Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), usually caused by a viral infection, is known to cause brain-centric symptoms of neuroinflammation, loss of homeostasis, brain fog, lack of restorative sleep, and poor response to even minor stressors. Long-COVID has similar effects in humans and is also thought to be caused by neuroinflammation. Lead author Emeritus Professor Warren Tate, of the University of Otago’s Department of Biochemistry, says how these debilitating effects develop in the brain is poorly understood. In a study published in Frontiers in Neurology, he and colleagues from Otago, Victoria University of Wellington and the University of Technology Sydney developed a unifying model to explain how the brain-centric symptoms of these diseases are maintained through a brain connection -body. They suggest that, after an initial viral infection or stressful event, the resulting systemic pathology moves to the brain via neurovascular pathways or through a dysfunctional blood-brain barrier. This leads to chronic neuroinflammation, leading to a prolonged illness with chronic relapse recovery cycles. The model suggests that healing does not occur because a signal is constantly cycling from the brain to the body, causing the patient to relapse. Creating this model is not only important for the “huge research effort ahead,” but also for providing recognition to ME/CFS and long-term COVID sufferers. “These diseases are very closely related and it is clear that the biological basis of Long COVID is undoubtedly linked to the original COVID infection – so there should no longer be any debate and doubt about the fact that post-viral fatigue syndromes such as ME /CFS is biologically based and involves very disturbed physiology,” says Emeritus Professor Tate. This work will enable the development of optimal evidence-based knowledge of these diseases and best management practices for medical professionals. “Patients need appropriate confirmation of their biological condition and help to alleviate the distressing symptoms of these very difficult, life-changing syndromes, which are difficult for patients to manage on their own. “This work highlighted that there is a sensitive subset of people who develop such syndromes when exposed to severe stress, such as infection with COVID-19 or Epstein Barr glandular fever virus, or in some individuals with vaccination interpreted as severe stress. “What should be a transient inflammatory/immune response in the body to clear infection, develop immunity and manage physiological stress, becomes chronic and so the disease persists.”
