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Biomedical subjects

D Bergner

Publications and source records attributed to D Bergner.

3 recordsLinked to original sources

In vitro activation of peripheral mononuclear cells by zinc in HIV-infected patients and healthy controls.

Zinc is a mitogen for peripheral blood mononuclear cells (PBMC). The optimal mitogenic concentration was found to be 0.05 mmol/l (327 micrograms/dl), four times higher than physiological serum levels. Maximal proliferation was observed after 6 days. Limited dilution technique revealed a frequency of zinc reactive cells of 1:3467 (median; range 1:1628-1:6235). Cord blood mononuclear cells from four of six healthy children could be stimulated to proliferate by zinc. A normal zinc-induced proliferative response could be demonstrated in all six HIV-infected patients in the Walter-Reed-stage I, in nine of 11 patients in Walter-Reed II and in only two of five patients in Walter-Reed III. In Walter-Reed IV to VI all eight patients showed a weak response to zinc (less than 50% of the healthy day control). Decreased zinc serum levels were found in 10 of 28 patients and in one of 16 controls. There was a significant correlation of a diminished zinc-induced proliferation with lower serum levels of zinc and a reduced proportion of CD4 helper cells in HIV-1-infected men. Because of a suppression of mitogenesis by high dose of zinc an excessive intake of zinc as used by some HIV-1-infected patients can presently not be recommended. The value of zinc-induced proliferation for monitoring HIV-infected patients has still to be established.

Cells, Cultured

[HIV-1 antigenemia and T-cell activation in HIV-1 infected patients].

In order to study a supposed association between T-cell activation in vivo and HIV-1-antigenemia in HIV-1-infected patients, the detection of p24-antigen in sera was correlated to serum levels of beta-2-microglobulin and C1q-binding immune complexes. Anti-p24-antibodies and the urinary excretion of neopterin were also analysed. In 24 of 80 patients (30%) p24-antigen could be detected, and in 15 of 59 (25.4%) there was a loss of anti-p24-antibodies. Tests revealed elevated serum levels of beta-2-microglobulin in 58 of 80 patients (72.5%), elevated levels of C1q-binding immune complexes in 15 of 66 (22.7%), and increased excretion of neopterin in 52 of 60 (86.7%). Detection of p24-antigen, loss of anti-p24-antibodies, serum levels of beta-2-microglobulin, and urinary excretion of neopterin were significantly correlated to advanced stages of HIV-1 infection. Patients with p24-antigen in the serum showed significantly more frequently elevated serum levels of beta-2-microglobulin and no significant association with increased urinary excretion of neopterin. Because of the high proportion of patients with elevated serum levels of beta-2-microglobulin and increased excretion of urinary neopterin in the absence of detectable p24-antigen in serum, we could not correlate HIV-1-antigenemia to T-cell activation in vivo.

Acquired Immunodeficiency Syndrome