Treatment as prevention: The breaking of taboos is required in the fight against hepatitis C among people who inject drugs

H igh prevalence and incidence rates contrast starkly with low detection and treatment uptake rates and that makes the hepatitis C epidemic among people who inject drugs (PWID) a serious public health issue. In expectance of new interferon (IFN)-free hepatitis C treatment regimens, Martin et al. present, in this issue of HEPATOLOGY, mathematical model calculations on an approach that is already well documented in the field of human immunodeficiency virus (HIV): treatment as prevention. Because future treatment regimens will be much better tolerated and even more efficient than current IFN-based dual or triple therapies, they have the potential of being widely used to treat PWID. Taking this into account, the model described in this study suggests that scaling up treatment uptake rates for people who inject drugs with the new direct-acting antivirals (DAAs) has the potential to, over time, significantly reduce the prevalence of chronic hepatitis C in this, so far, heavily underserved population. However, to increase treatment uptake rates in this major at-risk group requires drastic changes on several levels as well as the breaking of some taboos. Martin et al. calculated the necessary scale-up rates among PWID to half the prevalence of hepatitis C virus (HCV) infections within the next 15 years. Their mathematical model has been applied to a variety of settings and takes into account different levels of baseline prevalence and treatment uptake as well as the varying levels of primary prevention measures, such as the provision of sterile injection equipment and opioid substitution therapy. In settings with a high baseline chronic prevalence, such as in Melbourne, Australia (50%) and Vancouver, Canada (65%), the use of future DAAs over the next 15 years would, at the current treatment rates, only have a very low effect on prevalence (less than 2%). A 13to 15-fold increase of treatment uptake would be needed to half the prevalence in these settings. With a chronic baseline prevalence of 25%, such as in Edinburgh, Scotland, a mere 3-fold increase in treatment provision could reduce chronic HCV prevalence to less than 7%. As discussed by the researchers, various programs have proven that such annual numbers of treatment uptake rates are, in fact, feasible. However, from a more global point of view, such programs remain isolated examples of best practice in their respective regions and have, so far, had no relevant effect on the epidemic. Many Western countries show similar hepatitis C prevalence levels to the ones in Melbourne and Vancouver, with similarly low levels of treatment uptake rates, but with reasonably high coverage of primary prevention measures. To achieve nationwide treatment uptake rates among PWID that relevantly affect prevalence, groundbreaking changes in the currently inefficient HCV care system for this vulnerable population are urgently needed. First, and easiest to achieve: treating patients irrespective of their liver fibrosis stage, which is, in effect, treatment as primary prevention. Today, in many countries, fibrosis stage of at least F2 is a prerequisite to obtain antiviral treatment. Second, a paradigm shift concerning reinfection must be made: Risk of reinfection is one of the most mentioned reasons why PWID are not treated. Looking closely at the model of Martin et al., risk of reinfection actually becomes an indication for treatment because people at risk of reinfection are also the most likely to further spread the virus. From a public health perspective, treating those at high risk of reinfection should be a priority and, if indicated, they should be treated repeatedly. Similar model calculations for dualcombination therapies with pegylated IFN and ribavirin have shown that this is a cost-effective approach and, in Abbreviations: DAAs, direct acting antivirals; HCV, hepatitis C virus; HIV, human immunodeficiency virus; IFN, interferon; PWID, people who inject drugs. Address reprint requests to: Philip Bruggmann, M.D., Arud Centres for Addiction Medicine, Konradstrasse 32, 8005 Z€ urich, Switzerland. E-mail: p.bruggmann@arud.ch; fax: 1058-360-50-19. Copyright VC 2013 by the American Association for the Study of Liver Diseases. View this article online at wileyonlinelibrary.com. DOI 10.1002/hep.26539 Potential conflict of interest: The author has served as advisor/speaker for and has received project and research grants from Roche, MSD, Janssen, Abbott, Gilead, Viif and Bristol-Myers Squibb.