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Lab Invest. 1987 Jan;56(1):32-6.

Influenza B virus model of Reye's syndrome. Evidence for a nonpermissive infection of liver and brain.


Nonpermissive or abortive viral infections seldom have been recognized as damaging to organs. Concentrated infectious influenza B/Lee virus injected intravenously into Balb/c mice causes a microvesicular fatty metamorphosis of the liver and produces many features of Reye's syndrome. Evidence for a nonpermissive infection in brain and liver includes the following points: (a) no viral replication occurs in either organ; (b) no inflammation develops; (c) no virions are seen by electron microscopy; (d) influenza B viral hemagglutinin increases in the liver; (e) immunofluorescent and immunoperoxidase staining demonstrate viral antigens within hepatocytes and brain capillary endothelial cells; (f) viral antigens appear at 12 hours and disappear by 4 days without spread to adjacent cells; (g) inactivated influenza B virus does not kill mice; (h) mouse alpha- and beta- interferon and homologous B/Lee antiserum given before but not 2 hours after virus inoculation protects mice. These observations suggest a nonpermissive viral infection in hepatocytes and brain capillary endothelial cells which is important in the pathogenesis of the mouse illness and may play a role in the pathogenesis of Reye's syndrome.

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