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Genetic Variation in IL28B and Treatment-induced Clearance of HCV in HCV/HIV Co-infected Patients
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Reported by Jules Levin
CROI 2010
Jacob Nattermann*1, M Vogel1, A Baumgarten2, U Naumann3, H-J Stellbrink4, M Danta5, C Tural6, R Bruno7, U Spengler1, and J Rockstroh1
1Univ of Bonn, Germany; 2Private Practice, Berlin, Germany; 3Praxiszentrum Kaiserdamm, Berlin, Germany; 4ICH, Hamburg, Germany; 5St Vincent's Clin Sch, Australia; 6Hosp Univ Germans Trias i Pujol, Autonomos Univ of Barcelona, Spain; and 7Univ of Pavia IRCCS, San Matteo Hosp, Italy
Background: Co-infection with the hepatitis C virus (HCV) in HIV-positive patients is a health-problem worldwide. The factors affecting response to HCV-specific therapy are only partly understood at the moment. However, 3 recent reports demonstrated a genetic polymorphism near the IL28B gene, encoding interferon-λ-3, to be strongly associated with response to treatment with pegylated interferon-α and ribavirin in HCV mono-infected patients. Here, we studied whether IL28B gene polymorphism (rs 12979860) affects treatment outcome in HCV/HIV co-infection.
Methods: IL28B genotypes were determined in 183 HCV/HIV co-infected patients treated with pegylated interferon-α, including 65 patients with acute and 118 with chronic hepatitis C. Rates of sustained virological responses (SVR) were compared patients carrying different genotypes. As a control, 137 healthy and 199 HCV mono-infected subjects were studied.
Results: IL28B genotype distribution did not differ significantly between the groups. In HIV/HCV co-infection carriers of C/C genotype had significantly higher SVR rates than patients with other genotypes (C/T and T/T) (58.1% vs 40.6%; P =0.041). Interestingly, this effect reached statistical significance only in HIV+ patients with chronic (50% vs 29%; P =0.04) but not in those with acute (73.3% vs 60%; P =n.s.) hepatitis C.
Conclusions: The IL28B genetic polymorphism has only limited effect on treatment-induced clearance of hepatitis C virus in HCV/HIV co-infected patients. This is in strong contrast to observations in HCV mono-infected patients and may suggest interference of HIV with the interferon-λ signaling pathway.
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