Effect of gold(I) compounds on the virulence of an amyocarditic strain of coxsackievirus B3

• Published in: Biological trace element research 2001, Vol.84 (1-3), p.67-80
• Main Authors: Smith, A D, South, P K, Levander, O A
• Format: Article
• Language: English
• Subjects: Animals; Aurothioglucose - pharmacology; Blood Glucose - metabolism; Coxsackievirus B3; Coxsackievirus Infections - pathology; Enterovirus - pathogenicity; Enzymatic activity; Enzyme Inhibitors - pharmacology; Enzymes; Glucose - metabolism; Glutathione Peroxidase - antagonists & inhibitors; Gold; Gold - pharmacology; Immunohistochemistry; Maltose - analogs & derivatives; Maltose - pharmacology; Mice; Mice, Inbred C3H; Mortality; Myocardium - enzymology; Rodents; Selenium; Selenium - antagonists & inhibitors; Selenium - deficiency; Thioredoxin-Disulfide Reductase - antagonists & inhibitors; Time Factors; Vitamin E Deficiency - metabolism
• ISSN: 0163-4984; 0163-4984; 1559-0720
• DOI: 10.1385/bter:84:1-3:067

Coxsackieviruses, especially B strains (CVB), are known etiological agents of myocarditis. Both amyocardititc and myocarditic strains exist and at least one amyocarditic strain, CVB3/0, can convert to virulence when passaged through selenium or vitamin E-deficient mice. Gold(I)-containing compounds, such as aurothiomalate (ATM) and aurothioglucose (ATG), can act as selenium antagonists. In this study, we examined the effect of intraperitoneal administration of equal doses of ATM or ATG on the virulence of CVB3/0. ATM but not ATG increased mortality in CVB3/0-infected mice. CVB3/0-infected mice treated with ATM had total necrosis of the pancreatic exocrine tissue. Heart damage also occurred in ATM-treated mice but did not correlate with mortality. Increased viral titers and persistence were observed in ATM-treated mice and, to a lesser extent, in ATG-treated mice. Thus, under our conditions, only ATM increased the virulence of CVB3/0, whereas ATG did not. On the other hand, both ATG and ATM inhibited thioredoxin reductase activity in heart and pancreas, but neither affected glutathione peroxidase activity. In contrast, dietary selenium deficiency reduces both enzyme activities. Thus, it is unlikely that these compounds affect virulence by acting as selenium antagonists.