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Zinc status in human immunodeficiency virus infection Baum MK; Shor-Posner G; Campa AJ Nutr 2000[May]; 130 (5S Suppl): 1421S-3SThere is substantial evidence to support an important role for zinc in immune processes. Adequate zinc status is essential for T-cell division, maturation and differentiation; lymphocyte response to mitogens; programmed cell death of lymphoid and myeloid origins; gene transcription; and biomembrane function. Lymphocytes are one of the types of cells activated by zinc. Zinc is the structural component of a wide variety of proteins, neuropeptides, hormone receptors and polynucleotides. Among the best known zinc-dependent hormones/enzymes are Cu, Zn superoxide dismutase, an enzyme component of the antioxidant defense system, and thymulin, which is essential for the formation of T-lymphocytes. In animals and humans, zinc deficiency results in rapid and marked atrophy of the thymus, impaired cell-mediated cutaneous sensitivity and lymphopenia. Primary and secondary antibody responses are reduced in zinc deficiency, particularly for those antigens that require T-cell help, such as those in heterologous red blood cells. In addition, antibody response and the generation of splenic cytotoxic T cells after immunization are reduced. Zinc also inhibits the production of tumor necrosis factor, which is implicated in the pathophysiology of cachexia and wasting in acquired immune deficiency syndrome.|*HIV-1[MESH]|Disease Susceptibility[MESH]|HIV Infections/*immunology/physiopathology[MESH]|Humans[MESH]|Immune System/drug effects[MESH]|Nutritional Status[MESH]|Zinc/blood/deficiency/*immunology/pharmacology/physiology[MESH] |
