Thread by @MarekSJF

Very interesting podcast by @SessionsTlc with @Dr_B_Hohberger about her research on #LongCovid and #BC007.As someone who follows the research on GPCR autoantibodies in #MECFS/#LongCovid, this interview was very insightful and clarified some points for me.1 tlcsessions.net/episodes/episo…

Summary of the main points (I also added some notes):
Endothelial dysfunction was the starting point, well known in glaucoma (eye disease), in 2020 also after virus infection observed. Post-Covid patients had reduced blood flow to the eyes, therefore presumably to other parts
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of the body. Reduced blood flow causes problems in the long run, occlusion is not good for the surrounding tissue. At the same time it was found that patients had certain autoantibodies (AAB), it is known that in presence of these AAB the perfusion in the eyes is reduced, and
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probably in the rest of the body. These GPCR-autoantibodies activate target receptors in cells in a harmful way, different from the normal activation by physiological agents: over stimulation, and receptor desensitization. This causes many problems in the body, but it is
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unknown what happens exactly in the cellular target after such activation. LC patients have 4-5 different AAB, e.g. beta2-adrenergic receptors antibody. AAB can be present in patients with no symptoms, only when there is a coexisting factor do symptoms occur.
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There must be a preexisting factor for developing LC, but it is unknown what it is. (note: in we can see that also many healthy people have these AAB). The idea was to use BC007 to remove AAB and therefore increase blood flow in the eyes
6sciencedirect.com/science/articl…

(and body), and see which symptoms decrease or disappear. BC originally had the same idea for heart diseases with the same AAB. Healing attempts in Erlangen: 4 LC patients, only one 75-min infusion needed, no side effects, first brain fog improved, symptom-free in 3-4 weeks.
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BUT the outcome of the treatment depends on the severity of the symptoms, BC007 improves the blood flow, but irreversible damage to the cells may already be present.
(note: I assume that there have been unpublished healing attempts, I think the remark above is based on that).
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BC007 neutralizes the functional activity of AAB. Normally the body would produce new AAB after a short period of time, but new AAB no longer appear after treatment with BC007 (note: this is the crucial point, otherwise such treatment would be useless).
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AAB are produced by B-cells (note: In a talk Prof. Harrer said that BC007 actually acts on these B-cells and stops the production of AAB ).

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But there must be some kind of autoimmune predisposition in the patients with #LC/#MECFS, therefore even after successful treatment with BC007, other infections could trigger the production of these AAB again. #MECFS same as #LC, just a different name.
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Two projects in Erlangen:
1. Phase 2 clinical study with BC007 for LC with autoimmunity, 30 patients, start in autumn 2022 (waiting for BC007 from BC), currently developing protocols for study.

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2. Development of an algorithm for the diagnosis of LC; 300 patients, started in Dec 2021, pull patients for BC007 study, 3 LC subgroups: autoimmunity (BC007), viral persistence (further vaccination), organ dysfunction (e.g. fibrosis lungs) (rehabilitation).

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I will stop here, there is more info. It is an excellent podcast, I recommend listening to it.

Thank you both, @Dr_B_Hohberger and @SessionsTlc!

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PS: Many people with #MECFS have the 'tired but wired' feeling. Apparently, this is also related to GPCR AABs:

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Regarding the fact that healthy people also have these GPCR-AABs: Hohberger recently mentioned that animal studies show that the additional factor that makes GPCR-AABs pathogenic is the environment: ischemia and/or inflammation.

I wonder if this is related to clots & MCAS.

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More insight from a #MECFS conference at Charité, May 2023 👇

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#BC007 is not a newly developed drug, it was originally developed as a thrombin inhibitor (anticoagulant) under the name ARC183.

"Selection of single-stranded DNA molecules that bind and inhibit human thrombin"

18nature.com/articles/35556…