Viral infection and iron metabolism.
Fundamental cellular operations, including DNA synthesis and the generation of ATP, require iron. Viruses hijack cells in order to replicate, and efficient replication needs an iron-replete host. Some viruses selectively infect iron-acquiring cells by binding to transferrin receptor 1 during cell entry. Other viruses alter the expression of proteins involved in iron homeostasis, such as HFE and hepcidin. In HIV-1 and hepatitis C virus infections, iron overload is associated with poor prognosis and could be partly caused by the viruses themselves. Understanding how iron metabolism and viral infection interact might suggest new methods to control disease.
Molecular Immunology Group, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital and Oxford University, Oxford OX3 9DS, UK. hdrakes@hammer.imm.ox.ac.uk
Hal
H
Drakesmith
Andrew
A
Prentice
D000818:Animals; D023181:Antimicrobial Cationic Peptides / Q000378:metabolism; D064451:Hepcidins; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D007501:Iron / Q000378:metabolism*; D019190:Iron Overload; D014777:Virus Diseases / Q000378:metabolism*; D014779:Virus Replication / Q000502:physiology
D023181:Antimicrobial Cationic Peptides; C578702:HAMP protein, human; D064451:Hepcidins; D007501:Iron