Biochemical and morphological characteristics of a mouse model of Reye's syndrome induced by the interaction of influenza B virus and a chemical emulsifier.

One theory of the etiology of Reye's syndrome is that environmental toxins predispose the child to react abnormally to virus infection. Influenza B is the most commonly implicated virus. Suckling mice were exposed to a surfactant, Toximul MP8, either by a single intraperitoneal injection or by repeated applications to the skin. At various times after exposure, the mice were infected intranasally with influenza B virus. Mice exposed to a combination of chemical and virus had a higher mortality rate than that of the control groups. Serum ammonia levels were elevated and the mitochondrial urea cycle enzyme, ornithine transcarbamylase, had reduced activity in the livers of mice exposed to Toximul and infected with virus. The hepatocyte cytoplasmic urea cycle enzyme concentrations were variable. Livers of the animals with "chronic" skin application of Toximul followed by virus infection showed mitochondrial swelling and breakdown of cristae. Those animals who received one intraperitoneal injection of Toximul and those infected with virus alone showed either negative or mild morphologic changes in the liver. We conclude that young mice exposed to a chemical emulsifier and subsequently to influenza B develop histomorphic and urea cycle changes, as well as hyperammonemia analogous to human Reye's syndrome.