resistance can occur and become a clinical challenge to be solved[30,33].
However, before them, there are already some questions that should concern us. First one is why is the association of RBV with DAAs, in some cases, increasing the SVR12 rate and shortening the duration of treatment? Then, at what point is it no longer worth treating a patient? Will we have the financial capacity to treat reinfected-patients? Will this simplicity of therapeutic regimen encourage risk behaviors in the future?
References
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