Zinc status in human immunodeficiency virus infection

There is substantial evidence to support an important role for zinc in immu ne processes. Adequate zinc status is essential for T-cell division, matura tion 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 th e antioxidant defense system, and thymulin, which is essential for the form ation of T-lymphocytes. In animals and humans, zinc deficiency results in r apid and marked atrophy of the thymus, impaired cell-mediated cutaneous sen sitivity and lymphopenia. Primary and secondary antibody responses are redu ced 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 immunizatio n are reduced. Zinc also inhibits the production of tumor necrosis factor, which is implicated in the pathophysiology of cachexia and wasting in acqui red immune deficiency syndrome.