Hepatitis E virus (HEV) is a member of the genus Hepevirus within the family Hepeviridae. Hepatitis E is recognized as a zoonosis, and swine and wild boars (Sus scrofa) are known reservoirs of HEV infection. The aim of this study was to investigate the presence of HEV in wild boars and hunters exposed to infection in central Italy (Latium region). During the hunting season, blood samples were collected from 228 wild boars and 20 hunters. The seroprevalence of HEV infection was determined using a commercial enzyme-linked immunosorbent assay, previously validated for use in man, pigs and wild boars. The estimated HEV seroprevalence in wild boars and in hunters was 40.7% (93/228; 95% confidence interval [CI] 34.4–47.1%) and 25% (5/20; 95% CI 6.1–43.9%), respectively. Liver samples were collected from the boars and HEV RNA was detected by nested reverse transcriptase polymerase chain reaction. Fifty-five of 164 tested wild boar liver samples (33.5%; 95% CI 26.2–40.7%) and three of 20 (15.0%; 95% CI 1.3–28.7%) tested human serum samples were positive for HEV RNA. Phylogenetic analysis of the nucleotide sequences obtained from PCR products indicated that the HEV strains present in wild boars and the human population all belonged to genotype 3, supporting the zoonotic role of wild boars in the spread of HEV infection.

Constituting an integral part of a heme's porphyrin ring, iron is essential for supplying cells and tissues with oxygen. Given tight links between oxygen delivery and iron availability, it is not surprising that iron deprivation and oxygen deprivation (hypoxia) have very similar consequences at the molecular level. Under hypoxia, the expression of major iron homeostasis genes including transferrin, transferrin receptor, ceruloplasmin, and heme oxygenase-1 is activated by hypoxia-inducible factors to provide increased iron availability for erythropoiesis in an attempt to enhance oxygen uptake and delivery to hypoxic cells. Iron-response proteins (IRP1 and IRP2) and "cap-n-collar" bZIP transcriptional factors (NE-F2 p45; Nrf1, 2, and 3; Bach1 and 2) also control gene and protein expression of the key iron homeostasis proteins. In this article, we give an overview of the mechanisms by which iron pathways are regulated by hypoxia at multiple levels. In addition, potential clinical benefits of manipulating iron pathways in the hypoxia-related conditions anemia and ischemia are discussed.