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Much has been learned about hepatitis E virus (HEV) infection over the last years. We know today that hepatitis E of genotype 3 is a zoonotic infection in the Western world that can be transmitted through the consumption of raw or undercooked pork and game meat, with much higher than anticipated seroprevalence rates, a broad range of hepatic as well as extrahepatic manifestations, and a potential to persist and cause chronic hepatitis as well as cirrhosis in immunocompromised individuals, including transplant recipients as well as patients with haematologic malignancies or poorly controlled HIV infection.1 Fibrosis progression can be rapid in these patients, with a reported 10% developing cirrhosis within 2 years.2 ,3 Reduction of immunosuppressive treatment results in viral elimination in only about 30%.2 ,3 Therefore, antiviral treatment of chronic hepatitis E becomes an important issue. Ribavirin (RBV) is commonly used in this situation.4 However, some patients do not achieve sustained viral elimination even after repeated or prolonged courses and become non-responsive to RBV treatment.
On this background, Todt et al5 report in this issue an in-depth analysis of HEV genome sequence evolution during RBV treatment of chronic hepatitis E. Using deep sequencing technology, the authors observed in a series of nine patients with chronic HEV genotype 3 infection …
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