August 13, 2021
TELOMERES ARE BEING SHORTENED AND BECOMING DYSFUNCTIONAL DUE TO THE PATHOLOGICAL EFFECTS OF THE SPIKE PROTEIN
The cases of thrombocytopenia occurring post Spike Protein therapy may be due to shortened telomeres and telomere dysfyunction either already present, induced or accelerated by the pathological effects of the Spike Protein of the SARS-CoV-2 virus.
Interestingly, telomere dysfunction can explain the heretofore unexplained presence of megakaryocytes. This presence suggests extreme impact on telomeres. p53, ROS and mitochondrial dysfunction may all be involved, stemming from the signaling/interactions of the S1/S2 cleaved and circulating subunits.
The telomere length in refractory and non-refractory ITP patients were both significantly shorter than that in the controls (p?=?0.025; p?=?0.000). However no significant difference in telomere length of PBMC was found between refractory ITP patients and non-refractory ITP patients (p?=?0.234).
An abnormal regulating telomere/telomerase system might be involved in the pathogenesis of ITP. Further studies may elucidate whether the telomere length could be considered as a predictive biomarker for the prognosis of ITP.
Most certainly a bioweapon. Discovered by researching the effects of telomere shortening on cancer cells.
Telomere Dysfunction Drives Aberrant Hematopoietic Differentiation and Myelodysplastic Syndrome
Telomerase Activity Increased and Telomere Length Shortened in Peripheral Blood Cells from Patients with Immune Thrombocytopenia