Akabane orthobunyavirus (AKAV) is a negative sense, single-stranded, segmented RNA virus that belongs to the family Peribunyaviridae. AKAV is an arbovirus that primarily infects ruminants (cattle, sheep, goats) and other ungulates (including horses and pigs), is transmitted by bites from midges of the genus Culicoides, and is associated with abortion, stillbirth, and congenital abnormalities in infected pregnant animals. AKAV is prevalent in Asia, Africa, and Australia and in the absence of specific antivirals, the resulting livestock diseases can cause pronounced economic losses. Though orthobunyaviruses replicate in the cytoplasm, targeting host nuclear transport could be an effective antiviral strategy, as has been observed for many other RNA viruses. Our studies aim to unveil whether the host nuclear transport system may contribute to promoting AKAV infection. To address this, various inhibitors in different AKAV-infected cells lines are currently being examined to fully understand which nuclear import pathways modulate viral replication. Our initial screening indicates that importazole (which targets both classical and non-classical nuclear import) inhibited AKAV infection in Vero cells in a dose-dependent manner, whereas gossypol (which targets only classical nuclear import) did not. Additionally, importazole was shown to inhibit AKAV infection in mosquito-derived C6/36 cells. These preliminary results indicate that a factor promoting AKAV replication is transported into the nucleus in both mammalian and insect cells using non-classical, importin beta-mediated transport. The identity of this proviral factor and the stage of AKAV replication that it exerts influence are the focus of ongoing studies. Our research will reveal novel mechanisms of proviral signalling in infected cells and may lead to new avenues for targeting orthobunyaviruses with antivirals.