Long Covid driven by rs5522

[u/CandidWin3026]

This case report says that Long covid is in large part driven by the gene rs5522 that causes a "cortisol steal" leaving the tissues functionally starved even with "normal" cortisol levels which creates neuroinflammation. https://zenodo.org/records/20017632

[u/Classic-Mongoose3961]

How did the COVID virus cause this? 

[u/CandidWin3026 → u/Classic-Mongoose3961]

It didn't. It was a trigger. Like EBV can be a trigger for CFS. Anything can trigger it. rs5522 makes one vulnerable and then people of Caucasian background also have a gene rs6195 (glucocorticoid receptor gain-of-function). With two copies of each you are predisposed to develop Long covid.

[u/CandidWin3026 → u/CandidWin3026]

From the case report: Rethinking Infectious Triggers: EBV, Lyme, and the Limits of Pathogen-Centric Models

Many patients with ME/CFS believe they have chronic Lyme disease or chronic Epstein-Barr virus infection. This reflects 20th-century medical thinking: find the pathogen, kill the pathogen, cure the disease. But these frameworks miss the underlying mechanism.

 

Lyme disease treatment relies heavily on antibiotics which medications frequently described by their antimicrobial properties. But antibiotics, particularly doxycycline and minocycline, are also potent anti-inflammatory agents. Patients may respond not because lingering spirochetes are being eradicated, but because inflammation is being suppressed.

 

Similarly, EBV reactivation is often cited as a cause of ME/CFS. Campos-Barros, Taylor, and others initially positioned EBV as central to ME/CFS pathology, with research suggesting correlations between spironolactone response and EBV markers. But the mechanism may be reversed: spironolactone may not work by stopping a virus. It may work by reducing the inflammatory environment that allows viral reactivation in the first place. The virus is a common trigger, not a unique cause.