In mice treated with sodium aurothiomalate (myocrisin), prior to infection with Coxsackievirus B3, 90% of the animals died by the 11 th day postinfection (p.i.) A mortality of 10% was noted in mice receiving myocrisin only, and no deaths occurred in animals infected with virus alone. The highest amount of virus was recovered from the pancreas of myocrisin‐treated mice on day 3 p.i. This was over 500‐fold higher than the virus titer found in the pancreas of mice infected with virus only. Generally the titer of virus present in different organs was higher at every point in drug‐treated animals as compared to intact mice infected with the virus. A high and persistent viremia was present in myocrisin‐treated mice; in contrast a low viremia followed by virus clearance from the blood was observed in intact mice infected with the virus. The antibody response was studied in intact and myocrisin‐treated mice infected with the virus. In both groups, no neutralizing antibodies were detected on days 1, 2, and 3 p.i. On day 7 after infection, the titers of antibodies were 1:16 and 1:12 in intact and myocrisin‐treated mice, respectively. Administration of hyperimmune anti‐Coxsackievirus B3 serum 6 hours after infection protrected the myocrisin‐treated group of mice against lethal disease. The results of these studies suggest that (1) antibodies alone may not be sufficient to limit the spread and persistence of virus in natural infections and (2) in the absence of any apparent histopathological differences the increased multiplication of Coxsackievirus B3 could be the cause of death in myocrisintreated mice.

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   |texte=   Potentiation of coxsackievirus B3 infection in adult mice pretreated with a gold salt
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