Long COVID / post-COVID profile

Long COVID (post-COVID syndrome) covers symptoms persisting beyond 12 weeks after a SARS-CoV-2 infection. Mechanisms discussed (current research, partly disputed): viral reactivation (EBV, CMV, HHV6), autoantibodies (receptor antibodies against AT1R, β-receptors), mitochondrial dysfunction, neuroinflammation, microbiome dysbiosis and microglial activation. The long COVID base profile (43 parameters) covers catecholamines, tryptophan metabolism, mitochondrial markers and intestinal inflammation factors — full diagnostics only at the practice.

Which mechanisms are being researched in long COVID

Long COVID is not a uniform condition, and so far there is no single laboratory value that confirms it. Research is investigating several mechanisms that may be involved to differing degrees in different people and could overlap. One of these is persistence of the virus: in studies, genetic material or proteins of SARS-CoV-2 were still found in gut tissue or blood months after infection in some of those affected. Studies have also found antibody patterns suggesting reactivation of the Epstein-Barr virus more often in long COVID. What role these findings play in the complaints has not yet been settled.

How long COVID may affect the immune system, vessels and tryptophan metabolism

In some studies, autoantibodies were found against receptors through which adrenaline, acetylcholine or angiotensin act; other studies could not confirm this – the finding is disputed. Persistent activation of T cells and interferon signalling, damage to the inner lining of blood vessels and tiny clots in the blood have also been described, the significance of which is likewise debated. One study observed that persistent interferon signalling reduces the absorption of tryptophan in the gut; as a result, serotonin in the blood fell, which was linked with altered signalling via the vagus nerve. The profile's measurements of tryptophan metabolism are aimed at such connections.

Long COVID: what is observed in muscles, mitochondria and the nervous system

A hallmark for many of those affected is that complaints worsen after exertion. In a study with muscle samples taken before and after exertion, long COVID showed lower mitochondrial performance, a shift towards energy production without oxygen and damage to muscle fibres. In animal models, even a mild infection triggered persistent activation of microglia – the brain's immune cells – with fewer newly formed nerve cells and changes to the nerve sheaths; in humans this is being investigated with imaging techniques. For a racing heart on standing up, damage to fine nerve fibres, autoantibodies and reduced blood volume are being discussed.

The interpretation is given in your report.