PDF(Pubmed)
Abstract：
Rabies virus (RABV) causes a fatal neurological disease, consisting of unsegmented negative-strand RNA, which encodes five structural proteins (3\'-N-P-M-G-L-5\'). Apolipoprotein D (ApoD), a lipocalin, is upregulated in the nervous system after injury or pathological changes. Few studies have focused on the role of ApoD during virus infection so far. This study demonstrated that ApoD is upregulated in the mouse brain (in vivo) and C8-D1A cells (in vitro) after RABV infection. By upregulating ApoD expression in C8-D1A cells, we found that ApoD facilitated RABV replication. Additionally, Co-immunoprecipitation demonstrated that ApoD interacted with RABV glycoprotein (G protein). The interaction could promote RABV replication by upregulating the cholesterol level. These findings revealed a novel role of ApoD in promoting RABV replication and provided a potential therapeutic target for rabies.
摘要：
狂犬病病毒（RABV）会导致致命的神经系统疾病，由未分段的负链RNA组成，其编码五种结构蛋白(3'-N-P-M-G-L-5')。载脂蛋白D(ApoD),脂质运载蛋白，在损伤或病理变化后在神经系统中上调。迄今为止，很少有研究关注ApoD在病毒感染过程中的作用。这项研究表明，在RABV感染后，ApoD在小鼠大脑（体内）和C8-D1A细胞（体外）中上调。通过上调C8-D1A细胞中ApoD的表达，我们发现ApoD促进了RABV的复制。此外,免疫共沉淀表明ApoD与RABV糖蛋白(G蛋白)相互作用。这种相互作用可以通过上调胆固醇水平来促进RABV的复制。这些发现揭示了ApoD在促进RABV复制中的新作用，并为狂犬病提供了潜在的治疗靶标。
