A study led by the University of Cambridge has revealed that an inflammatory protein could be a new potential biomarker and target for the treatment of long COVID.
Published in Science Advances, the study found that the production of a protein called interferon gamma (IFN-Y), a pro-inflammatory molecule, persisted until symptoms improved in long COVID patients.
Continuing to affect millions of people globally, long COVID refers to the progressive signs, symptoms and conditions that continue or develop after acute COVID-19 infection caused by the SARS-CoV-2 virus.
According to the Office for National Statistics (ONS), 2.9% of the UK population were experiencing self-reported long COVID as of March 2023.
Beginning in 2020, researchers studied 111 COVID-19-confirmed patients admitted to Addenbrooke’s Hospital, Cambridge University Hospital, Royal Papworth Hospital and Cambridge and Peterborough NHS Foundation Trusts at 28 days, 90 days and 180 days following symptom onset.
For nearly three years, researchers monitored patients with long COVID fatigue – the most common and debilitating symptom of the condition – to determine why some patients recovered more than others.
The 55 patients recruited between August 2020 and July 2021 from the long COVID clinic at Addenbrooke’s all experienced severe symptoms for at least five months after acute COVID-19.
After analysing patients’ blood samples for signs of cytokines – small proteins that play a key role in the function of immune system cells and blood cells – they found that white blood cells of individuals infected with SARS-CoV-2 produced IFN-Y.
More specifically, in patients living with long COVID, higher levels of IFN-Y persisted for up to 31 months.
After conducting cell depletion assays, researchers identified that immune cells known as CD8-positive T cells were the precise cell types responsible for producing IFN-Y but required contact with another immune cell type: CD14 monocytes.
Additionally, the team measured the release of IFN-Y participants before and after vaccination and discovered a reduction in IFN-Y post-vaccination in patients whose symptoms resolved.
Co-author of the study, Dr Benjamin Krishna, Cambridge Institute of Therapeutic Immunology and Infectious Diseases, said: “We hope that this could help to pave the way to develop therapies and give some patients a firm diagnosis.”