Autophagy impairment by African swine fever virus.
Autophagy impairment by African swine fever virus.
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DOI：
10.1099/jgv.0.001637
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发表时间：
2021-08
期刊：
影响因子：
--
通讯作者：
Netherton CL
中科院分区：
文献类型：
--
作者：
Shimmon GL;Hui JYK;Wileman TE;Netherton CL
非洲猪瘟是一种由编码150多个开放阅读框的大型双链DNA病毒引起的家猪和野猪的毁灭性疾病。目前还没有获得许可的疫苗用于该疾病，目前最有希望的候选疫苗是通过删除毒力因子而减毒的修饰活病毒。与许多病毒一样，非洲猪瘟病毒显著改变宿主细胞机制以利于其复制，并且改变宿主途径的病毒基因代表了开发基因缺失疫苗的有希望的靶点。自噬是一种重要的细胞途径，参与细胞内稳态、先天性和适应性免疫，因此被许多不同的病毒操纵。自噬是由一个复杂的蛋白质级联调节的，在这里，我们表明非洲猪瘟病毒可以通过至少两种不同的机制阻断自噬体的形成，这是自噬途径的一个关键功能步骤。有趣的是，这并不需要A179 L基因，该基因已被证明与Beclin-1相互作用，Beclin-1是一种重要的自噬调节因子。
African swine fever is a devastating disease of domestic swine and wild boar caused by a large double-stranded DNA virus that encodes for more than 150 open reading frames. There is no licensed vaccine for the disease and the most promising current candidates are modified live viruses that have been attenuated by deletion of virulence factors. Like many viruses African swine fever virus significantly alters the host cell machinery to benefit its replication and viral genes that modify host pathways represent promising targets for development of gene deleted vaccines. Autophagy is an important cellular pathway that is involved in cellular homeostasis, innate and adaptive immunity and therefore is manipulated by a number of different viruses. Autophagy is regulated by a complex protein cascade and here we show that African swine fever virus can block formation of autophagosomes, a critical functional step of the autophagy pathway through at least two different mechanisms. Interestingly this does not require the A179L gene that has been shown to interact with Beclin-1, an important autophagy regulator.
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