We assessed the effects of sustained viral response (SVR), after treating with interferon–ribavirin (IF-RB), on mortality, liver-related (LR) events (decompensation, hepatocellular carcinoma), HIV progression, and liver stiffness in HIV/hepatitis C virus (HCV)-coinfected patients with nonadvanced liver fibrosis.
From a cohort of HIV/HCV-coinfected patients treated with IF-RB, we selected those with baseline liver fibrosis stages F0, F1, or F2 according to METAVIR. The study started when IF-RB was stopped and ended at death or at the last follow-up visit.
A total of 695 patients were included (HCV genotype 1 or 4, 431; F0, 77; F1, 290; and F2, 328), and 274 patients achieved SVR. After a median follow-up of 4.9 years, the adjusted hazard ratio (aHR) [95% confidence interval (CI)] of LR events or overall death, for patients with SVR taking the group of patients with no SVR as a reference was 0.217 (0.079 to 0.599) (P = 0.003) for the whole cohort with F0 to F2. For patients with F0, the aHR (95% CI) was 0.514 (0.040 to 6.593) (P = 0.609), for patients with F1, the aHR (95% CI) was 0.305 (0.053 to 1.762) (P = 0.185), and for patients with F2, it was 0.075 (0.009 to 0.662) (P = 0.020). We also found that, in comparison with no SVR, SVR was followed by less frequent HIV progression for the entire population (F0 to F2) and less frequent liver stiffness across all categories of fibrosis.
SVR in HIV/HCV-coinfected patients with moderate stages of liver fibrosis is associated with a reduction of mortality and LR events, and with a reduction of progression of HIV and liver fibrosis.
*Department of Infectious Diseases, Hospital General Universitario Gregorio Marañón, Madrid, Spain;
†Department of Infectious Diseases, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Madrid, Spain;
‡Department of Infectious Diseases, Hospital Universitario La Paz, Madrid, Spain;
§Department of Infectious Diseases, Instituto de Investigación Sanitaria La Paz (IdiPAZ), Madrid, Spain;
‖Department of Infectious Diseases, Hospital Donostia, San Sebastián, Spain;
¶Department of Infectious Diseases, Hospital Universitari Vall d'Hebron, Barcelona, Spain;
#Hospital Universitario La Fe, Valencia, Spain;
**Department of Infectious Diseases, Hospital Universitario Ramón y Cajal, Madrid, Spain;
††Department of Infectious Diseases, Hospital Clínico San Carlos, Madrid, Spain;
‡‡Department of Infectious Diseases, Hospital Clínico Universitario, Valencia, Spain;
§§Department of Infectious Diseases, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Spain;
‖‖Department of Infectious Diseases, Hospital Universitario La Princesa, Madrid, Spain;
¶¶Department of Infectious Diseases, Hospital Santa Creu i Sant Pau, Barcelona, Spain; and
##Department of Infectious Diseases, Fundación SEIMC-GESIDA, Madrid, Spain.
Correspondence to: Juan Berenguer, MD, PhD, Unidad de Enfermedades Infecciosas/VIH (4100), Hospital General Universitario Gregorio Marañón, Doctor Esquerdo 46, 28007 Madrid, Spain (e-mail: email@example.com).
Supported by grants from the Fundación para la Investigación y la Prevención del SIDA en España (FIPSE) (Refs. 36,443/03, 36,702/07, and 361020/10), by grants from Fondo de Investigacion de Sanidad en España (FIS) (Spanish Health Funds for Research) (Refs. EC07/90,734, PI11/01556, and EC11/241), and by Red de Investigación en SIDA (AIDS Research Network) (RIS). Ref RD12/0017. Dr Juan Berenguer is an investigator from the Programa de Intensificación de la Actividad Investigadora en el Sistema Nacional de Salud (I3SNS) (Refs. INT10/009 and INT12/154).
Presented as an oral communication at the 53rd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC), Denver, CO, September 10–13 (abstract 1499).
The authors have no conflicts of interest to disclose.
Juan Berenguer and Juan González-García contributed equally to this study.
Received December 13, 2013
Accepted March 25, 2014