Nassim Kamar, Toulouse, France

Hepatitis E virus (HEV) infection is an emerging disease in developed countries. Locally acquired HEV genotype-3-infection is thought to be a porcine zoonosis. Until recently, it has been thought to be responsible for acute hepatitis that does not evolve to chronic hepatitis. However, over the last three years, a number of cases of chronic hepatitis caused by HEV genotype 3 have been reported in the immunosuppressed, i.e., solid-organ-transplant (SOT) recipients, and hematological, and HIV patients. Chronic HEV infection can cause rapidly progressive cirrhosis, necessitating liver transplantation. Nearly, 60% of solid-organ-transplant patients infected by HEV develop chronic hepatitis. The use of tacrolimus rather than cyclosporin A, and a low platelet count at HEV diagnosis have been identified as independent predictive factors associated with chronic HEV infection. A decrease of dose and trough levels of immunosuppressive therapy targeting T-cells (i.e., cyclosporin A and tacrolimus) led to HEV clearance in one-third of chronically infected SOT patients. Furthermore, it has been recently shown that pegylated-interferon α or ribavirin alone can successfully treat HEV infection, producing a sustained virological response. Finally, HEV-induced neurological symptoms have been reported and HEV RNA has been detected in the cerebrospinal fluid. Hence, HEV infection should be looked for systematically in organ-transplant patients with unexplained hepatitis.