Tissue uptake of mercury is changed during the course of a common viral infection in mice.

Mercury (Hg) has been shown to have immunotoxic effects and to influence the severity of infection. However, the impact of infection on the normal Hg homeostasis in different target organs involved in the disease process has not been studied. In this study, Hg was measured through inductively coupled plasma-mass spectrometry (ICP-MS) in the intestine, serum, liver, and brain on days 3, 6, and 9 of coxsackievirus B3 (CVB3) infection in female Balb/c mice. The severity of the infection was assessed from clinical signs of disease and the number of virus particles in infected organs. CVB3 and gene expression of metallothionein 1 (MT1) was measured by reverse transcription-polymerase chain reaction (RT-PCR). Gene expression of MT1 increased and peaked on day 3 in the brain (93%, p<0.01) and liver (19-fold, p<0.01) and on day 6 in the intestine (seven-fold, p<0.01). This peak in MT1 in the liver and brain corresponded to the peak in virus numbers in these tissues. Hg in the intestine and serum tended to decrease on all days of infection. The maximum decrease, in comparison with non-infected mice, occurred in the intestine (78%, p<0.001) on day 9 and in serum (50%, p<0.05) on day 6. However, in the brain, Hg increased by 52% (p<0.05) on day 6. Hg went unchanged in the liver. An infection-induced increase of Hg in the brain but unchanged level in the liver may be due to the peak of virus replication and an associated infection-induced expression of MT1. Moreover, the decrease of Hg in serum and the intestine but a concomitant intestinal increase in MT1 on day 6 may reflect a flux and increased retention of Hg to infected organs such as the brain. The pathophysiological interpretation of these preliminary findings requires further research.