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o. t.i.d.; faldaprevir: 240?mg p.o. OD; daclatasvir: http://en.wikipedia.org/wiki/Resveratrol 90?mg p.o. OD [15-17]. The integrase inhibitor raltegravir does not interact significantly with the telaprevir, boceprevir or simeprevir [15, 18, 19]. The HIV protease inhibitors (PI) are more complicated. Atazanavir boosted with ritonavir (/r) is considered to be an acceptable combination with telaprevir, while significant interactions have been noted for lopinavir/r, darunavir/r and fosamprenavir/r [20]. Even if they have been used in the phase II trials, PI should not be combined with boceprevir to avoid HIV escape [21]. Boceprevir reduces lopinavir/r, atazanavir/r and darunavir/r concentrations [22]. Although PI were tested in trials on daclatasvir and faldaprevir for co-infected patients, the dose of the DAA had to be reduced http://www.selleckchem.com/products/DMXAA(ASA404).html in both cases (daclatasvir: 30?mg p.o. OD; faldaprevir: 120?mg p.o. OD) [13, 14]. Darunavir/r is not recommended with simeprevir [15]. Before initiating HCV treatment, it is important to identify if the patient has cirrhosis. Currently PEG-IFN-based regimens are contraindicated in patients with decompensated cirrhosis. Treatment can be attempted in patients with compensated cirrhosis but the patient's medical condition should be optimized first. Cirrhosis should be managed with regular procedures such as screening for hepatocellular carcinoma and oesophageal varices. Historically, didanosine use, bilirubin above the normal limit and pre-existent cirrhosis have been associated with a higher risk of liver decompensation in the treatment of co-infected patients [23]. The CUPIC study evaluated the outcome of mono-infected patients with cirrhosis treated with telaprevir or boceprevir in an early access program. This study found that low albumin ( http://www.selleckchem.com/products/Aloxistatin.html were associated with a significantly increased risk of severe on treatment complications or death [24]. Patients at risk of decompensation should be transferred to a liver transplant centre before beginning treatment of HCV. Criteria for liver transplantation in patients with HIV are much stricter than those for patients without, and not all transplant centres offer liver transplantation to patients with HIV. The Food and Drug Administration (FDA) has recently accepted a SVR at post-treatment week 12 (SVR12) as a primary outcome for clinical trials instead of the previously used SVR24 [25]. In a large cohort of HCV mono-infected patients treated with PEG-IFN/RBV therapy, it has been demonstrated that 12?weeks post-treatment follow-up appears to be as relevant as 24?weeks to define SVR [26]. Even if the data are limited, this new outcome also seems to be acceptable in co-infected patients. A retrospective analysis of the results of APRICOT and PARADIGM have shown that only 2/941 patients treated with combination IFN or PEG-IFN/RBV relapsed between post-treatment weeks 12 and 24 [27].