Zinc status in human immunodeficiency virus infection.
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.
Baum
M K
MK
Center for Disease Prevention, Department of Psychiatry and Behavioral Medicine, University of Miami School of Medicine, Miami, FL 33136, USA.
Shor-Posner
G
G
Campa
A
A
D004198:Disease Susceptibility; D015658:HIV Infections / Q000276:immunology* / Q000503:physiopathology; D015497:HIV-1; D006801:Humans; D007107:Immune System / Q000187:drug effects; D009752:Nutritional Status; D015032:Zinc / Q000097:blood / Q000172:deficiency / Q000276:immunology* / Q000494:pharmacology / Q000502:physiology
D015032:Zinc