Mechanism of encephalitis after influenza virus infection based on defect of β-oxidation in liver

许多人认为流感病毒感染后的脑炎与β-氧化缺陷有关。然而，其机制仍不清楚。由于幼年内脏脂肪变性（JVS）小鼠具有缺陷的OCTN-2（肉毒碱转运蛋白），因此细胞中的β-氧化被抑制。因此，JVS小鼠在感染流感病毒后，很可能会发生高频率的脑炎。因此，我们首先分析了JVS小鼠的特征。1.断乳期死亡机制新生JVS小鼠90%左右在断乳期死亡。据报道，与正常对照组相比，JVS小鼠的血清氨水平较高。但水平略高于正常对照组。高肉毒碱饲料可使JVS小鼠免于死亡和低血糖。2.上调和下调基因的分析我们在JVS小鼠心脏中发现了一些有趣的分子方面，包括一些离子通道的下调和参与细胞周期进程的上调基因。

It is thought that many case of encephalitis after infection of influenza virus are associated with the defect of β-oxidation. However, the mechanism remain unclear. Because juvenile visceral steatosis(JVS)mouse has a defective OCTN-2(carnitine transporter), the β-oxidation is suppressed in the cell. Therefore, after infection of influenza virus, JVS mouse is supposed to be suffered from encephalitis at high frequency. So, first of all, we analyzed the characteristics of JVS mouse.1.Mechanism of death in weaning periodAbout 90% of new born JVS mouse die in weaning period. It has been reported that serum level of ammonia is high in JVS mouse in comparison with normal control. However, the level was a little higher than the normal control. In contract to it, serum level of glucose was low.JVS mouse given high carnitine diet can escape the death and hypoglycemia. These mechanism remains still unknown.2.Analysis of up-and down-regulation genesWe found several interesting molecular aspects that have not yet been identified in the hearts of JVS mice, including down-regulation of a number of ion channels and up-regulators involved in cell cycle progression.