There is a critical need to identify the underlying biomedical mechanisms associated with Long Covid and ME/CFS. Many studies have shown that COVID-19 can have long-term health impacts, including but not limited to increased cardiovascular disease risk, neurological/cognitive impairments, and immune system disturbances.

While evidence demonstrates a link between Long Covid and immune dysfunction, characterised by disruptions or ‘exhaustion’ of specific immune cell populations, our understanding of the precise nature and extent of their functional abnormalities remains incomplete. Further research is necessary to elucidate the specific mechanisms involved, particularly focusing on the functional impairments of affected immune cells or processes.

To fully understand why our immune system malfunctions, especially in scenarios like post-infection associated illnesses, we must delve deeper into the intricate workings of our cells, specifically focusing on the critical role of mitochondria. Often likened to powerhouses of the cell, these tiny organelles are not only responsible for energy production, but also play a crucial role in influencing how our immune system fights off pathogens and maintains overall health.

When these essential “energy centres” are damaged, a cascade of effects can occur, potentially contributing to a range of symptoms such as muscle weakness, fatigue, and cognitive impairment. Interestingly, these symptoms often overlap with those observed in infection-associated chronic conditions, suggesting a potential link between mitochondrial dysfunction and certain post-infection complications. This overlap highlights the importance of incorporating the study of immune cell metabolic function, or immunometabolic programming, into our understanding of immune dysfunction, particularly in the context of infection-associated chronic conditions.