Author

R. Datir

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Microbiology· 3

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 3 Organism:human· 3 Assay:proteomics· 1 Assay:whole-genome sequencing· 1

Frequent Co-Authors

B. Meng· 3 shared D. Collier· 2 shared G. Papa· 2 shared I. Ferreira· 2 shared R. K. Gupta· 2 shared A. Abdullahi· 1 shared A. Carabelii· 1 shared A. Lever· 1 shared

Activity by Year

2020-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 36 mutual co-author links

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3 shared papersMicrobiology

B. Meng

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3 papers

Recent·Most cited

SARS-CoV-2 Spike N-Terminal Domain modulates TMPRSS2-dependent viral entry and fusogenicity

B. Meng, R. Datir, J. Choi, CITIID-NIHR BioResource COVID-19 Collaboration, J. Bradley, K. G. Smith, J. H. Lee, R. K. Gupta

This study examines how mutations in the SARS-CoV-2 Spike N-Terminal Domain affect viral entry and fusogenicity, showing context-dependent modulation of spike function.

bioRxiv · May 7, 2022Microbiology

SARS-CoV-2 B.1.617.2 Delta variant replication, sensitivity to neutralising antibodies and vaccine breakthrough

P. Mlcochova, S. A. Kemp, M. Shanker Dhar, G. Papa, B. Meng, S. Mishra, C. Whittaker, T. Mellan, I. Ferreira, R. Datir, D. Collier, S. Singh, R. Pandey, K. Ponnusamy, V. S. Radhakrishnan, , Saliba

This study evaluates the replication, antibody sensitivity, and vaccine efficacy of the SARS-CoV-2 B.1.617.2 Delta variant compared to other variants and vaccine-elicited immunity.

bioRxiv · May 8, 2021 · PreprintMicrobiology

Recurrent emergence and transmission of a SARS-CoV-2 Spike deletion H69/V70

S. Kemp, B. Meng, I. Ferreira, R. Datir, W. Harvey, D. Collier, COVID-19 Genomics UK (COG-UK) consortium, G. Papa, A. Carabelii, S. Lytras, J. Kenyon, A. Lever, L. James, D. L. Robertson, R. K. Gupta

This paper identifies a recurrent SARS-CoV-2 Spike deletion (H69/V70) that increases infectivity and compensates for RBD mutations, suggesting it may facilitate immune escape and variant emergence.

bioRxiv · Dec 14, 2020Microbiology