Polymorphisms near the IL28B gene, which code for interferon (IFN)-k3, predict response to pegylated interferon-a (PEG-IFN) and ribavirin treatment in hepatitis C virus (HCV) genotype 1 infected patients. Follow-up studies of the effect of IL28B gene in HCV non-genotype 1 infected patients have almost always used predominantly HCV genotype 2-infected or mixed genotype 2/3-infected cohorts with results partly conflicting with HCV genotype 1. We performed a retrospective analysis of 281 patients infected with HCV genotype 3 for association of response to therapy with IL28B polymorphisms. We found that the HCV genotype 1 responder genotypes at rs12979860 and rs8099917 did not associate with sustained virological response to PEG-IFN/ribavirin therapy. However, the responder genotypes of both SNPs showed association with rapid viral response measured at 4 weeks (rs12979860, P 5 3 3 10 25 ; rs8099917, P 5 3 3 10 24 ). In multivariate analysis, age (<40 years), baseline viral load (<4 3 10 5 IU/mL) and the responder genotypes of SNPs rs12979860 or rs8099917 remained significant independent predictors of rapid viral response to therapy. Furthermore, we show that IL28B polymorphisms are associated with relapse in patients who achieve rapid viral response to PEG-IFN/ribavirin therapy. The responder genotypes also showed association with markers of stage and activity of liver disease, namely high aspartate aminotransferase platelet ratio index (APRI, rs12979860, P 5 0.018; rs8099917, not significant) and high alanine aminotransferase (ALT, rs12979860, P 5 0.002; rs8099917, P 5 0.001), in addition to a high baseline viral load (rs12979860, P 5 1.4 3 10 25 ; rs8099917, P 5 7.3 3 10 26 ). Conclusion: Polymorphisms near the IL28B gene show association with rapid viral response but not sustained viral response to PEG-IFN/ribavirin therapy in HCV genotype 3-infected patients. (HEPATOLOGY 2011;53:746-754)

There are no evidence-based guidelines for the treatment of Mycoplasma genitalium-positive genital infection. In a retrospective survey, we analysed the treatment results of patients tested for M. genitalium at Olafia, Unit for Sexual Transmitted Diseases in Oslo. Out of 10,109 patients, 452 had a positive polymerase chain reaction. Between 72% and 100% of patients in the different treatment groups returned for test of cure after four to five weeks. First-line treatment with 1 g single dose azithromycin had a recovery rate of 79%. It was as effective as an extended five-days' course of azithromycin. Ofloxacin 200 mg b.i.d for 10 days cured 56% and moxifloxacin 400 mg o.d. for seven days as either second-, third- or fourth-line treatment after azithromycin or ofloxacin failure cured 100%. Azithromycin 1 g as a single dose seems to be the best choice of treatment for M. genitalium, with moxifloxacin 400 mg x 1 for seven days if treatment fails.

This data support the hypothesis that M genitalium causes urethritis in women and that M genitalium infection of the genitourinary tract leads to different clinical manifestations depending on whether the site of infection is the urethral or the cervical epithelium.

These data add further evidence to the association of M genitalium infection with NGU and should allow better risk analysis of recent recommendations of not performing urethral smears in asymptomatic men attending STI clinics.

Our results supports the European findings that the MSM population carries a high burden of STIs and that testing the anorectum and oropharynx will identify a significantly higher percentage of infected patients and reservoirs of STIs.