Effect of Iron on Viral Infections

Abstract

Iron is a cofactor in various biological processes, primarily obtained through dietary intake and also through oral or intravenous supplementation. Elevated iron levels are associated with increased production of reactive oxygen species, causing cellular damage. Additionally, iron influences the body’s response to infections and participates in the synthesis of genetic material and cellular functions. Therefore, this review aims to explore the complex interplay between iron homeostasis and viral infections, analyzing how iron availability affects viral replication, possible mutations, and pathogenesis. The interaction between viruses and iron, although less explored in the literature, indicates the influence of host iron bioavailability on parasite–host interactions. Furthermore, iron absorption is regulated by hepcidin, a peptide hormone produced by the liver, which reduces blood iron levels by inhibiting ferroportin function. Iron is important in viral growth and activities, potentially promoting replication, possible mutations, and increased virulence as seen in some studies with respiratory, enteric, and other viral models. Thus, iron chelators can be a promising preventive therapeutic strategy to limit iron availability and thereby reduce viral infectivity.