Ancestral SARS-CoV-2-specific T cells cross-recognize the Omicron variant.
Nat Med
; 28(3): 472-476, 2022 03.
Article
in English
| MEDLINE | ID: covidwho-1632511
ABSTRACT
The emergence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron (B.1.1.529) variant of concern (VOC) has destabilized global efforts to control the impact of coronavirus disease 2019 (COVID-19). Recent data have suggested that B.1.1.529 can readily infect people with naturally acquired or vaccine-induced immunity, facilitated in some cases by viral escape from antibodies that neutralize ancestral SARS-CoV-2. However, severe disease appears to be relatively uncommon in such individuals, highlighting a potential role for other components of the adaptive immune system. We report here that SARS-CoV-2 spike-specific CD4+ and CD8+ T cells induced by prior infection or BNT162b2 vaccination provide extensive immune coverage against B.1.1.529. The median relative frequencies of SARS-CoV-2 spike-specific CD4+ T cells that cross-recognized B.1.1.529 in previously infected or BNT162b2-vaccinated individuals were 84% and 91%, respectively, and the corresponding median relative frequencies for SARS-CoV-2 spike-specific CD8+ T cells were 70% and 92%, respectively. Pairwise comparisons across groups further revealed that SARS-CoV-2 spike-reactive CD4+ and CD8+ T cells were functionally and phenotypically similar in response to the ancestral strain or B.1.1.529. Collectively, our data indicate that established SARS-CoV-2 spike-specific CD4+ and CD8+ T cell responses, especially after BNT162b2 vaccination, remain largely intact against B.1.1.529.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
CD4-Positive T-Lymphocytes
/
CD8-Positive T-Lymphocytes
/
Cross Protection
/
SARS-CoV-2
/
COVID-19
Type of study:
Experimental Studies
/
Observational study
/
Randomized controlled trials
Topics:
Vaccines
/
Variants
Limits:
Humans
Language:
English
Journal:
Nat Med
Journal subject:
Molecular Biology
/
Medicine
Year:
2022
Document Type:
Article
Affiliation country:
S41591-022-01700-x
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