The data presented here show that the orbivirus genome encodes four distinct non-structural proteins (NS1-NS4). NS1 and NS3 play an important role in orbivirus exit mechanisms from infected cells [15] . BTV infects mammalian cells, usually resulting in a lytic infection, while infection of KC cells derived from the BTV vector Culicoides sonorensis, become persistently infected with little or no evidence of cell lysis [56, 57] . Previous work showed that intracellular expression of an NS1 specific antibody fragment (scFv) destabilised the formation of NS1 tubules in BTV infected cells [14] . As a consequence, cells became persistently infected and viruses exited by budding instead of via cell lysis. Although BTV NS3 is effectively expressed in insect cells [15] , it is much less abundant in mammalian cells [4] . It was suggested previously [14] that the relative levels of NS1 to NS3 synthesised during infection dictate the fate of cellular pathogenesis as of whether the virus exit occurs by lysis or budding.