Literature detail

Cross-Neutralisation of Novel Bombali Virus by Ebola Virus Antibodies and Convalescent Plasma Using an Optimised Pseudotype-Based Neutralisation Assay.

Emma M Bentley1 Samuel Richardson1 Mariliza Derveni2 Pramila Rijal3 Alain R Townsend3 Jonathan L Heeney4 Giada Mattiuzzo1 Edward Wright2
Affiliations 4 institutions
  1. Division of Virology, National Institute for Biological Standards and Control-MHRA, Blanche Lane, South Mimms EN6 3QG, UK.
  2. School of Life Sciences, University of Sussex, Brighton BN1 9QG, UK.
  3. MRC Human Immunology Unit, MRC Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 9DS, UK.
  4. Department of Veterinary Medicine, University of Cambridge, Cambridge CB3 OES, UK.
PMID 34449756 2021 Trop Med Infect Dis eng epublish
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Article

Publication summary

Ebolaviruses continue to pose a significant outbreak threat, and while Ebola virus (EBOV)-specific vaccines and antivirals have been licensed, efforts to develop candidates offering broad species cross-protection are continuing. The use of pseudotyped virus in place of live virus is recognised as an alternative, safer, high-throughput platform to evaluate anti-ebolavirus antibodies towards their development, yet it requires optimisation. Here, we have shown that the target cell line impacts neutralisation assay results and cannot be selected purely based on permissiveness. In expanding the platform to incorporate each of the ebolavirus species envelope glycoprotein, allowing a comprehensive assessment of cross-neutralisation, we found that the recently discovered Bombali virus has a point mutation in the receptor-binding domain which prevents entry into a hamster cell line and, importantly, shows that this virus can be cross-neutralised by EBOV antibodies and convalescent plasma.

cross-neutralisation ebolavirus pseudotyped virus

Structured evidence records

Evidence records

2 total
1 records
Extraction confidence 0.90
Key finding

A point mutation in the Bombali virus glycoprotein receptor-binding domain inhibits its entry into hamster cells, indicating molecular adaptation affecting host tropism.

Virus
Host
Not specified
Location
Not specified
Supporting text

We found that the recently discovered Bombali virus has a point mutation in the receptor-binding domain which prevents entry into a hamster cell line.

Genes or proteins
envelope glycoprotein
Mutations
point mutation
Mechanism types
receptor_binding; cell_entry; host_range
1 records
Extraction confidence 0.85
Key finding

A point mutation in the receptor-binding domain of Bombali virus glycoprotein prevents entry into hamster cells.

Virus
Host
Location
Not specified
Supporting text

We found that the recently discovered Bombali virus has a point mutation in the receptor-binding domain which prevents entry into a hamster cell line.

Method
pseudotype-based neutralisation assay
Receptors
receptor-binding domain