Post-Covid POTS and alpha-1 adrenergic AABs (G-Protein receptors)

[marcjf]

A couple of weeks after I contracted Covid, I developed symptoms that resemble Hyperadrenergic POTS, which have persisted for the past ~10.5 months.

I went for a POTS panel, and ended having elevated levels for
* Alpha-1 Adrenergic AABs

As well as at risk for
* AT1R AABs

These are not too surprising, given that a majority of POTS patients have elevated levels for these. These G-Protein AABs are also are one of the major problems in Long Covid in general: https://www.ahajournals.org/doi/full/10.1161/JAHA.119.013602

They are only part of the issue. But I hope scientists can connect the dots, and figure out why these AABs are still being produced for this long.

Has anyone here that has these AABs elevated tried treating it by targeting the AABs via immunoadsorption? This is not exactly a new concept, and there are papers detailing hypertension treatment via this process, like this one https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0003742#pone-0003742-g001

Is there any other treatment that is effective against GPCR AABs in general? There is also BC007, but it is still in trial for another condition.

 

[Pyrrhus]

Has anyone here that has these AABs elevated tried treating it by targeting the AABs via immunoadsorption?

Carmen Sheibenbogen's group in Germany published an article on this topic:

Immunoadsorption to remove ß2 adrenergic receptor antibodies in CFS/ME.
https://forums.phoenixrising.me/thr...renergic-receptor-antibodies-in-cfs-me.58277/

 

[pechius]

https://www.sciencedirect.com/science/article/pii/S2589909021000204

Functional autoantibodies against G-protein coupled receptors in patients with persistent post-COVID-19 symptoms

Highlights

•
Sera from post-COVID syndrome patients contained functionally active autoantibodies which target G-protein coupled receptors.
•
The list included pathogenic autoantibodies targeting the nociception receptor, the β2-and α1-adrenoceptors, angiotensin II AT1-, muscarinic M2-, MAS-, and ETA-receptors.
•
Included syndromes were of neurological and cardiological origin, or a combination of both.
•
This type of pathogenic autoantibody and specific autoantibody pattern were described before the first appearance of SARS-CoV2 in distinct neurological deficits and cardiovascular diseases.

 

[marcjf]

Carmen Sheibenbogen's group in Germany published an article on this topic:

Immunoadsorption to remove ß2 adrenergic receptor antibodies in CFS/ME.
https://forums.phoenixrising.me/thr...renergic-receptor-antibodies-in-cfs-me.58277/

Interesting, this is still in a research setting though. Do we find these kind of treatments commercially available? I am assuming not. I find people posting about their IVIG treatment, or Rituximab, but not Immunoadsorption.

 

[marcjf]

https://www.sciencedirect.com/science/article/pii/S2589909021000204

Functional autoantibodies against G-protein coupled receptors in patients with persistent post-COVID-19 symptoms

Highlights

•
Sera from post-COVID syndrome patients contained functionally active autoantibodies which target G-protein coupled receptors.
•
The list included pathogenic autoantibodies targeting the nociception receptor, the β2-and α1-adrenoceptors, angiotensin II AT1-, muscarinic M2-, MAS-, and ETA-receptors.
•
Included syndromes were of neurological and cardiological origin, or a combination of both.
•
This type of pathogenic autoantibody and specific autoantibody pattern were described before the first appearance of SARS-CoV2 in distinct neurological deficits and cardiovascular diseases.

That is a good one, I bumped into this, but forgot to link it, thanks for doing that.
I feel G-protein receptor AABs are a big part of the Long Covid puzzle. While they do not explain the ethiology, they give a good explanation of the symptoms. The majority of my issues are explained by disruption of the alpha-1 receptor. Hopefully we bump into less articles like "Mistery about long-haulers", "Scientists struggle to figure out why these people are still sick.".

 

[Pyrrhus]

Interesting, this is still in a research setting though. Do we find these kind of treatments commercially available?

I think it's still all experimental, but I'm not sure.
Same for "plasma exchange", where you swap your blood plasma with someone else...

 

[pattismith]

https://www.sciencedirect.com/science/article/pii/S2589909021000204

Functional autoantibodies against G-protein coupled receptors in patients with persistent post-COVID-19 symptoms

Highlights

•
Sera from post-COVID syndrome patients contained functionally active autoantibodies which target G-protein coupled receptors.
•
The list included pathogenic autoantibodies targeting the nociception receptor, the β2-and α1-adrenoceptors, angiotensin II AT1-, muscarinic M2-, MAS-, and ETA-receptors.
•
Included syndromes were of neurological and cardiological origin, or a combination of both.
•
This type of pathogenic autoantibody and specific autoantibody pattern were described before the first appearance of SARS-CoV2 in distinct neurological deficits and cardiovascular diseases.

In Sjogren, a 2021 study (with Celltrend team) found

Compared to healthy subjects, sera of patients with pSS showed significantly higher binding to β2AR and ETAR,

Autoantibodies against G-protein coupled receptors (GPCR) in Sjogren 2021 | Phoenix Rising ME/CFS Forums

In the long covid study, there is useful information about AAB that increase the HR (positive chronotropic) or decrease the HR (negative chronotropic)

The positive chronotropic GPCR-fAABs identified in the blood of Long-COVID patients targeted

- the β2-adrenoceptor (β2-fAAB),
- the α1-adrenoceptor (α1-fAAB),
- the angiotensin II AT1-receptor (AT1-fAAB),
- and the nociceptin—like opioid receptor (NOC-fAAB).

The negative chronotropic GPCR-fAABs identified targeted

-the muscarinic M2-receptor (M2-fAAB),
- the MAS-receptor (MAS-fAAB), and
- the ETA-receptor (ETA-fAAB).