Hepatitis E virus (HEV) infection is recognised as a major cause of acute hepatitis, with different transmission patterns and disease characteristics depending on regions of the world.1 While human-restricted genotypes, HEV-1 and HEV-2, known as the most pathogenic, cause primarily waterborne epidemics in endemic areas, zoonotic HEV-3 and HEV-4 are mostly transmitted after consumption of contaminated pork meat products in industrialised regions. In the general population, acute HEV infection is usually self-limited and treatment mostly only entails supportive care. However, HEV-3, and to some extent HEV-4, can lead to persistent infection in immunocompromised individuals, which in turn can lead to rapid development of liver fibrosis and cirrhosis, and in some cases to decompensation. In these circumstances, virus elimination can be achieved by relieving the immunosuppression regimen, when possible, or by 3–6 months off-label treatment with ribavirin (RBV), a broad-spectrum antiviral drug.1 However, the use of RBV,…