Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.
Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.
Virus Res. 2018 Mar 15;248:44-52. doi: 10.1016/j.virusres.2018.02.004. Epub 2018 Feb 13.
Autophagy of cytoplasmic components plays an essential role in the pathogenic infection process. Furthermore, research suggests that autophagy is an extremely important component of the innate immune response. Our study aimed to reveal the effect of virus-induced autophagy on pseudorabies virus (PRV) replication. Our results confirmed that light chain 3 (LC3)-I was converted into LC3-II after PRV infection; this transition is considered an important indicator of autophagy. Transmission electron microscopy (TEM) revealed that PRV infection could notably increase the number of autophagosomes in mouse neuro-2a (N2a) cells. In addition, LC3-II accumulated in response to chloroquine (CQ) treatment, indicating that PRV infection induced a complete autophagic flux response. Furthermore, our analyses verified differences in the magnitude of autophagy induction by two different PRV isolates, LA and ZJ01. Subsequent analysis showed that the induction of autophagy by rapamycin facilitated PRV replication, while inhibition of autophagy by 3-methyladenine (3-MA) reduced PRV replication. These results indicated that PRV induced autophagy via the classical Beclin-1-Atg7-Atg5 pathway to enhance viral replication in N2a cells in vitro.
细胞质成分的自噬在致病感染过程中起着至关重要的作用。此外，研究表明自噬是先天免疫反应的一个极其重要的组成部分。本研究旨在揭示病毒诱导的自噬对伪狂犬病病毒（PRV）复制的影响。我们的结果证实，PRV 感染后轻链 3（LC3）-I 转化为 LC3-II；这种转变被认为是自噬的一个重要指标。透射电子显微镜（TEM）显示，PRV 感染可显著增加小鼠神经瘤-2a（N2a）细胞中自噬体的数量。此外，氯喹（CQ）处理后 LC3-II 积累，表明 PRV 感染诱导了完整的自噬流反应。此外，我们的分析还验证了两种不同 PRV 分离株 LA 和 ZJ01 诱导自噬的程度存在差异。随后的分析表明，雷帕霉素诱导的自噬促进了 PRV 的复制，而 3-甲基腺嘌呤（3-MA）抑制自噬则降低了 PRV 的复制。这些结果表明，PRV 通过经典的 Beclin-1-Atg7-Atg5 途径诱导自噬，以增强体外 N2a 细胞中病毒的复制。
