The impact of viral mutations on recognition by SARS-CoV-2 specific T cells
Authors: de Silva, T.I., Buchan, S.L. et al.
Journal: iScience
Volume: 24
Issue: 11
eISSN: 2589-0042
DOI: 10.1016/j.isci.2021.103353
Abstract:We identify amino acid variants within dominant SARS-CoV-2 T cell epitopes by interrogating global sequence data. Several variants within nucleocapsid and ORF3a epitopes have arisen independently in multiple lineages and result in loss of recognition by epitope-specific T cells assessed by IFN-γ and cytotoxic killing assays. Complete loss of T cell responsiveness was seen due to Q213K in the A∗01:01-restricted CD8+ ORF3a epitope FTSDYYQLY207-215; due to P13L, P13S, and P13T in the B∗27:05-restricted CD8+ nucleocapsid epitope QRNAPRITF9-17; and due to T362I and P365S in the A∗03:01/A∗11:01-restricted CD8+ nucleocapsid epitope KTFPPTEPK361-369. CD8+ T cell lines unable to recognize variant epitopes have diverse T cell receptor repertoires. These data demonstrate the potential for T cell evasion and highlight the need for ongoing surveillance for variants capable of escaping T cell as well as humoral immunity.
https://eprints.bournemouth.ac.uk/36742/
Source: Scopus
The impact of viral mutations on recognition by SARS-CoV-2 specific T cells.
Authors: de Silva, T.I. et al.
Journal: iScience
Volume: 24
Issue: 11
Pages: 103353
eISSN: 2589-0042
DOI: 10.1016/j.isci.2021.103353
Abstract:We identify amino acid variants within dominant SARS-CoV-2 T cell epitopes by interrogating global sequence data. Several variants within nucleocapsid and ORF3a epitopes have arisen independently in multiple lineages and result in loss of recognition by epitope-specific T cells assessed by IFN-γ and cytotoxic killing assays. Complete loss of T cell responsiveness was seen due to Q213K in the A∗01:01-restricted CD8+ ORF3a epitope FTSDYYQLY207-215; due to P13L, P13S, and P13T in the B∗27:05-restricted CD8+ nucleocapsid epitope QRNAPRITF9-17; and due to T362I and P365S in the A∗03:01/A∗11:01-restricted CD8+ nucleocapsid epitope KTFPPTEPK361-369. CD8+ T cell lines unable to recognize variant epitopes have diverse T cell receptor repertoires. These data demonstrate the potential for T cell evasion and highlight the need for ongoing surveillance for variants capable of escaping T cell as well as humoral immunity.
https://eprints.bournemouth.ac.uk/36742/
Source: PubMed
The impact of viral mutations on recognition by SARS-CoV-2 specific T cells
Authors: de, S.T.I. et al.
Journal: ISCIENCE
Volume: 24
Issue: 11
eISSN: 2589-0042
DOI: 10.1016/j.isci.2021.103353
https://eprints.bournemouth.ac.uk/36742/
Source: Web of Science (Lite)
The impact of viral mutations on recognition by SARS-CoV-2 specific T cells
Authors: de Silva, T.I., Buchan, S.L. et al.
Journal: iScience
Volume: 24
Issue: 11
eISSN: 2589-0042
DOI: 10.1016/j.isci.2021.103353
Abstract:We identify amino acid variants within dominant SARS-CoV-2 T cell epitopes by interrogating global sequence data. Several variants within nucleocapsid and ORF3a epitopes have arisen independently in multiple lineages and result in loss of recognition by epitope-specific T cells assessed by IFN-γ and cytotoxic killing assays. Complete loss of T cell responsiveness was seen due to Q213K in the A∗01:01-restricted CD8+ ORF3a epitope FTSDYYQLY207-215; due to P13L, P13S, and P13T in the B∗27:05-restricted CD8+ nucleocapsid epitope QRNAPRITF9-17; and due to T362I and P365S in the A∗03:01/A∗11:01-restricted CD8+ nucleocapsid epitope KTFPPTEPK361-369. CD8+ T cell lines unable to recognize variant epitopes have diverse T cell receptor repertoires. These data demonstrate the potential for T cell evasion and highlight the need for ongoing surveillance for variants capable of escaping T cell as well as humoral immunity.
https://eprints.bournemouth.ac.uk/36742/
Source: Manual
The impact of viral mutations on recognition by SARS-CoV-2 specific T cells.
Authors: de Silva, T.I. et al.
Journal: iScience
Volume: 24
Issue: 11
Pages: 103353
eISSN: 2589-0042
ISSN: 2589-0042
DOI: 10.1016/j.isci.2021.103353
Abstract:We identify amino acid variants within dominant SARS-CoV-2 T cell epitopes by interrogating global sequence data. Several variants within nucleocapsid and ORF3a epitopes have arisen independently in multiple lineages and result in loss of recognition by epitope-specific T cells assessed by IFN-γ and cytotoxic killing assays. Complete loss of T cell responsiveness was seen due to Q213K in the A∗01:01-restricted CD8+ ORF3a epitope FTSDYYQLY207-215; due to P13L, P13S, and P13T in the B∗27:05-restricted CD8+ nucleocapsid epitope QRNAPRITF9-17; and due to T362I and P365S in the A∗03:01/A∗11:01-restricted CD8+ nucleocapsid epitope KTFPPTEPK361-369. CD8+ T cell lines unable to recognize variant epitopes have diverse T cell receptor repertoires. These data demonstrate the potential for T cell evasion and highlight the need for ongoing surveillance for variants capable of escaping T cell as well as humoral immunity.
https://eprints.bournemouth.ac.uk/36742/
Source: Europe PubMed Central
The impact of viral mutations on recognition by SARS-CoV-2 specific T cells
Authors: de Silva, T.I. et al.
Journal: iScience
Volume: 24
Issue: 11
ISSN: 2589-0042
Abstract:We identify amino acid variants within dominant SARS-CoV-2 T cell epitopes by interrogating global sequence data. Several variants within nucleocapsid and ORF3a epitopes have arisen independently in multiple lineages and result in loss of recognition by epitope-specific T cells assessed by IFN-γ and cytotoxic killing assays. Complete loss of T cell responsiveness was seen due to Q213K in the A∗01:01-restricted CD8+ ORF3a epitope FTSDYYQLY207-215; due to P13L, P13S, and P13T in the B∗27:05-restricted CD8+ nucleocapsid epitope QRNAPRITF9-17; and due to T362I and P365S in the A∗03:01/A∗11:01-restricted CD8+ nucleocapsid epitope KTFPPTEPK361-369. CD8+ T cell lines unable to recognize variant epitopes have diverse T cell receptor repertoires. These data demonstrate the potential for T cell evasion and highlight the need for ongoing surveillance for variants capable of escaping T cell as well as humoral immunity.
https://eprints.bournemouth.ac.uk/36742/
Source: BURO EPrints
Preferred by: Anna Mantzouratou