Researchers demonstrate that Long Covid is marked by activation of the body’s immune inflammatory response system (IRS) and increased immune-associated neurotoxicity.
Years after lockdown, ‘Long Covid’ is still proving to be a serious challenge worldwide. The evidence suggests that an increasing number of people who have contracted coronavirus suffer persistent long-term effects such as chronic fatigue, cognitive disfunction and insomnia. This impacts on their quality of life and puts additional pressure on healthcare systems.
In seeking to develop effective treatment for such conditions, research continues into understanding the mechanisms that cause Long Covid. The new issue of medical journal Brain, Behaviour and Immunity includes a meta-analysis of more than 100 separate such studies, using them to draw conclusions about the way the disease can impact the immune system.
The authors analysed the results of 103 studies, comprising a total of 5,502 patients with Long Covid and 5,962 patients without, in what’s thought to be the first such meta-analysis on such a large scale. Indeed, the analysis covers all available literature on the subject up to July 5, 2024.
Between them, the studies explored a range of different factors. For example, some examined such matters as the profile of a patient’s immune inflammatory response system (IRS) and compensatory immunoregulatory system (CIRS). There were also studies of levels of proteins called cytokines and associated chemokines. These normally defend the body from germs; too many cytokines, however, can result in excess inflammation and such conditions as autoimmune diseases. Growth factors, levels of C-reactive proteins (CRP) and immune-associated neurotoxicity were also covered in these studies.
By looking at these various studies as a whole, the researchers found that patients with Long Covid typically exhibit heightened immune-inflammation, enhanced cell-mediated immunity and immune-related neurotoxicity than patients without Long Covid.
The authors say that more extensive examination of cytokines, chemokines and growth factor profiles in relation to Long Covid will be ‘instrumental’ in better understanding the mechanisms involved in this illness. They also admit certain limitations to their meta-analysis, not least that they did not have the opportunity to ‘investigate the interplay between neuro-oxidative and neuroimmune-inflammatory pathways’ in the context of Long Covid. Clearly, more research is needed.
Yet these findings are a significant step forward in our understanding of the mechanisms involved in Long Covid, which in turn makes it possible to develop better targeted and so more effective treatments.
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