Schmallenberg virus (SBV) is a newly emerged orthobunyavirus that has caused widespread disease in cattle, sheep and goats in Europe. Like other orthobunyaviruses SBV is characterized by a tripartite negative sense RNA genome that encodes four structural and two nonstructural proteins. in vitro, SBV has a wide in vitro host range, and BHK-21 cells are a convenient host for both SBV propagation and assay by plaque titration.
In this paper, the three SBV genome segments were cloned as cDNA and a three-plasmid rescue system was established to recover infectious virus. Recombinant virus behaved similarly in cell culture to authentic virus. The open reading frame for the nonstructural NSs protein, encoded on the smallest genome segment, was disrupted by introduction of translation stop codons in the appropriate cDNA, and when this plasmid was used in reverse genetics, a recombinant virus that lacks NSs expression was recovered. This virus had reduced capacity to shut-off host cell protein synthesis compared to wild type virus. In addition, the NSs-deleted virus induced interferon in cells, indicating that like other orthobunyaviruses, NSs functions as an interferon antagonist most probably by globally inhibiting host cell metabolism.
Development of a reverse genetic system for SBV will aid investigation of its pathogenic mechanisms as well as creation of attenuated strains that could be candidate vaccines.