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Iron metabolism and HIV infection: reciprocal interactions with potentially harmful consequences?
Author(s) -
Savarino Andrea,
Pescarmona Gian Piero,
Boelaert Johan R.
Publication year - 1999
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/(sici)1099-0844(199912)17:4<279::aid-cbf833>3.0.co;2-j
Subject(s) - ferritin , oxidative stress , human immunodeficiency virus (hiv) , metabolism , in vitro , biology , virus , viral replication , virology , immunology , genetics , biochemistry
Humans with advanced human immunodeficiency virus (HIV) infection present some evidence suggestive of iron accumulation. Ferritin concentrations increase with HIV disease progression, and iron accumulates in several tissues. Iron excess may exert negative effects in individuals with HIV. Indeed, iron accumulation seems to be associated with shorter survival, and a number of investigations point to an iron‐mediated oxidative stress in subjects with HIV infection. The observations on humans infected with HIV are in part supported by in‐vitro findings. Indeed, in‐vitro HIV infection is associated with changes in iron metabolism, and an iron‐mediated oxidative stress is likely to contribute to viral cytopathogenicity. Furthermore, it is interesting to point out that the interaction between iron and HIV may be reciprocal, since viruses with a life‐cycle involving a DNA phase require chelatable iron for optimum replication. This combined evidence suggests that iron metabolism is an important area for virus/host interaction. These observations may be relevant to both laboratory monitoring and clinical treatment of individuals with HIV. Copyright © 1999 John Wiley & Sons, Ltd.