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© 1987 Oxford University Press

research-article

Effects of NiCI2 and CdCI2 on Susceptibility to Murine Cytomegalovirus and Virus-Augmented Natural Killer Cell and Interferon Responses1

MARY J. DANIELS*, MARGARET G. Ménache{dagger}, GARY R. BURLESON{dagger}, JUDITH A. GRAHAM* and MARYJANE K. SELGRADE*

*Health Effects Research Laboratory, U.S. Environmental Protection Agency Research Triangle Park, North Carolina 27711 {dagger}Inhalation Toxicology Group, Northrop Services, Inc. Research Triangle Park, North Carolina 27709

Effects of NiCl2 and CdCl2 on Susceptibility to Murine Cytomegalovirus and Virus-Augmented Natural Killer Cell and Interferon Responses. DANIELS, M. J., MéNACHE, M. G., BURLESON, G. R., GRAHAM, J. A., and SELGRADE, M. K. (1987). Fundam. Appl. Toxicol. 8, 443–453. Female C3H/HeJ or CD-1 mice were infected with a sublethal dose of murine cytomegalovirus (MCMV) and then exposed to nickel chloride (NiCl2) or cadmium chloride (CdCl2) intramuscularly (im) or by inhalation. Effects of these treatments on disease susceptibility, virus-augmented and spontaneous natural killer (NK) cell activity, and virus induction of interferon (IFN) were determined. NiCl2 (20 mg/kg, im) enhanced mortality due to MCMV in both mouse strains, and a reduction in virus-augmented NK cell activity was seen at doses as low as 10 mg NiCl2/kg im. At 6.25 mg CdCl2/kg im there was a significant depression of NK cell activity, but there was no effect on mortality due to infection. Effects on NK activity did not appear to be due to effects on IFN production since neither of the metal treatments caused depression of this response. Neither metal when given by inhalation had any effect on these parameters.


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