Letter: chronic hepatitis C genotype 3
infection – still a hurdle toward a
direct-acting anti-viral-induced HCV cur

Angarano, G.

Bruno, G.

Milella, M.

Saracino, A.

English

Archivio istituzionale della ricerca - Università di Bari

Letter to the EditorLetter: chronic hepatitis C genotype 3infection – still a hurdle toward adirect-acting anti-viral-induced HCV cure?G. Bruno , M. Milella, G. Angarano & A. SaracinoClinic of Infectious Diseases, University of Bari, Bari, Italy.E-mail: giusbruno85@gmail.comdoi:10.1111/apt.14042SIRS, We read with interest the article of Cornberg et al.1who reported effectiveness and safety of different regimensagainst HCV (hepatitis C virus) genotype (GT) threeinfection from a large real-world experience. Untilrecently, HCV GT3-infection was widely recognised as achallenge in the era of direct-acting anti-virals (DAAs),particularly in cirrhotic and treatment-experienced sub-jects.2 However, treatment options for HCV GT3-infec-tion are rapidly evolving thanks to the recent introductionof sofosbuvir (SOF)+ daclatasvir (DCV)Ribavirin (RBV)and, more recently, sosfosbuvir/velpatasvir in severalcountries.3 These regimens represent the best option forHCV GT3 infection as currently recommended by inter-national guidelines.4In our centre, from February 2015 until December2016, a total of 61 DAA-based regimens were prescribedfor 57 HCV GT3-infected individuals (four patients wereretreated), of whom 14 were HV/HCV co-infected. Cir-rhosis was found in 34/57 subjects (59.6%); no patienthad a decompensated cirrhosis. Forty-six treatments werecompleted and could be evaluated for sustained virologi-cal response (SVR). The following regimens were used:SOF+RBV for 24 weeks in 20 cases; SOF+DCV for 12 or24 weeks in two and five cases respectively; SOF+DCV+RBV for 12 or 24 weeks in 4 and 13 cases, respectively,and SOF+ ledipasvir (LDV)+RBV for 24 weeks in onesubject.SVR12 was achieved in 38/46 cases (82.6%) at theintention-to-treat analysis; 22/24 (91.6%) withSOF+DCVRBV; 15/21 (71.4%) with SOF+RBV; and1/1 (100%) with SOF+LDV+RBV. Among the sevenindividuals who did not obtain SVR, five had a relapse,one cirrhotic patient died because of non-Hodgkin lym-phoma and one discontinued treatment for varicealbleeding and then he was lost to follow-up. Of the fiverelapsers, four underwent retreatment. Clinical character-istics of the seven patients, who had a treatment failureare shown in Table 1.The lower SVR rate in the group of SOF+RBV-treatedpatients compared to other regimens was expected, as 10patients with an advanced liver disease, for whom anti-AP&T invited editorial and correspondence columns are restricted to letters discussing papers that have been publishedin the journal. A letter must have a maximum of 500 words, may contain one table or figure, and should have no morethan 10 references. It should be submitted electronically to the Editors via http://mc.manuscriptcentral.com/apt.Table 1 | Clinical characteristics of HCV GT3-infected patients who failed a DAA-based treatmentN. Age HIV Cirrhosis CPIFN-experienced Therapy Outcome RetreatmentSVR12 afterretreatment1. 55 No Yes B No SOF+DCV (24w) Died (LNH) – –2. 48 No Yes A No SOF+RBV (24w) L-FU – –3. 47 No Yes A Yes SOF+RBV (24w) Relapse SOF+DCV+RBV (24w) Yes4. 57 No Yes A Yes SOF+RBV (24w) Relapse SOF+DCV+RBV (24w) Yes5. 52 Yes Yes A Yes SOF+RBV (24w) Relapse SOF+DCV+RBV (24w) Yes6. 51 Yes Yes A Yes SOF+RBV (24w) Relapse SOF+DCV+RBV (24w) Yes7. 49 Yes No – Yes SOF+DCV (12w) Relapse – –CP, Child–Pugh score; IFN, interferon; SOF, sofosbuvir; DCV, daclatasvir; RBV, Ribavirin; w, weeks; LNH, non-Hodgkin lymphoma;L-FU, lost to follow-up.ª 2017 John Wiley & Sons Ltd1376Alimentary Pharmacology and TherapeuticsHCV treatment could not be further delayed, were trea-ted with this combination because of the non-availabilityof DCV in our centre until July 2015.In agreement with Cornberg, our clinical practiceexperience confirmed that a 24-week course ofSOF+DCVRBV can be already considered a goodoption for GT3-infected patients, including DAA treat-ment-experienced individuals with cirrhosis. Further-more, a recent study reported high rates of SVR (90.5%)also in Child–Pugh score B/C individuals treated withsofosbuvir plus an NS5A inhibitor (daclatasvir or ledi-pasvir).5 In the near future, HCV GT3 treatment optionswill be enriched leading to even higher rates of eradica-tion in patients with advanced liver disease includingthose with renal impairment.6ACKNOWLEDGEMENTDeclaration of personal and funding interests: None.REFERENCES1. Cornberg M, Petersen J, Schober A, et al. Real-world use,effectiveness and safety of anti-viral treatment in chronic hepatitisC genotype 3 infection. Aliment Pharmacol Ther 2017; 45: 688–700.2. Ampuero J, Romero-Gomez M, Reddy KR. Review article: HCVgenotype 3 – the new treatment challenge. Aliment PharmacolTher 2014; 39: 686–98.3. Foster GR, Afdhal N, Roberts SK, et al. Sofosbuvir andvelpatasvir for HCV genotype 2 and 3 infection. N Engl J Med2015; 373: 2608–17.4. EASL recommendations on treatment of hepatitis C 2016.European association for the study of the liver. J Hepatol 2017;66: 153–94.5. Alonso S, Riveiro-Barciela M, Fernandez I, et al. Effectivenessand safety of sofosbuvir-based regimens plus an NS5A inhibitorfor patients with HCV genotype 3 infection and cirrhosis. Resultsof a multicenter real-life cohort. J Viral Hepat 2016. doi: 10.1111/jvh.12648 [Epub ahead of print]6. Gane E, Poordad F, Wang S, et al. High efficacy of ABT-493 andABT-530 treatment in patients with HCV genotype 1 or 3infection and compensated cirrhosis. Gastroenterology 2016; 151:651–659 e1.Aliment Pharmacol Ther 2017; 45: 1376–1377 1377ª 2017 John Wiley & Sons LtdLetter to the Editor

Letter: chronic hepatitis C genotype 3 infection - still a hurdle toward a direct-acting anti-viral-induced HCV cure?

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Letter: chronic hepatitis C genotype 3 infection - still a hurdle toward a direct-acting anti-viral-induced HCV cure?

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