Infection with the HCV is one of the major causes of chronic liver disease with an estimated 184 million persons worldwide positive for HCV antibodies1 and 3–4 million newly infected each year. The situation is worrying in emerging countries of Central and Southeast Asia, North Africa and Middle East with seroprevalence around 3%–5%. Central Africa and Egypt remain regions of very high endemicity with a 25% prevalence in the latter. Hepatitis C is therefore a global health problem with striking inequalities in the access to healthcare and implementation of treatments between world regions.

HCV is an enveloped RNA virus classified into seven genotypes, and virions are found associated to β-lipoproteins in the serum of patients.2 A generally asymptomatic initial infection phase is followed by signs of liver injury after 20–30 years, and patients develop cirrhosis or hepatocellular carcinoma in severe cases for which liver transplantation (LT) is the only alternative. In the absence of preventive vaccine, the current standard of care treatment relies on a combination of interferon α (IFNα) and ribavirin, to which direct-acting antivirals (DAA) have been recently added. DAA target viral enzymes of the replication complex and raise great hopes of eradication in treated patients. At present, filed DAA are only effective on genotype 1, induce viral resistance and severe adverse effects, and their costs are out of reach for patients of emerging countries.3 Novel DAA currently in clinical trials are pan-genotypic and usable in IFN-free regimens in a near-future perspective of all-oral therapies.3 HCV-positive patients undergoing LT experience graft infection and recurrence of hepatitis C, shortening their survival compared with uninfected transplant recipients.4 In these particular clinical cases, antiviral therapies aimed at preventing …