Virological response and resistance mutations to NS3/4A inhibitors in hepatitis C virus-human immunodeficiency virus coinfection

作     者：Alissa Naqvi Valérie Giordanengo Brigitte Dunais Francine de Salvador-Guillouet Isabelle Perbost Jacques Durant Pascal Pugliese Aline Joulié Pierre Marie Roger Eric Rosenthal 

作者机构：Infectious Diseases Department Archet Hospital Centre Hospitalier Universitaire Virology Laboratory Archet Hospital Centre Hospitalier Universitaire Internal Medicine Department Archet Hospital Centre Hospitalier Universitaire 

出 版 物：《World Journal of Hepatology》 (世界肝病学杂志（英文版）（电子版）)

年 卷 期：2015年第7卷第18期

页      面：2177-2183页

学科分类：1004[医学-公共卫生与预防医学(可授医学、理学学位)] 100401[医学-流行病与卫生统计学] 10[医学] 

基　　金：Abbvie Bristol-Myers Squibb Gilead Sciences Inc Janssen Merck 

主　　题：Telaprevir Boceprevir Hepatitis C virushuman immun 

摘      要：AIM: To evaluate virological response to telaprevir or boceprevir in combination with pegylated interferon and ribavirin and resistance mutations to NS3/4A inhibitors in hepatitis C virus-human immunodeficiency virus(HCV-HIV) coinfected patients in a real life setting. METHODS: Patients with HCV genotype 1-HIV coinfection followed in Nice University Hospital internal medicine and infectious diseases departments who initiated treatment including pegylated interferon and ribavirin(Peg IFN/RBV) + telaprevir or boceprevir, according to standard treatment protocols, between August 2011 and October 2013 entered this observational study. Patient data were extracted from an electronic database(Nadis®). Liver fibrosis was measured by elastometry(Fibroscan®) with the following cut-off values: F0-F1: 7.1 k Pa, F2: 7.1-9.5 k Pa, F3: 9.5-14.5 k Pa, F4: ≥ 14.5 k Pa. The proportion of patients with sustained virological response(SVR) twelve weeks after completing treatment, frequency and type of adverse events, and NS3/4A protease inhibitor mutations were described. RESULTS: Forty-one patients were included: 13(31.7%) patients were HCV-treatment na?ve, 22(53.7%) had advanced liver fibrosis or cirrhosis(Fibroscan stage F3 and F4); none had decompensated cirrhosis or hepatocellular carcinoma; all were receiving antiretroviral treatment, consisting for most them(83%) in either a nucleoside reverse-transcriptase inhibitor/protease inhibitor or/integrase inhibitor combination; all patients had undetectable HIV-RNA. One patient was lost to follow-up. SVR was achieved by 52.5% of patients. Five patients experienced virological failure during treatment and four relapsed. Seven discontinued treatment due to adverse events. Main adverse events included severe anemia(88%) and rash(25%). NS3/4A protease mutations were analyzed at baseline and at the time of virological failure in the 9 patients experiencing non-response, breakthrough or relapse. No baseline resistance mutation cou