Abstract
A mouse model of Reye's syndrome (RS), in which exposure to an emulsifier prior to Influenza B virus infection induced most of the biochemical and histologic features of human RS, was used to investigate ASA and AAP as initiators and enhancers of this syndrome. Mortalities of mice increased when ASA and AAP was given to 2 week old mice previously exposed to emulsifier and Influenza B (p=0.02 and p=0.001 respectively). In 5 week old mice, mortalities increased in mice infected with ASA coincident with administration of the drug but independent of the emulsifiers (p=0.01). In vitro work with MDCR (dog kidney) cell cultures were used to study the cytotoxic effect of ASA and AAP on Influenza B infection. Neither ASA or AAP, up to cytotoxic concentration, had any effect on the sensitivity of MDCR cells to Influenza B infection. Both drugs, however, substantially reduced the sensitivity of these cells to exogenously provided interferon. As both drugs are mitochondrial toxins and displayed similar interactions with the virus, these studies question the substitution for ASA in young patients with influenza infection.
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Crocker, J., Digout, S., Lee, S. et al. 636 ACETYLSALICYLIC ACID (ASA) AND ACETAMINOPHEN (AAP) AS POSSIBLE CONTRIBUTORY FACTORS IN THE ETIOLOGY OF REYE'S SYNDROME. Pediatr Res 19, 216 (1985). https://doi.org/10.1203/00006450-198504000-00666
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DOI: https://doi.org/10.1203/00006450-198504000-00666
