AI Article Synopsis
- A study in Japan from 2000-2005 explored the causes of influenza-associated encephalopathy (IAE), revealing that more than half of affected patients had mitochondrial beta-oxidation disorders due to carnitine palmitoyltransferase II variations.
- Model mice with impaired mitochondrial functions showed significant changes in brain chemistry (like increased trypsin) after being infected with the influenza A virus, which led to damage to the blood-brain barrier.
- The research indicates that IAE can cause serious neurological issues, highlighting the relationship between metabolic problems and viral infections.
Article Abstract
To assess the etiology of influenza-associated encephalopathy(IAE), a surveillance effort was conducted during 2000-2005 in Japan. Over half of fatal and handicapped IAE patients exhibited a disorder of mitochondrial beta-oxidation and ATP generation evoked by the thermolabile phenotype of carnitine palmitoyltransferase II variations with transiently elevated serum acylcarnitine during high-grade fever. Model mice having impaired mitochondrial beta-oxidation exhibited significant accumulation of mini-plasmin and up-regulation of trypsin in the cerebral capillaries after infection with influenza A virus, resulting in the destruction of blood-brain barrier and increased brain vascular permeability. Trypsin up-regulation was also evident in the neuronal cells in the hippocampus, suggesting a severe neurologic complication of IAE.
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