Reply to Menard et al

To the Editor—I thank Amélie Menard and colleagues for their interest in my article and for pointing out that the data I reviewed came from clinical trials rather than “real-life” treatment cohorts [1]. Participants in clinical trials are often highly motivated patients with few comorbidities and concomitant medications, and they are usually seen at a higher frequency than patients treated outside clinical trials. Several studies have reported lower hepatitis C virus (HCV) sustained virological response (SVR) rates in real-world cohorts compared with results obtained with the same direct-acting antiviral (DAA)-containing regimens in clinical trials [2–4], especially with interferon-containing therapy [2, 3]. However, recent data suggest that SVR rates in real-world patients treated with current the American Association for the Study of Liver Diseases and the Infectious Diseases Society of America recommended interferon-free therapy for genotype 1 do not have lower SVR rates than observed in clinical trials [5]. The principal thrust of my article was that human immunodeficiency virus (HIV)-coinfected patients have the same SVR rates as do HCV monoinfected patients treated with the same anti-HCV regimen, at least in clinical trials. Thus, the issue is not so much whether there is a reduced SVR rate in real world patients, but rather whether there is a differential in SVR rates between HCV monoinfected patients and HIV-HCV coinfected patients in the real world. Menard and colleagues report on 55 HIV-HCV coinfected patients treated for HCV with sofosbuvir-containing therapy, of whom 2 received interferon, and observed an SVR rate of 94.5% (52/55), similar to that observed in clinical trials [1]. Schaerer and colleagues similarly observed that the SVR rate in HCV genotype 1-HIV coinfected patients treated with an HCV protease inhibitor in combination with pegylated interferon plus ribavirin in the Swiss Cohort Study was similar to that observed in clinical trials [6]. Two groups of investigators have reported similar SVR rates in HCV genotype 1 monoinfected patients and HCV genotype 1-HIV coinfected patients treated with telaprevir plus pegylated interferon and ribavirin in the very same clinic [7, 8], thereby showing no differential in SVR rate between the HCV monoinfected and the HIV-HCV coinfected in a real-world setting. The report by Menard and colleagues is consistent with data from Switzerland [6], the United States [7], and Canada [8] in demonstrating that HIV-HCV coinfected patients have similar SVR rates as HCV monoinfected patients in real-world practice using DAA-containing therapy and, therefore, taking a different approach to treating HCV in the HIV-coinfected compared with the HCV monoinfected (“HIV exceptionalism”) is unjustifiable. Potential conflict of interest. Author certifies no potential conflicts of interest. The author has submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.

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