Golding Josephine P, Goatley Lynnette, Goodbourn Steve, Dixon Linda K, Taylor Geraldine, Netherton Christopher L
Vaccinology Group, The Pirbright Institute, Ash Road, Pirbright, Surrey GU24 0NF, UK.
ASFV Group, The Pirbright Institute, Ash Road, Pirbright, Surrey GU24 0NF, UK.
Virology. 2016 Jun;493:154-61. doi: 10.1016/j.virol.2016.03.019. Epub 2016 Apr 1.
African swine fever virus (ASFV) causes a lethal haemorrhagic disease of pigs. There are conflicting reports on the role of interferon in ASFV infection. We therefore analysed the interaction of ASFV with porcine interferon, in vivo and in vitro. Virulent ASFV induced biologically active IFN in the circulation of pigs from day 3-post infection, whereas low virulent OUR T88/3, which lacks genes from multigene family (MGF) 360 and MGF505, did not. Infection of porcine leucocytes enriched for dendritic cells, with ASFV, in vitro, induced high levels of interferon, suggesting a potential source of interferon in animals undergoing acute ASF. Replication of OUR T88/3, but not virulent viruses, was reduced in interferon pretreated macrophages and a recombinant virus lacking similar genes to those absent in OUR T88/3 was also inhibited. These findings suggest that as well as inhibiting the induction of interferon, MGF360 and MGF505 genes also enable ASFV to overcome the antiviral state.
非洲猪瘟病毒(ASFV)会引发猪的致命性出血性疾病。关于干扰素在ASFV感染中的作用,存在相互矛盾的报道。因此,我们在体内和体外分析了ASFV与猪干扰素的相互作用。强毒力的ASFV在感染后第3天就会在猪的血液循环中诱导产生具有生物活性的干扰素,而缺乏多基因家族(MGF)360和MGF505基因的低毒力OUR T88/3毒株则不会。体外使用ASFV感染富含树突状细胞的猪白细胞会诱导产生高水平的干扰素,这表明在经历急性非洲猪瘟的动物体内,干扰素可能有一个潜在来源。在经干扰素预处理的巨噬细胞中,OUR T88/3毒株的复制受到抑制,但强毒力病毒不受影响,并且一种缺乏与OUR T88/3中缺失基因相似基因的重组病毒也受到抑制。这些发现表明,MGF360和MGF505基因除了能抑制干扰素的诱导外,还能使ASFV克服抗病毒状态。