THE SARS-COV-2 VIRUS (SPIKE PROTEIN) IS A GENETIC “TIME MACHINE”

August 28, 2021

THE SARS-COV-2 VIRUS (SPIKE PROTEIN) IS A GENETIC “TIME MACHINE" THAT RECREATES THE VERY EARLY STAGES OF DEVELOPMENT, WHEN TRANSPOSABLE ELEMENTS ARE MOST ACTIVE. THIS RESULTS IN REACTIVATION OF DEVELOPMENTAL GENETIC PATHWAYS AND DEDIFFERENTIATED CELLS, CELLS THAT “HAVE NOT GROWN UP" DO NOT KNOW THEIR “JOB" OR “NAME." THE SAME MECHANISM AS CANCER. THE REACTIVATED DEVELOPMENTAL PATHWAYS ALSO EXPLAIN THE EMERGENCE OF GENETIC DISEASES (EXAPTATION) IN MID LIFE.

Published: 16 July 2021

SARS-CoV-2 infection induces the dedifferentiation of multiciliated cells and impairs mucociliary clearance

Expression of transposons has long been implicated in cancer development. The documented silencing of these elements in healthy somatic tissues led to the assumption that transcription of TEs was deleterious. Indeed, transposon activity can interrupt gene expression and function by inserting into the promoter or coding sequence. Additionally, the repetitive nature of these sequences can result in incorrect recombination events and lead to translocations, deletions and insertions. The predominant mode of retrotransposon-driven oncogenesis was considered to be by these mechanisms, resulting in genomic instability. Sporadic evidence exists for de
novo insertions contributing to oncogenesis however this was not extensive enough to account for the entirety of this phenomenon. An upregulation of TEs on a genome-wide scale as a result of loss of DNA methylation has also been documented.

This has been linked to changes in response to immune therapies as a result of ACTIVATION OF THE INNATE IMMUNE RESPONSE.

Environmental Conditions Shared by the Placenta, Cancer and COVID

During early placentation the invading trophoblastic cells are exposed to severe hypoxic conditions. Hypoxia is also well-documented in tumors and occurs to varying degrees both spatially and temporally during tumorigenesis. The implications of hypoxic conditions are not fully understood. However, it has been shown that exposure to hypoxia can increase the rate of cell division in order to seek out an oxygen supply.
Hypoxia can also induce hypomethylation in cancer cells, however the extent to which this occurs is unknown. The hypoxia inducible factor (HIF) is known to be expressed in both placental and tumor cells in response to low oxygen levels.
HIF expression has downstream effects on a number of different pathways including metabolism, angiogenesis and immune modulation. Notably, temporal expression of PDL-1 in invading trophoblast cells has been linked to oxygen availability. HIF knockout mice demonstrate embryonic lethality owing to abnormal placentation. HIF dysregulation has also been observed in a number of cancers. A recent review by Macklin et al. highlights the similarities between the placental and cancer microenvironments, and discusses hypoxia and
subsequent HIF expression as a potential link between some of the shared functions carried out by both tissues.

The term used is onco-exaptation. The ‘exaptation,’ an LTR promoter, provides the means with which an otherwise fate-restricted proto-oncogene may be accessed. In otherwords, it had NOT been activated during early development. It has been awakened by the spike’s literal carnival of transposon activity.

Please read the extremely important Frontiers
paper.

References/Related Papers

SARS-CoV-2 infection induces the dedifferentiation of multiciliated cells and impairs mucociliary clearance

https://www.nature.com/articles/s41467-021-24521-x

Onco-exaptation of an endogenous retroviral LTR drives IRF5 expression in Hodgkin lymphoma

https://www.nature.com/articles/onc2015308

Reawakening the Developmental Origins of Cancer Through Transposable Elements

https://www.frontiersin.org/articles/10.3389/fonc.2020.00468/full