In this study, SPIKE antigen detected most often in 60% of the PASC patients and in > 70% of patients who reported ongoing cardiovascular, systemic, head-eye-ear-nose-throat, and musculoskeletal symptoms.
If viral reservoirs persist in the body of PASC patients, why do we not also detect N in more patients? Active viral reservoirs could cause PASC symptoms, but circulating spike may also give rise to symptoms.
Although spike does not instigate a cytokine storm in PASC patients, spike alone has been shown to induce dysfunction in pericytes, vascular endothelial cells, and the blood–brain barrier
the presence of circulating spike in PASC patients up to 12 months after diagnosis suggests that SARS-CoV-2 viral reservoirs may persist in the body.
There are likely many overlapping immunological and inflammatory phenomena contributing to PASC and the detection of spike cannot alone confirm the presence of active viral reservoirs.
However, if our finding can be validated in a larger cohort, it would provide strong support for the use of spike as a biomarker for PASC, making it easier to identify patients and assess treatment strategies.
Serum Amyloid A has been found in Spike Protein produced #microclots. SAA amyloidosis has a 10 year median survival rate. It has not been established that Spike amyloids only affect some people. Indeed, it may be a ticking time bomb of #diedsuddenly in billions. #teamclots
If untreated, AA amyloidosis is a serious disease with a significant mortality due to end-stage kidney disease, infection, heart failure, bowel perforation, or gastrointestinal bleeding [3-5].
Patients with persistently high circulating levels of serum amyloid A protein (SAA) are at particular risk of these complications [6,7].