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2026, Number 1

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Invest Med ISSSTE 2026; 1 (1)

Interaction between iron and the human immunodeficiency virus: an analysis of its influence on pathogenesis and immune response

Rodríguez-Hernández SA, García-Oropesa EM, Hernández-Martínez JC, Flores-Gómez JF, Gaspar-Coronado JA, Nolasco-Quiroga M, Rosas-Díaz M

Language: Spanish
References: 19
Page: 41-44
PDF size: 644.56 Kb.


ABSTRACT

Human immunodeficiency virus (HIV) infection disrupts iron metabolism, thereby influencing disease progression and the host immune response. This article reviews the current evidence on how iron overload or deficiency affects HIV pathogenesis. Iron acts as a cofactor for key enzymes in viral replication (ribonucleotide reductase) and for NF-κB activation via reactive oxygen species (ROS). Iron overload increases viral transcription, impairs the function of macrophage and T-lymphocytes, and raises the risk of opportunistic infections. Conversely, deficiency resulting from chronic bleeding, malabsorption, or elevated hepcidin causes iron-deficiency anemia, blunts immune responses, and is associated with higher mortality. Maintaining iron within physiological ranges should therefore be a therapeutic goal in HIV infection.


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