Modelling the evolution of Schmallenberg virus seroprevalence in a sheep flock after natural infection.

Modelling the long-term seroprevalence evolution against Schmallenberg virus (SBV) is of first interest to plan vaccination strategies and to predict viral resurgence. The objectives of this study were first to estimate the duration of colostral immunity and the persistence of active immunity in a sheep flock that encountered two episodes of natural SBV infection and then to model the evolution of SBV seroprevalence by considering immune status as well as zootechnical variables. The entire sheep flock of the University of Namur composed by around 400 ewes producing 600 lambs a year and characterized by an annual 24.0% renewal rate was used for this study from January 2012 until December 2016. Antibody titers were estimated by performing Virus Neutralization Test (VNT) from blood and colostrum samples collected in lambs and adult sheep. Colostral antibodies against SBV of lambs born to seropositive ewes were detectable during four months. A significant increase of anti-SBV antibody titers was observed in lambs' serum as well as in ewes' colostrum between the time of first viral episode (2011) and the time of SBV reemergence (2012) suggesting a booster effect of viral resurgence on immune status. In naturally SBV infected adult sheep, the active immunity was estimated to last at least four years. These results combined with flock management data allowed to develop a mathematical model to predict the evolution of SBV seroprevalence at a herd scale. The accuracy of this model was assessed by VNT experiment performed at the end of the study. By applying this model to the sheep flock of the University of Namur, it was estimated that an annual 24.0% renewal rate led to total seronegativity, and so high susceptibility to viral resurgence, in 50 months after time of last natural infection. The third SBV episode detected in this research sheep flock within the expected time demonstrated huge within-flock susceptibility.

S segment variability during the two first years of the spread of Schmallenberg virus.

A large sheep flock screened over a two-year period showed active spreading of Schmallenberg virus (SBV) during the summers of 2011 and 2012. Transplacental infections were observed during the two associated lambing periods (the winters of 2012 and 2013). Analysis of small (S) segment sequences of 38 SBV-positive samples, collected during periods of viral spreading and lambing revealed intra-herd sequences diversity and sub-consensus variability occurring after transplacental infections. In comparison with the nucleoprotein (N), which appeared to be conserved, the non-structural protein (NSs) showed the highest level of variability at the time of viral emergence and over the two-year analysis period.

Schmallenberg virus infection of ruminants: challenges and opportunities for veterinarians.

In 2011, European ruminant flocks were infected by Schmallenberg virus (SBV) leading to transient disease in adult cattle but abortions and congenital deformities in calves, lambs, and goat kids. SBV belonging to the Simbu serogroup (family Bunyaviridae and genus Orthobunyavirus) was first discovered in the same region where bluetongue virus serotype 8 (BTV-8) emerged 5 years before. Both viruses are transmitted by biting midges (Culicoides spp.) and share several similarities. This paper describes the current knowledge of temporal and geographical spread, molecular virology, transmission and susceptible species, clinical signs, diagnosis, prevention and control, impact on ruminant health, and productivity of SBV infection in Europe, and compares SBV infection with BTV-8 infection in ruminants.

Characterization of messenger RNA termini in Schmallenberg virus and related Simbuviruses.

Schmallenberg virus (SBV) is an emerging arbovirus infecting ruminants in Europe. SBV belongs to the Bunyaviridae family within the Simbu serogroup. Its genome comprises three segments, small (S), medium (M) and large (L), that together encode six proteins and contain NTRs. NTRs are involved in initiation and termination of transcription and in genome packaging. This study explored the 3' mRNA termini of SBV and related Simbuviruses. In addition, the 5' termini of SBV messenger RNA (mRNA) were characterized. For the three SBV segments, cap-snatching was found to initiate mRNA transcription both in vivo and in vitro. The presence of extraneous nucleotides between host RNA leaders and the viral termini fits with the previously described prime-and-realign theory. At the 3' termini, common features were identified for SBV and related Simbuviruses. However, different patterns were observed for the termini of the three segments from the same virus type.

Schmallenberg virus among female lambs, Belgium, 2012.

Reemergence of Schmallenberg virus (SBV) occurred among lambs (n = 50) in a sheep flock in Belgium between mid-July and mid-October 2012. Bimonthly assessment by quantitative reverse transcription PCR and seroneutralization demonstrated that 100% of lambs were infected. Viremia duration may be longer in naturally infected than in experimentally infected animals.

In vivo and in vitro identification of a hypervariable region in Schmallenberg virus.

Detected for the first time in 2011, Schmallenberg virus (SBV) is an orthobunyavirus of the Simbu serogroup that caused a large outbreak in European ruminants. In a tight time frame, data have been obtained on SBV epidemiology and the clinical pictures associated with this new viral infection, but little information is available on the molecular biology of SBV. In this study, SBV sequence variability was characterized from the central nervous system of two stillborn lambs in a naturally infected herd. A hypervariable region (HVR) was detected in the N-terminal region of the SBV Gc glycoprotein through sequencing and analysis of the two full-length genomes representative of intra-herd SBV dissemination. In vitro growth assays coupled with full-length genome sequencing were performed on the two isolates after successive cellular passages, showing an in vitro adaptation of SBV and mutation accumulation inside the HVR in the absence of immune selective pressure.