The effects of dietary T-2 toxin on the immunological function and herpes simplex reactivation in Swiss mice.

Abstract

T-2 toxin, a trichothecene mycotoxin, is a potently cytotoxic and immunosuppressive secondary metabolite produced by Fusarium fungi. Young male white Swiss mice were fed a diet supplemented with T-2 toxin at levels of 5, 10, or 20 ppm, control diet ad libitum, or control diet at a restricted rate for 1, 2, 3, 4, and 6 weeks. The effect of the toxin on the immune system of these mice was assessed by counting total spleen cell numbers and the in vitro proliferative response of spleen cells from these mice to the polyclonal mitogens, concanavalin A (Con A), and lipopolysaccharide (LPS). Body weight gains were also measured. Initially, the ingestion of T-2 toxin and restricted diet depressed total spleen cell counts, but after 3 weeks, only the spleen cell counts of mice fed 20 ppm of T-2 toxin were significantly lower. Consumption of 20 ppm of T-2 toxin by mice for 1 to 4 weeks depressed the spleen proliferative responses to the T-cell mitogen Con A; however, the response to LPS, a B-cell mitogen, was depressed in mice fed 10 and 20 ppm of T-2 toxin as well as in mice fed a control diet at a restricted rate. In order to determine whether T-2 toxin could induce reactivation of herpes simplex virus type 1 (HSV-1), latency was established in the trigeminal ganglia of mice. Feeding of T-2 toxin at 5, 10, and 20 ppm levels for 3 or 6 weeks did not reactivate virus; however, treatment with liquid nitrogen and cyclophosphamide did reactivate virus. These results demonstrate that although T-2 can cause immunosuppression, this response is not sufficient to reactivate HSV-1.