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Long COVID pathophysiology
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== Comparison to other conditions == {| class="wikitable" !Findings !Long COVID !Post-acute SARS !ME/CFS !POTS !MCAS !Chronic Lyme disease |- |G-protein coupled receptor autoantibodies |β2- and α1-adrenoceptors, angiotensin II AT1-, muscarinic M2-, MAS-, nociceptin- and ETA-receptors | |M3 and M4 [[Muscarinic acetylcholine receptor|muscarinic acetylcholine receptors]], as well as ß2 [[Adrenergic receptor|adrenergic receptors]] |α1, β1 and β2 adrenergic receptor autoantibodies | | |- | | | | | | | |} === Post-SARS syndrome === {{Main|page_name=Post-SARS syndrome}} === ME/CFS === {{Main article|page_name=Myalgic encephalomyelitis}} === Postviral fatigue syndrome === {{Main|page_name=Postviral fatigue syndrome}} === Chronic fatigue and Idiopathic chronic fatigue === {{Main|page_name=Idiopathic chronic fatigue}} === POTS === {{Main|page_name=Postural orthostatic tachycardia syndrome}} === MCAS === {{Main|page_name=Mast cell activation syndrome}} === Post-Ebola syndrome === {{Main|page_name=Post-Ebola syndrome}} === Chronic Epstein-Barr virus === {{Main|page_name=Chronic Epstein-Barr virus}} === Post-Treatment Lyme disease syndrome === Post-treatment Lyme disease syndrome (PTLDS) is hypothesized to be caused by the presence of residual bacterial debris (possibly bacterial cell envelope fragments) stimulating the immune system. The relapsing character and the symptoms of this syndrome are very similar to the symptom presentation of Long COVID. The discovery of antigen-presenting non-classical monocytes in Long COVID<ref name="Patterson2021" /> supports the theory that both syndromes are similarly caused by residual debris of pathogens after the infection is cleared. === Alzheimer's disease === === Traumatic Brain Injury ===
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