The homologous recombination DNA repair pathway is one of the mechanisms that the body uses to stop your cells turning cancerous in response to environmental stress.
One of the most important components of this pathway is Tumor protein P53 (p53), the “guardian of the genome”. It protects our cells from cellular damage. Under cellular stress, p53 jumps into action, regulating gene expression to control DNA repair, cell division and cell death. It is the most commonly mutated gene in cancer.
In October 2021, two revered scientists, called Jiang and Mei, had a paper published, after peer review, in MDPI, showing that the SARS-Cov-2 spike protein obliterated the DNA repair mechanism in lymphocytes.
The viral spike protein was so toxic to this pathway that it knocked 90% of it out. If the whole spike protein got into the nucleus (in the ovaries), and enough of it was produced and hung around long enough before the body was able to get rid of it all, it would cause cancer. Fortunately, in the case of naturally infection, this is unlikely to occur.
Unfortunately, the experimental mRNA toxshot induces spike protein to be produced (the full length spike exactly matching – amino acid for amino acid – the full length of the viral spike protein¹) in and around the cell nucleus² and is produced for at least 60 days and almost certainly longer³.
“Fact checkers” said the viral spike protein doesn’t get in the nucleus despite the expert scientists showing that it absolutely does.