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Hepatitis B virus (HBV) infection was defined by having a positive HBsAg test known for more than 6 months. Analyses of HIV-RNA, find more anti-HCV antibodies, and HBV serology were performed utilising routine techniques at the local virological laboratories. HCV-RNA was analysed in anti-HCV positive individuals with the Roche TaqMan Test (detection limit of 15 IU/ml). HCV genotyping was performed with a line probe assay or an in-house method. Anti-HCV positive patients from the Stockholm area (n = 263) were tested for IL28B rs12979860 SNP with a Taqman-based allele-specific PCR method (Applied Biosystems Inc, Foster City, CA, USA), using the ABI 7500 Fast equipment. Human DNA was extracted from plasma obtained from EDTA blood kept at −70 °C.The SNP was defined as rs12979860 genotype CC, CT or TT genotype. Differences between groups were compared with the χ2 test for categorical variables and the Wilcoxon Rank Sum test for continuous variables. A p value of <0.05 was considered statistically significant. All data were analysed using JMP software version 9.0.0. The study was performed in accordance with the Declaration of Helsinki and was approved by the Regional Ethics committee (Dnr 2010/1782-31). Three patients in the IL28B tested anti-HCV and HCV-RNA positive subgroup spontaneously cleared their chronic hepatitis C infection after introduction of ART. These individuals became HCV-RNA negative without any specific HCV treatment after previously being diagnosed to have chronic HCV infection with at least 2 positive HCV-RNA tests 6 months apart. All three had IL28B genotype CC.Their cases are briefly reported here ( Fig. 1A–C). (1) A 58-year-old homosexual male seroconverted simultaneously for both HIV and HCV genotype 4 in July 2008. He had fluctuating HCV-RNA levels between 847,000, 268,000, and 3,700,000 IU/ml repeatedly during 2008–2010. He had markedly elevated aminotransferases in August 2009 when a liver elasticity measurement by Fibroscan showed a mean elasticity of 16.9 kPa indicating cirrhosis and/or active inflammation. ART (raltegravir, tenofovir, and emtricitabine) was started in February 2010 when his CD4+ T-cell count was 384 × 109/L, but was interrupted after one month due to an ALT flare. At this time his bilirubin value was 83–193 μmol/L (ULN <26), ALT 3.39–6.43 μkat/L (ULN <1.20), AST 6.03–22.82 μkat/L (ULN <0.76), and the HCV-RNA level 225,000 IU/ml. The CD4+ T-cell count was 390 × 109/L. The flare subsided within 2 months (22 months after the HCV diagnosis) and HCV-RNA became negative. He was restarted with the same ART regimen and had no flare reaction. Hereafter, HCV-RNA has repeatedly been tested negative during 2 years (Fig. 1A). These three patients have repeatedly been tested negative for HCV-RNA three times after their first negative HCV-RNA test. Anti-HCV test results were available in 4765/5315 (90%) known HIV infected persons in Sweden.