Journal
IMMUNITY
Volume 54, Issue 5, Pages 1055-+Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2021.04.006
Keywords
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Categories
Funding
- QIMR Berghofer COVID-19 appeal
- Monash University
- Australian Nuclear Science and Technology Organisation (ANSTO)
- AINSE
- ECR
- Australian Research Council (ARC)
- National Health and Medical Research Council (NHMRC) [GNT1132519]
- Medical Research Future Fund (MRFF) [APP2005654]
- Australian Government Research Training Program scholarship
- NHMRC C.J. Martin fellowship [1110429]
- Australian Research Council DECRA [DE210101479, DE180100512]
- NHMRC SRF [1159272]
- National Health and Medical Research Council of Australia [1110429, 1159272] Funding Source: NHMRC
- Australian Research Council [DE210101479] Funding Source: Australian Research Council
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Efforts are being made to understand the immune response to SARS-CoV-2, with a focus on T cell immunity and cross-recognition with seasonal coronaviruses. Research has shown that the N protein of SARS-CoV-2 induces an immunodominant response and T cells demonstrate cross-reactivity towards certain coronaviruses through specific peptide conformations.
Efforts are beingmade worldwide to understand the immune response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for the coronavirus disease 2019 (COVID-19) pandemic, including the impact of T cell immunity and cross-recognition with seasonal coronaviruses. Screening of SARS-CoV-2 peptide pools revealed that the nucleocapsid (N) protein induced an immunodominant response in HLA-B7(+) COVID-19-recovered individuals that was also detectable in unexposed donors. A single N-encoded epitope that was highly conserved across circulating coronaviruses drove this immunodominant response. In vitro peptide stimulation and crystal structure analyses revealed T cell-mediated cross-reactivity toward circulating OC43 and HKU-1 betacoronaviruses but not 229E or NL63 alphacoronaviruses because of different peptide conformations. T cell receptor (TCR) sequencing indicated that cross-reactivity was driven by private TCR repertoires with a bias for TRBV27 and a long CDR3b loop. Our findings demonstrate the basis of selective T cell cross-reactivity for an immunodominant SARS-CoV-2 epitope and its homologs from seasonal coronaviruses, suggesting long-lasting protective immunity.
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