I'm going to share a hypothesis that is not mine, but we should consider it.
RNA viruses like cov2 may enter a low replication state in tissues like the brain.
They may (likely imo) contribute to long-term issues like MS and parkinson's.
RNA viruses like cov2 may enter a low replication state in tissues like the brain.
They may (likely imo) contribute to long-term issues like MS and parkinson's.
The problem I see is that cov2 has a superantigen.
This means in the low replication state, cov2 can shed a hyperinflammatory payload.
This would, in my opinion, accelerate disease processes.
This means in the low replication state, cov2 can shed a hyperinflammatory payload.
This would, in my opinion, accelerate disease processes.
The only thing we have going right now is wishful thinking and acceptance
The basis of wishful thinking is thin; in animals the neural decay is pronounced and fairly rapid
Even in humans the neurocognitive impact is pronounced
The basis of wishful thinking is thin; in animals the neural decay is pronounced and fairly rapid
Even in humans the neurocognitive impact is pronounced
I think we all have accepted the unknown and this risk because most of our peers and loved ones have already been infected
I also think we have shifted the risk we deem acceptable because our locus of control is limited
I also think we have shifted the risk we deem acceptable because our locus of control is limited
I think Long Covid may represent a manifestation of this 'low replication state'
timesofisrael.com/more-than-10-o…
timesofisrael.com/more-than-10-o…
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