7-10 Genome-wide

find more association studies have demonstrated that genetic variations in the region near the interleukin-28B (IL28B) gene, which encodes interferon-λ3 (IFN-λ3), are associated with chronic HCV treatment response.11-14 In one candidate gene study15 and one genome-wide association study,14 it was demonstrated that genetic variations in the IL28B gene region are also associated with absence of HCV RNA in anti-HCV antibody–positive individuals (presumed spontaneous HCV clearance). However, studies performed to date are limited to chronic infection, lack longitudinal data to enable an examination of the effects of genetic variations in the IL28B gene region on the time to spontaneous HCV clearance, and are cross-sectional Midostaurin mouse in nature. We investigated the effect of genetic variations in the IL28B gene region on time to spontaneous HCV clearance and treatment-response following recent HCV infection in the Australian Trial in Acute Hepatitis C (ATAHC), a prospective trial of the natural history and

treatment of recently acquired HCV infection. AHR, adjusted hazards ratio; ALT, alanine aminotransferase; ATAHC, Australian Trial in Acute Hepatitis C; CI, confidence interval; HCV, hepatitis C virus; HIV, human immunodeficiency virus; IFN-λ3, interferon-λ3; IL-28B interleukin-28B; PEG-IFN, pegylated interferon-α2a; RVR, rapid virological response; SNP, single-nucleotide polymorphism; SVR, sustained virological response. The ATAHC study was a multicenter, prospective cohort click here study of the natural history and treatment of recent HCV infection, as previously described.3 Recruitment of HIV-infected and HIV-uninfected participants was from June 2004 through November 2007. Recent infection with either acute or early chronic HCV infection with the following eligibility

criteria: First positive anti-HCV antibody within 6 months of enrollment; and either: 1 Acute clinical hepatitis C infection, defined as symptomatic seroconversion illness or alanine aminotransferase (ALT) level greater than 10 times the upper limit of normal (>400 IU/mL) with exclusion of other causes of acute hepatitis, at most 12 months before the initial positive anti-HCV antibody; or All participants with detectable HCV RNA during the screening period (maximum 12 weeks) were assessed for HCV treatment eligibility. Participants unwilling to undergo treatment assessment and those with undetectable HCV RNA at screening continued to be followed. From screening, participants were followed for up to 12 weeks to allow for spontaneous HCV clearance and if HCV RNA remained detectable were offered treatment. Participants were then seen at baseline and 12 weekly intervals for up to 144 weeks (individuals receiving HCV treatment were also seen at 4-weekly intervals up to week 12). All study participants provided written informed consent.