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.

中文翻译：

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非洲猪瘟病毒对自噬的损害

非洲猪瘟是家猪和野猪的一种毁灭性疾病，由编码超过 150 个开放阅读框的大型双链 DNA 病毒引起。没有针对该疾病的许可疫苗，目前最有希望的候选疫苗是通过删除毒力因子而减毒的改良活病毒。像许多病毒一样，非洲猪瘟病毒显着改变了宿主细胞机制，使其复制受益，而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目标。自噬是一种重要的细胞通路，涉及细胞稳态、先天免疫和适应性免疫，因此受到许多不同病毒的操纵。自噬受复杂的蛋白质级联调节，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止自噬体的形成，这是自噬途径的关键功能步骤。有趣的是，这不需要A179L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剂。