Serum hepcidin levels in women infected with HIV-1 under antiviral therapy

Malvoisin, Etienne; Makhloufi, Djamila; Livrozet, Jean-Michel

doi:10.1002/jmv.24019

Cited by 12 publications

(4 citation statements)

References 35 publications

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“…Hepcidin levels were shown to be increased in HIV infection with or without ART, which is consistent with reduced serum iron levels, 45 but another study demonstrated reduced hepcidin levels in HIV-positive women, which can lead to increased iron release into the circulation. 46 Our results are more consistent with reduced hepcidin levels leading to increased serum iron, although we did not measure hepcidin levels in our studies.…”

Section: Relationship Among Iron Hiv and Art 309supporting

confidence: 82%

Short Communication: High Cellular Iron Levels Are Associated with Increased HIV Infection and Replication

Chang

Bayeva²,

Taiwo

et al. 2015

AIDS Research and Human Retroviruses

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Section: Relationship Among Iron Hiv and Art 309supporting

confidence: 82%

Short Communication: High Cellular Iron Levels Are Associated with Increased HIV Infection and Replication

Chang

Bayeva²,

Taiwo

et al. 2015

AIDS Research and Human Retroviruses

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“…These conflicting data need further investigation. Malvoisin et al also demonstrated higher levels of hepcidin in individuals with high viremia, which is consistent with our results [ 20 ].…”

Section: Discussionsupporting

confidence: 93%

Asymptomatic Human Immunodeficiency Virus-1 Infection with High CD4+ T Cell Count Does Not Alter Iron Metabolism or Hepcidin Levels: The Pilot Study

Szymczak

Zalewska

Rymer³

et al. 2021

Infect Dis Ther

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Introduction The purpose of the study was to assess hepcidin levels and iron metabolism in otherwise healthy human immunodeficiency virus-1 (HIV-1)-infected males and the influence of antiretroviral therapy on hepcidin production, as data in this group are scarce. Methods A total of 89 HIV-1-infected males, 42 on effective antiretroviral therapy (ART)—group A, 47 treatment-naïve—group B, and 27 healthy controls—group C, were enrolled. Erythrocytes parameters, iron metabolism parameters, hepcidin, highly sensitive C-reactive protein (hsCRP), interleukin 6 (IL-6), and soluble transferrin receptor (sTfR) levels were assessed. Conditions related to inflammatory activity, systemic metabolic diseases and iron supplementation were exclusion criteria. Convenience sampling was used. Results Median age in HIV-1 group was 33 years, and 27 years in the control group. Median CD4 + T-cell count was 724 cells/μl in group A, and 488 cells/μl in group B ( p = 0.0000). Nadir CD4 + T-cell count was 397 cells/μl in group A and 475 cells/μl in group B ( p = 0.0001). Median value of HIV-1 viral load (VL) in group B was 16 900 copies/mL. The hepcidin value was lower in group A than in groups B ( p = 0.0008) or C ( p = 0.0004), without differences between groups B and C. The hepcidin value correlated with ferritin in groups A ( r 2 = 0.16; p = 0.008) and B ( r 2 = 0.39; p = 0.000), but not in group C ( r 2 = 0.11; p = 0.09). In group A, the hepcidin value correlated with current CD4 + count ( r = 0.48, p = 0.0012), but there was no correlation in group B. There were no correlations of hepcidin values with CD4 + T cell nadir in group A ( p = 0.371) or in group B ( p = 0.477); ART period ( p = 0.614); VL in group B ( p = 0.71). No abnormalities of iron metabolism, hsCRP, IL-6, or sTfR were noted. Conclusions Asymptomatic HIV-1 infection does not cause clinically important iron metabolism alterations or increased hepcidin production. Hepcidin values decrease on effective antiretroviral therapy.

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“…Hepcidin levels remained elevated in patients in the chronic phase of the disease without the use of HAART, increasing the viral load. This effect was not found in patients with HBV or HCV, indicating that hypoferraemia is pathogen-specific and that the HIV-1 virus utilizes intracellular iron for viral replication [163,164,165,166]. …”

Section: Hepcidinmentioning

confidence: 99%

Hepcidin: Homeostasis and Diseases Related to Iron Metabolism

et al. 2017

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Iron is an essential metal for cell survival that is regulated by the peptide hormone hepcidin. However, its influence on certain diseases is directly related to iron metabolism or secondary to underlying diseases. Genetic alterations influence the serum hepcidin concentration, which can lead to an iron overload in tissues, as observed in haemochromatosis, in which serum hepcidin or defective hepcidin synthesis is observed. Another genetic imbalance of iron is iron-refractory anaemia, in which serum concentrations of hepcidin are increased, precluding the flow and efflux of extra- and intracellular iron. During the pathogenesis of certain diseases, the resulting oxidative stress, as well as the increase in inflammatory cytokines, influences the transcription of the HAMP gene to generate a secondary anaemia due to the increase in the serum concentration of hepcidin. To date, there is no available drug to inhibit or enhance hepcidin transcription, mostly due to the cytotoxicity described in the in vitro models. The proposed therapeutic targets are still in the early stages of clinical trials. Some candidates are promising, such as heparin derivatives and minihepcidins. This review describes the main pathways of systemic and genetic regulation of hepcidin, as well as its influence on the disorders related to iron metabolism.

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Serum hepcidin levels in women infected with HIV-1 under antiviral therapy

Cited by 12 publications

References 35 publications

Short Communication: High Cellular Iron Levels Are Associated with Increased HIV Infection and Replication

Short Communication: High Cellular Iron Levels Are Associated with Increased HIV Infection and Replication

Asymptomatic Human Immunodeficiency Virus-1 Infection with High CD4+ T Cell Count Does Not Alter Iron Metabolism or Hepcidin Levels: The Pilot Study

Hepcidin: Homeostasis and Diseases Related to Iron Metabolism

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