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Hepatitis C virus (HCV) infection is a leading cause of death in individuals infected with human immunodeficiency virus (HIV), as HCV-related liver disease is accelerated by HIV. Therefore, effective treatment of both diseases is crucial to prevent liver related morbidity and mortality in this population. Fortunately, due to the potent antiretroviral therapy (ART), almost normal life expectancy can be expected if antiviral therapy is commenced before the onset of acquired immunodeficiency syndrome or advanced immunodeficiency. In terms of antiviral therapy for HCV infection, treatment with pegylated interferon and ribavirin had been challenging in HIV infected patients because of severe adverse events, drug-drug interaction as well as low cure rates, with sustained virologic response (SVR) rates ranging from 27% to 40%. Interferon-free all direct-acting antiviral (DAA) has opened a new era of HCV treatment even in patients with HCV/HIV coinfection. The SVR rates in several clinical trials, where various regimens including ledipasvir/sofosbuvir, daclatasvir plus sofosbuvir, sofosbuvir/velpatasvir, glecaprevir/pibrentasvir were used, ranged from 95% to 98%, which is similar to those in patients with HCV monoinfection. The question is that such high SVR rates in coinfected patients in clinical trial settings could be translated in the real-life practice. As is known well, there are strict inclusion and exclusion criteria for patient recruitment in clinical trials. Whereas, patients in real-life setting are quite heterogeneous, have concomitant diseases and medications. Specifically, patients coinfected with HCV/HIV in real clinical setting have a possibility of lower adherence to DAA and drugdrug interaction between DAA and ART medications. More importantly, in clinical trial, only patients with undetectable HIV RNA are enrolled, while in real practice the HIV status is variable. Indeed, the reported SVR rates of coinfected patients in real practice is rather lower than in clinical trials. In a recent prospective Spanish cohort study, the SVR12 rates in subjects with HIV-coinfection treated with DAAs were 86.3% (221/256 patients), which were significantly lower than 94.9% (205/216) in subjects with HCV monoinfection treated with DAAs (p=0.002). In addition, HIV infection was found to be an independent predictor of non-achievement of SVR12 in the multivariate logistic regression analysis. However, it should be noted that around one half (42%, 108/256) of the HCV/HIV coinfected patients received simeprevir + sofosbuvir, which has been associated with treatment failure. In the article by Gayam et al., the efficacy and tolerability of DAAs were retrospectively studied in patients (n=74) with HCV/ HIV coinfection compared to those (n=253) with HCV monoinfection. The black was the most frequent race, accounting for 64.5% of the entire population. There were 68 (20.8%) prior treatment-experienced patients, and the most common genotype was 1a in the both groups (62.2% in coinfection vs 53.4% in monoinfection). The proportion of patients with compensated cirrhosis was comparable (14% vs 23%, p=0.103). Unlike in clinical trials, some coinfected patients had detectable HIV RNA in blood. The overall SVR rates in all the patients were 94%. The SVR was higher in HCV monoinfected patients compared to those with HCV/HIV coinfection (96% vs 86%, p=0.005). In multivariate regression analysis, positive HIV was the only in-

gut and liver

Efficacy of Direct-Acting Antivirals in Patients with Hepatitis C Virus/Human Immunodeficiency Virus Coinfection: A Gap between Clinical Trial and Real Practice