Schmallenberg virus non-structural proteins NSs and NSm are not essential for experimental infection of Culicoides sonorensis biting midges
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The teratogenic orthobunyavirus Schmallenberg virus (SBV) is transmitted between its mammalian hosts by Culicoides biting midges. The genome of circulating SBV, i.e. variants present in viraemic ruminants or insect vectors, is very stable, while variants found in malformed ruminant foetuses display a high genetic variability. It was suggested that foetal infection provides an environment that favours viral mutations that enable immune escape in the unborn, but at the costs of limiting the ability of the virus to spread further. To investigate infection and dissemination rates of different SBV variants in the insect vectors, we fed laboratory-reared Culicoides sonorensis with blood containing the prototype strain BH80/11-4 from a viraemic cow or strain D281/12, which was isolated from the brain of a sheep foetus and harbours multiple mutations in all three genome segments. Further, virus variants lacking NSs, NSm or both non-structural proteins were included. Six days after feeding, virus replication was found in about 2% of the midges exposed to wild-type strain BH80/11-4. The absence of the non-structural proteins had no obvious effect on the oral susceptibility to virus infection, as 2.78% of the midges fed with the NSs-deletion mutant displayed after six days viral loads higher than the respective day-0-group, 1.92% of the midges exposed to the NSm-deletion mutant and 1.55% of midges exposed to the NSs/NSm-deletion mutant. In contrast, strain D281/12 did not replicate at all in the midges, supporting the assumption that SBV variants arising in infected foetuses are unable to enter the normal insect-mammalian host cycle.
Importance
Biting midges are responsible for the transmission of Schmallenberg virus (SBV), a pathogen of veterinary importance that primarily infects ruminants. Although SBV has been extensively studied in the mammalian host, the virus-intrinsic factors allowing infection of, and replication in, biting midges are largely unknown. Therefore, we infected laboratory-reared Culicoides sonorensis midges with SBV variants by feeding them with virus-containing blood. The SBV variants differed in their genome composition, as we used the prototype wild-type strain, a strain with multiple mutations that was isolated from the brain of a malformed foetus, and recombinants lacking either NSs or NSm or both of these non-structural proteins. While the non-structural proteins had no obvious effect, the variant from the malformed foetus did not replicate at all, indicating that virus variants with characteristic genomic mutations present in foetuses lose their ability to infect the insect vector and will be excluded from the natural transmission cycle.
