CB2 BOOK END REGISTRATION

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CB2 BOOK END REGISTRATION

I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as. 'NIHR BioResource' REC ref 17/EE/0025, and 'Genetic variation AND Altered Leucocyte Function in health and disease - GANDALF' REC ref 08/H0308/176Īll necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived.

The details of the IRB/oversight body that provided approval or exemption for the research described are given below: I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. is a Wellcome Senior Fellow and was supported by funding from the Wellcome (Ref: 207498/Z/17/Z). was funded by the MRC (CSF MR/P008801/1) and NHSBT (WPA15-02) I.G.G. was funded by a Wellcome COVID-19 Rapid Response DCF and the Fondation Botnar N.M. is the recipient of Wellcome Senior Clinical Research Fellowship (108070/Z/15/Z) C.H. is the recipient of a Wellcome Investigator Award (200871/Z/16/Z) M.P.W. We are grateful for the generous support of CVC Capital Partners, the Evelyn Trust (20/75), UKRI COVID Immunology Consortium, Addenbrooke's Charitable Trust (12/20A) and the NIHR Cambridge Biomedical Research Centre for their financial support. The authors have declared no competing interest. These late immunometabolic inflammatory changes and unresolved immune cell defects, if persistent, may contribute to “long COVID”.

Immune recovery is complex, with profound persistent cellular abnormalities correlating with a change in the nature of the inflammatory response, where signatures characteristic of increased oxidative phosphorylation and reactive-oxygen species-associated inflammation replace those driven by TNF and IL-6. Viral load does not correlate with the development of this pathological response, but does with its subsequent severity. Such early evidence of inflammation suggests immunopathology may be inevitable in some individuals, or that preventative intervention might be needed before symptom onset.

Those presenting to hospital had delayed adaptive responses and systemic inflammation already evident at around symptom onset.

In a study of 207 SARS-CoV2-infected individuals with a range of severities followed over 12 weeks from symptom onset, we demonstrate that an early robust immune response, without systemic inflammation, is characteristic of asymptomatic or mild disease.

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