Virulent ASFV induced biologically active interferon in pigs, whereas low virulent strains lacking MGF360 and MGF505 did not, and replication of the latter was reduced in interferon-pretreated cells.
MGF360 and MGF505 genes in African swine fever virus are linked to the virus's ability to overcome the antiviral state induced by type I interferon.
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.
Golding et al. (2016) studied African swine fever virus (ASFV) infection. African swine fever virus (virulent vs low virulent OUR T88/3) vs. Interferon pretreated macrophages was evaluated on Interferon induction and viral replication. Virulent ASFV induced biologically active interferon in pigs, whereas low virulent strains lacking MGF360 and MGF505 did not, and replication of the latter was reduced in interferon-pretreated cells.