Researchers have shown for the first time that malfunctioning behaviour of a type of immune cell is linked to specific symptoms of Long Covid.
Normally functioning monocytes, made in the bone marrow, would travel through the blood to the lungs where they surround and kill the virus and boost the immune response.
However, scientists and clinicians discovered that in Long Covid, abnormal migration of these cells corresponds to the most commonly reported symptom, shortness of breath. A different migration profile alongside changes to other functions correspond to fatigue.
The unique monocyte signatures defining subgroups of Long Covid patients reveal new pathways that could targeted for novel therapeutic opportunities in Long Covid patients.
The research team was from The University of Manchester, Manchester University NHS Foundation Trust (MFT), Northern Care Alliance Foundation Trust (NCA), and the National Institute for Health and Care Research (NIHR) Manchester Biomedical Research Centre (BRC).
Dr Elizabeth Mann, Wellcome Trust/Royal Society Sir Henry Dale Fellow at The University of Manchester’s Lydia Becker Institute said: “There is now a wealth of evidence indicating that chronic morbidity persists in many Covid-19 patients during convalescence manifesting as Long Covid which remains a global public health problem despite vaccination programmes and milder strains of SARS-CoV-2.
“These debilitating symptoms including extreme fatigue, shortness of breath, myalgia, brain fog, depression, fibrotic lung disease and pulmonary vascular disease and we now know this can last for many months or even years following infection.
“But treatment options for Long Covid are currently limited, since the development of targeted therapeutic strategies requires an in depth understanding of the underlying immunological pathophysiology. Our work finding a link between monocyte function and specific Long Covid symptoms may provide an important first step on the road to possible treatments.”
