Sepehrvand et al. demonstrated a considerable seroprevalence rate of anti-HEV in Iranian kidney transplant recipients. The impact of HEV infection on renal transplantation and the risk of chronic HEV infection in this group are debated-issues that I would like to discuss. HEPATITIS E VIRUS (HEV) was first discovered in New Delhi, India, in 1955. The VIRUS is transmitted via the oral-fecal route. Other possible routes of transmission include blood transfusions, drug vertical transmission, person-to-person contact, and zoonotic transmission. The frequency of HEV transmission by non-fecal-oral routes remains unknown. In endemic areas, exposure occurs in childhood. In high-income countries, most cases of HEPATITIS E appear to be acquired locally and are not imported from endemic regions. In these areas, it likely has a zoonotic origin. In immunocompetent individuals, HEPATITIS E is a self-limited disease. However, HEV can cause chronic infection in solid organ transplants, patients who receive chemotherapy, and HIV-infected persons. HEV infection causes chronic HEPATITIS in more than 60% of recipients of solid organ transplants. Factors that increase the risk of chronic HEPATITIS in solid organ transplant recipients are shorter interval since the transplant, lower levels of liver enzymes and serum creatinine, lower platelet counts, and tacrolimus-based immunosuppression (compared with cyclosporin A), the most significant of which are tacrolimus use and low platelet count.