Fu Z F, Li X, Dhingra V
Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA 30606, USA.
Dev Biol (Basel). 2008;131:83-91.
Proteomics technology was employed to profile host responses to rabies virus (RABV) infection in order to understand how RABV infection results in neuronal dysfunction. In mice infected with wild-type (wt) RABV, the expression of proteins involved in ion homeostasis was altered. H+ ATPase and Na+/K+ ATPase were up-regulated while Ca2+ ATPase was downregulated, which resulted in reduction of intracellular Na+ and Ca2+ concentrations. Furthermore, infection with wt RABV resulted in down-regulation of SNAREs such as alpha-SNAP, TRIM9, syntaxin, and pallidin, all of which are involved in docking and fusion of synaptic vesicles to and with the presynaptic membrane. As a consequence, the accumulation of synaptic vesicles was observed in the presynapses of mice infected with wt RABV. These data demonstrate that infection with wt RABV results in the alteration of host protein expression, particularly those involved in ion homeostasis and docking and the fusion of synaptic vesicles to the presynaptic membrane, which may lead to neuronal dysfunction.
为了了解狂犬病病毒（RABV）感染如何导致神经元功能障碍，采用蛋白质组学技术分析宿主对RABV感染的反应。在感染野生型（wt）RABV的小鼠中，参与离子稳态的蛋白质表达发生了改变。H + ATP酶和Na + / K + ATP酶上调，而Ca2 + ATP酶下调，导致细胞内Na +和Ca2 +浓度降低。此外，感染wt RABV导致SNARE蛋白如α-SNAP、TRIM9、 syntaxin和pallidin下调，所有这些蛋白都参与突触小泡与突触前膜的对接和融合。因此，在感染wt RABV的小鼠突触前观察到突触小泡的积累。这些数据表明，感染wt RABV会导致宿主蛋白表达的改变，特别是那些参与离子稳态以及突触小泡与突触前膜对接和融合的蛋白，这可能导致神经元功能障碍。
