After some comments on biomarkers, I thought to add further thoughts.
I do not believe there is a single one and novel biomarker for #LongCOVID.
This is a multi-system disease, affecting different organ systems. Sometimes the organs that have already been vulnerable before acute infection(s), will be most affected.
By looking at various pathology lab biomarkers (e.g the list shared in a previous post), we can identify possible treatment targets.
Another point is that microclot complexes are definitely not unique to LongCOVID. The processes driving their presence, is circulating inflammatory molecules, immune dysfunction and vascular damage. Therefore we have been looking at their content, and searching for various modifications on proteins associated with them.
Something to keep in mind:
Each disease will have specific types of inflammatory molecules in circulation. We now know that even every patient will have a unique inflammatory molecule load.
We need to determine which inflammatory molecules, which post-translation modifications, and thus which pathways we should look at, to eventually decide on treatment.
Why is it so difficult?
There is not 1 single symptom or organ that is affected. Some patients will develop a diabetes profile, some will have an immune driven disease. The list goes on. Some will have viral persistence.
Because of this heterogeneous picture, we need personalised treatment, multiple biomarker panels and a clear understanding what each dysregulated lab result means.
I do not believe there is a single one and novel biomarker for #LongCOVID.
This is a multi-system disease, affecting different organ systems. Sometimes the organs that have already been vulnerable before acute infection(s), will be most affected.
By looking at various pathology lab biomarkers (e.g the list shared in a previous post), we can identify possible treatment targets.
Another point is that microclot complexes are definitely not unique to LongCOVID. The processes driving their presence, is circulating inflammatory molecules, immune dysfunction and vascular damage. Therefore we have been looking at their content, and searching for various modifications on proteins associated with them.
Something to keep in mind:
Each disease will have specific types of inflammatory molecules in circulation. We now know that even every patient will have a unique inflammatory molecule load.
We need to determine which inflammatory molecules, which post-translation modifications, and thus which pathways we should look at, to eventually decide on treatment.
Why is it so difficult?
There is not 1 single symptom or organ that is affected. Some patients will develop a diabetes profile, some will have an immune driven disease. The list goes on. Some will have viral persistence.
Because of this heterogeneous picture, we need personalised treatment, multiple biomarker panels and a clear understanding what each dysregulated lab result means.
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