Abstract
Background: Hepcidin is the principal regulator of iron absorption and its tissue distribution. Its correlation with iron homeostasis in individuals infected with human immunodeficiency virus type-1 (HIV-1) treated with different regimens of highly active antiretroviral therapy (HAART) was investigated. Methods: Serum hepcidin levels were determined in 448 volunteers. Of these, 372 were HIV-1-infected individuals, and 93 did not receive HAART (ART-naive) while 279 received HAART consisting of a non-nucleoside reverse transcriptase inhibitor (NNRTI-based) and protease inhibitors (PI-based); both were used in association with a nucleoside reverse transcriptase inhibitor (NRTI). Seventy-six additional HIV-1 seronegative individuals were enrolled in the study. The following parameters were quantified: hematological parameters, iron biomarkers and markers of infection (CD4+ and CD8+ T-cells), and HIV-1 RNA (viral load). Results: Serum hepcidin, iron and ferritin levels, as well as the marker of infection, CD4+ T-cells, were significantly lower in the ART-naive group compared with other groups. Additionally, transferrin saturation, iron binding capacity, hemoglobin level and erythrocyte level were not significantly different, and anemia was not observed in the different groups. Conclusions: HIV-1 infection affected serum hepcidin, iron and ferritin levels in the ART-naive group, and the different HAART regimens restored the levels of hepcidin and iron homeostasis in HIV-1-infected individuals who have undetectable HIV-1 RNA levels.
Highlights
The control of absorption, storage and circulation of iron in the body is regulated by complex mechanisms to maintain an appropriate amount of iron in the circulation and within tissues and avoid deficiency or overload [1]
These data showed that the groups of human immunodeficiency virus type-1 (HIV-1)-infected individuals treated with highly active antiretroviral therapy (HAART) had an acceptable immune status while they were participating in the study
We demonstrated that serum hepcidin levels, as well as iron and ferritin, were reduced in the ART-naïve group and showed a positive correlation with the number of CD4+ T-cells, but not with HIV-1 RNA levels
Summary
The control of absorption, storage and circulation of iron in the body is regulated by complex mechanisms to maintain an appropriate amount of iron in the circulation and within tissues and avoid deficiency or overload [1]. Hepcidin is considered an acute-phase protein induced by interleukin-6 (IL-6) during infection and inflammation processes that decrease circulating iron and iron delivery to cells [11] In this context, different studies suggest that cellular stores of iron could affect the course and progression of HIV-1 infection in humans. Xu and colleagues (2010) have suggested that hepcidin and the efflux of ferroportin-mediated iron could affect the regulation of HIV-1 transcription In this way, the increase in iron stores was associated with a rapid progression of HIV-1 in patients with thalassemia major who received oral iron and in HIV-1-infected individuals who had haptoglobin polymorphisms [13]. We investigated serum hepcidin levels, biomarkers of iron homeostasis, and markers of HIV-1 in a large number of individuals receiving different regimens of highly active antiretroviral therapy (HAART), as well as in individuals without therapy (ART-naïve). Conclusions: HIV-1 infection affected serum hepcidin, iron and ferritin levels in the ART-naïve group, and the different HAART regimens restored the levels of hepcidin and iron homeostasis in HIV-1-infected individuals who have unde-
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