Robust SARS-CoV-2-specific T-cell immunity is maintained at 6 months following primary infection

10.1101/2020.11.01.362319

bioRxiv

2nd November 2020

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This research has not been peer-reviewed, and has been posted on pre-print repository bioRxiv. This is a preliminary report that should not be regarded as conclusive, guide clinical practice/health-related behaviour, or be reported in news media as established information.


Abstract

The immune response to SARS-CoV-2 is critical in both controlling primary infection and preventing re-infection. However, there is concern that immune responses following natural infection may not be sustained and that this may predispose to recurrent infection. We analysed the magnitude and phenotype of the SARS-CoV-2 cellular immune response in 100 donors at six months following primary infection and related this to the profile of antibody level against spike, nucleoprotein and RBD over the previous six months. T-cell immune responses to SARS-CoV-2 were present by ELISPOT and/or ICS analysis in all donors and are characterised by predominant CD4+ T cell responses with strong IL-2 cytokine expression. Median T-cell responses were 50% higher in donors who had experienced an initial symptomatic infection indicating that the severity of primary infection establishes a ‘setpoint’ for cellular immunity that lasts for at least 6 months. The T-cell responses to both spike and nucleoprotein/membrane proteins were strongly correlated with the peak antibody level against each protein. The rate of decline in antibody level varied between individuals and higher levels of nucleoprotein-specific T cells were associated with preservation of NP-specific antibody level although no such correlation was observed in relation to spike-specific responses. In conclusion, our data are reassuring that functional SARS-CoV-2-specific T-cell responses are retained at six months following infection although the magnitude of this response is related to the clinical features of primary infection.


 

Author list:

Zuo J1*, Dowell A1*, Pearce H1*, Verma K1*, Long HM1, Begum J1, Aiano F2, Amin-ChowdhuryZ2, Hallis B3, Stapley L3, Borrow R4, Linley E4, Ahmad S5, Parker B6, Horsley A7, AmirthalingamG2, Brown K2, Ramsay ME2, Ladhani S2,8*, Moss P1*. 

 

1. Institute of Immunology and Immunotherapy, University of Birmingham, UK. B15 2TA
2. Immunisation and Countermeasures Division, National Infection Service, PHE Colindale. 61 Colindale Avenue, London NW9 5EQ.
3. Immunoassay Lab, National Infection Service, Porton Down SP4 0JG
4. Sero-epidemiology Unit, Public Health England, Public Health Laboratory Manchester, Manchester Medical Microbiology Partnership, Manchester Royal Infirmary, Oxford Road, Manchester, M13 9WL
5. The NIHR Manchester Clinical Research Facility at Wythenshawe Hospital, Charles Blackley Ward, North West Lung Research Centre, Manchester University NHS Foundation Trust, Wythenshawe Hospital, South moor Road, Manchester, M23 9LT
6. NIHR Manchester Clinical Research Facility, Manchester Royal Infirmary, Oxford Rd, Manchester, M13 9WL & Kellgren Centre for Rheumatology, NIHR Manchester Biomedical Research Centre, Manchester University NHS Foundation Trust, Manchester, M13 9WL
7. University of Manchester and NIHR Manchester Clinical Research Facility, Manchester University NHS Foundation Trust, Manchester M23 9LT
8. Paediatric Infectious Diseases Research Group (PIDRG), St. Georges University of London, (SGUL), London, UK