Media release
From:
Springer Nature
Resistance to detectable SARS-CoV-2 infection highlights new vaccine targets
Past exposure to other coronaviruses may speed up the clearance of SARS-CoV-2 because the immune system remembers viral replication proteins that are highly conserved across coronaviruses, a paper in Nature indicates. Healthcare workers at high risk of SARS-CoV-2 exposure were studied, and, despite testing negative for SARS-CoV-2 infection or antibodies, they showed signs of elevated memory T cell response against the conserved complex, suggesting that they were able to rapidly clear SARS-CoV-2. The findings highlight the highly conserved proteins as targets for future vaccines against endemic and emerging coronaviruses.
Some individuals at high risk of exposure to the highly infectious SARS-CoV-2 display negative results with standard diagnostic tests. Previous research has suggested that exposure to coronaviruses produces memory T cells that may be effective in attenuating SARS-CoV-2 infection. Mala Maini, Leo Swadling and colleagues hypothesize that pre-existing memory T cells that recognize the proteins of the replication–transcription complex (RTC), a conserved structure involved in viral replication, might facilitate the rapid control of SARS-CoV-2. Designing vaccines that could mimic this expansion of cross-reactive T cells may offer protection against a range of endemic or emerging coronaviruses, the authors conclude.
The authors studied 58 healthcare workers from hospitals in London, UK, who did not test positive for SARS-CoV-2 infection despite high risk of exposure during the first wave of the pandemic in the UK. They compared T cell responses in this cohort with those in matched healthcare workers who did develop laboratory-confirmed SARS-CoV-2 infection. Those individuals who seemed to evade infection had stronger T cell responses, particularly directed against the RTC, than those of individuals who tested positive.
Journal/
conference:
Nature
Organisation/s:
University College London, UK
Funder:
The COVIDsortium is supported by funding donated by individuals, charitable Trusts, and corporations including
Goldman Sachs, Citadel and Citadel Securities, The GUy Foundation, GW Pharmaceuticals,
Kusuma Trust, and Jagclif Charitable Trust, and enabled by Barts Charity with support from
UCLH Charity. Wider support is acknowledged on the COVIDsortium website. Institutional
support from Barts Health NHS Trust and Royal Free NHS Foundation Trust facilitated study
processes, in partnership with University College London and Queen Mary University London.
This study was funded by UKRI/NIHR UK-CIC (supporting LS and MKM). MKM is also supported
by Wellcome Trust Investigator Award (214191/Z/18/Z) and CRUK Immunology grant (26603)
and LS by a Medical Research Foundation fellowship (044-0001). MN is supported by the
Wellcome Trust (207511/Z/17/Z) and by NIHR Biomedical Research Funding to UCL and
UCLH. AB is supported by Grant support a Special NUHS COVID-19 Seed Grant Call, Project
NUHSRO/2020/052/RO5+5/NUHS-COVID/6 (WBS R-571-000-077-733). JCM, CM and TAT are
directly and indirectly supported by the University College London Hospitals (UCLH) and
Barts NIHR Biomedical Research Centres and through the British Heart Foundation (BHF)
Accelerator Award (AA/18/6/34223). TAT is funded by a BHF Intermediate Research
Fellowship (FS/19/35/34374). AMV, ÁM, CM and JCM were supported by the UKRI/MRC
Covid-19 Rapid response grant COV0331. ÁM and CP are supported by Rosetrees Trust,
The John Black Charitable Foundation, and Medical College of St Bartholomew’s Hospital
Trust and NIHR-MRC grant MR/V027883/1. RJB and DMA are supported by MRC (MR/S019553/1,
MR/R02622X/1, MR/V036939/1, MR/W020610/1), NIHR Imperial Biomedical Research
Centre (BRC): ITMAT, Cystic Fibrosis Trust SRC (2019SRC015), and Horizon 2020 Marie
Skłodowska-Curie Innovative Training Network (ITN) European Training Network (No 860325).
Funding for the HLA imputed data was provided by UKRI/MRC Covid-19 rapid response
grant (Cov-0331 - MR/V027883/1). LEM is supported by a Medical Research Council Career
Development Award (MR/R008698/1). LVD is supported by a UCL Excellence Fellowship.
The funders had no role in study design data collection, data analysis, data interpretation,
or writing of the report.