An immunodominant NP<inf>105–113</inf>-B*07:02 cytotoxic T cell response controls viral replication and is associated with less severe COVID-19 disease
Issued Date
2022-01-01
Resource Type
ISSN
15292908
eISSN
15292916
Scopus ID
2-s2.0-85120634509
Pubmed ID
34853448
Journal Title
Nature Immunology
Volume
23
Issue
1
Start Page
50
End Page
61
Rights Holder(s)
SCOPUS
Bibliographic Citation
Nature Immunology Vol.23 No.1 (2022) , 50-61
Suggested Citation
Peng Y., Felce S.L., Dong D., Penkava F., Mentzer A.J., Yao X., Liu G., Yin Z., Chen J.L., Lu Y., Wellington D., Wing P.A.C., Dominey-Foy D.C.C., Jin C., Wang W., Hamid M.A., Fernandes R.A., Wang B., Fries A., Zhuang X., Ashley N., Rostron T., Waugh C., Sopp P., Hublitz P., Beveridge R., Tan T.K., Dold C., Kwok A.J., Rich-Griffin C., Dejnirattisa W., Liu C., Kurupati P., Nassiri I., Watson R.A., Tong O., Taylor C.A., Kumar Sharma P., Sun B., Curion F., Revale S., Garner L.C., Jansen K., Ferreira R.C., Attar M., Fry J.W., Russell R.A., Stauss H.J., James W., Townsend A., Ho L.P., Klenerman P., Mongkolsapaya J., Screaton G.R., Dendrou C., Sansom S.N., Bashford-Rogers R., Chain B., Smith G.L., McKeating J.A., Fairfax B.P., Bowness P., McMichael A.J., Ogg G., Knight J.C., Dong T. An immunodominant NP<inf>105–113</inf>-B*07:02 cytotoxic T cell response controls viral replication and is associated with less severe COVID-19 disease. Nature Immunology Vol.23 No.1 (2022) , 50-61. 61. doi:10.1038/s41590-021-01084-z Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/85063
Title
An immunodominant NP<inf>105–113</inf>-B*07:02 cytotoxic T cell response controls viral replication and is associated with less severe COVID-19 disease
Author(s)
Peng Y.
Felce S.L.
Dong D.
Penkava F.
Mentzer A.J.
Yao X.
Liu G.
Yin Z.
Chen J.L.
Lu Y.
Wellington D.
Wing P.A.C.
Dominey-Foy D.C.C.
Jin C.
Wang W.
Hamid M.A.
Fernandes R.A.
Wang B.
Fries A.
Zhuang X.
Ashley N.
Rostron T.
Waugh C.
Sopp P.
Hublitz P.
Beveridge R.
Tan T.K.
Dold C.
Kwok A.J.
Rich-Griffin C.
Dejnirattisa W.
Liu C.
Kurupati P.
Nassiri I.
Watson R.A.
Tong O.
Taylor C.A.
Kumar Sharma P.
Sun B.
Curion F.
Revale S.
Garner L.C.
Jansen K.
Ferreira R.C.
Attar M.
Fry J.W.
Russell R.A.
Stauss H.J.
James W.
Townsend A.
Ho L.P.
Klenerman P.
Mongkolsapaya J.
Screaton G.R.
Dendrou C.
Sansom S.N.
Bashford-Rogers R.
Chain B.
Smith G.L.
McKeating J.A.
Fairfax B.P.
Bowness P.
McMichael A.J.
Ogg G.
Knight J.C.
Dong T.
Felce S.L.
Dong D.
Penkava F.
Mentzer A.J.
Yao X.
Liu G.
Yin Z.
Chen J.L.
Lu Y.
Wellington D.
Wing P.A.C.
Dominey-Foy D.C.C.
Jin C.
Wang W.
Hamid M.A.
Fernandes R.A.
Wang B.
Fries A.
Zhuang X.
Ashley N.
Rostron T.
Waugh C.
Sopp P.
Hublitz P.
Beveridge R.
Tan T.K.
Dold C.
Kwok A.J.
Rich-Griffin C.
Dejnirattisa W.
Liu C.
Kurupati P.
Nassiri I.
Watson R.A.
Tong O.
Taylor C.A.
Kumar Sharma P.
Sun B.
Curion F.
Revale S.
Garner L.C.
Jansen K.
Ferreira R.C.
Attar M.
Fry J.W.
Russell R.A.
Stauss H.J.
James W.
Townsend A.
Ho L.P.
Klenerman P.
Mongkolsapaya J.
Screaton G.R.
Dendrou C.
Sansom S.N.
Bashford-Rogers R.
Chain B.
Smith G.L.
McKeating J.A.
Fairfax B.P.
Bowness P.
McMichael A.J.
Ogg G.
Knight J.C.
Dong T.
Author's Affiliation
Siriraj Hospital
Beijing YouAn Hospital, Capital Medical University
The Wellcome Centre for Human Genetics
University of Cambridge
University of Oxford
Helmholtz Center Munich German Research Center for Environmental Health
Xinjiang Medical University
University College London
Sir William Dunn School of Pathology
Nuffield Department of Medicine
Kennedy Institute of Rheumatology
University of Oxford Medical Sciences Division
ProImmune Limited
Beijing YouAn Hospital, Capital Medical University
The Wellcome Centre for Human Genetics
University of Cambridge
University of Oxford
Helmholtz Center Munich German Research Center for Environmental Health
Xinjiang Medical University
University College London
Sir William Dunn School of Pathology
Nuffield Department of Medicine
Kennedy Institute of Rheumatology
University of Oxford Medical Sciences Division
ProImmune Limited
Other Contributor(s)
Abstract
NP105–113-B*07:02-specific CD8+ T cell responses are considered among the most dominant in SARS-CoV-2-infected individuals. We found strong association of this response with mild disease. Analysis of NP105–113-B*07:02-specific T cell clones and single-cell sequencing were performed concurrently, with functional avidity and antiviral efficacy assessed using an in vitro SARS-CoV-2 infection system, and were correlated with T cell receptor usage, transcriptome signature and disease severity (acute n = 77, convalescent n = 52). We demonstrated a beneficial association of NP105–113-B*07:02-specific T cells in COVID-19 disease progression, linked with expansion of T cell precursors, high functional avidity and antiviral effector function. Broad immune memory pools were narrowed postinfection but NP105–113-B*07:02-specific T cells were maintained 6 months after infection with preserved antiviral efficacy to the SARS-CoV-2 Victoria strain, as well as Alpha, Beta, Gamma and Delta variants. Our data show that NP105–113-B*07:02-specific T cell responses associate with mild disease and high antiviral efficacy, pointing to inclusion for future vaccine design.