Study summary · research use only
Zinc status in human immunodeficiency virus infection
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses the role of zinc in immune function, particularly relevant to human immunodeficiency virus infection. The authors describe zinc as essential for T-cell division, maturation and differentiation, lymphocyte responses to mitogens, programmed cell death, gene transcription, and biomembrane function, and as a structural component of many proteins, neuropeptides, hormone receptors, and polynucleotides. They note zinc-dependent enzymes including Cu,Zn superoxide dismutase and the thymic hormone thymulin, described as essential for T-lymphocyte formation. The authors state that in animals and humans zinc deficiency leads to thymic atrophy, impaired cell-mediated cutaneous sensitivity, lymphopenia, and reduced antibody responses, especially for antigens requiring T-cell help. They also note zinc inhibits tumor necrosis factor production, which is implicated in cachexia and wasting in acquired immune deficiency syndrome.
Abstract
There 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.
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