It is recognized that iron overload is associated with excess mortality in HIV/AIDS, and that this may be due to iron acting as an HIV-1 transcriptional activator. In vitro evidence using iron chelators suggests that therapeutic iron depletion may be beneficial in HIV-1 infection. We describe the clinical course of a Caucasian man with hereditary haemochromatosis and HIV infection where a significant drop in HIV viral load accompanied venesection over an 18-month period in the absence of HAART. We propose that further research should be undertaken to explore the relationship between HIV viral load and serum iron markers in hereditary haemochromatosis, with a view to evaluating the therapeutic benefit of venesection on HIV viral load in this setting.
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