Journal of Ardabil University of Medical Sciences (Apr 2015)
Methimazole-Induced Hypothyroidism Enhances HSV-1 Infectivity without Altering Circulating Leukocytes in the Rat
Abstract
Backgrounds & objectives: In addition to their genomic actions, thyroid hormones (THs) can modulate the immune responses through cell surface receptors. One of these is the antiviral effect of THs. Methimazole, as an anti-thyroid compound, is widely used to treat hyperthyroid patients. It also reduces blood leukocytes, granulocytes in particular, and thereby may affect the immune response. Recently, we reported that methimazole-induced hypothyroidism intensifies herpes simplex virus-1(HSV-1) infectivity. To determine whether the effect is mediated through alterations in circulating leukocytes, we assessed the HSV-1 infectivity and circulating leukocytes in methimazole-induced hypothyroid rat. Methods: Male Sprague Dawley rats received methimazole (200 μg/ml) in their drinking water for 2 weeks. Rats were then inoculated with a non-lethal single dose of HSV-1, and sacrificed 3 days later to harvest their spleen. Spleen extract was prepared, and virus yield was determined by evaluation of cytopathic effects (CPE) induced by the extract in a Vero cell culture system. For quantitative analysis, standard method of Reed-Muench was employed. The routine Wright’s staining protocol was used for blood leukocytes differential count. Results: The CPE development was significantly increased in the cell cultures exposed to the spleen extract of methimazole-treated animals (P < 0.05), indicating a higher virus yield and intensified virus infectivity. However, the effect of methimazole on blood leukocytes was minimal. Conclusion: Our data suggest that methimazole increases the susceptibility to HSV-1 infection, at least in part, by blocking THs synthesis but not alterations in circulating leukocytes.
