Evidence map›Paper›PMID 33497419›Full record

ArticlePLoS pathogens2021

High genetic variability of Schmallenberg virus M-segment leads to efficient immune escape from neutralizing antibodies.

Kerstin Wernike, Ilona Reimann, Ashley C Banyard, Franziska Kraatz, S Anna La Rocca, Bernd Hoffmann, Sarah McGowan, Silke Hechinger, Bhudipa Choudhury, Andrea Aebischer and 2 more

Abstract read
In one paragraph

Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
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  6. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Kerstin WernikeInstitute of Diagnostic Virology, Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany.ORCID 0000-0001-8071-0827
Ilona ReimannInstitute of Diagnostic Virology, Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany.
Ashley C BanyardDepartment of Virology, Animal and Plant Health Agency Weybridge, Addlestone, United Kingdom.ORCID 0000-0002-1286-9825
Franziska KraatzInstitute of Diagnostic Virology, Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany.
S Anna La RoccaDepartment of Virology, Animal and Plant Health Agency Weybridge, Addlestone, United Kingdom.
Bernd HoffmannInstitute of Diagnostic Virology, Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany.ORCID 0000-0001-5358-6445
Sarah McGowanDepartment of Virology, Animal and Plant Health Agency Weybridge, Addlestone, United Kingdom.ORCID 0000-0003-1507-0813
Silke HechingerInstitute of Diagnostic Virology, Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany.
Bhudipa ChoudhuryDepartment of Virology, Animal and Plant Health Agency Weybridge, Addlestone, United Kingdom.
Andrea AebischerDepartment of Experimental Animal Facilities and Biorisk Management, Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany.
Falko SteinbachDepartment of Virology, Animal and Plant Health Agency Weybridge, Addlestone, United Kingdom.ORCID 0000-0003-1236-2837
Martin BeerInstitute of Diagnostic Virology, Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schmallenberg virus (SBV) is the cause of severe fetal malformations when immunologically naïve pregnant ruminants are infected. In those malformed fetuses, a "hot-spot"-region of high genetic variability within the N-terminal region of the viral envelope protein Gc has been observed previously, and this region co-localizes with a known key immunogenic domain. We studied a series of M-segments of those SBV variants from malformed fetuses with point mutations, insertions or large in-frame deletions of up to 612 nucleotides. Furthermore, a unique cell-culture isolate from a malformed fetus with large in-frame deletions within the M-segment was analyzed. Each Gc-protein with amino acid deletions within the "hot spot" of mutations failed to react with any neutralizing anti-SBV monoclonal antibodies or a domain specific antiserum. In addition, in vitro virus replication of the natural deletion variant could not be markedly reduced by neutralizing monoclonal antibodies or antisera from the field. The large-deletion variant of SBV that could be isolated in cell culture was highly attenuated with an impaired in vivo replication following the inoculation of sheep. In conclusion, the observed amino acid sequence mutations within the N-terminal main immunogenic domain of glycoprotein Gc result in an efficient immune evasion from neutralizing antibodies in the special environment of a developing fetus. These SBV-variants were never detected as circulating viruses, and therefore should be considered to be dead-end virus variants, which are not able to spread further. The observations described here may be transferred to other orthobunyaviruses, particularly those of the Simbu serogroup that have been shown to infect fetuses. Importantly, such mutant strains should not be included in attempts to trace the spatial-temporal evolution of orthobunyaviruses in molecular-epidemiolocal approaches during outbreak investigations.

Indexed as

Genetic VariationAnimalsAntibodies, NeutralizingAntibodies, ViralBunyaviridae InfectionsCattleCattle DiseasesFemaleFetusGlycoproteinsMutationOrthobunyavirusRNA, ViralSequence DeletionSheepSheep DiseasesAntibodies, NeutralizingAntibodies, ViralGlycoproteinsRNA, ViralViral Envelope Proteins

Identifiers

PMID33497419
PMCPMC7872300

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.