The Transposon Theory of Aging and SARS-CoV-2

Even mild COVID infection accelerates aging by activating Transposable Elements.

Readers of this Substack know that I have, for years, hypothesized that Transposable Elements (TEs), including Retrotransposons, are almost certainly activated by SARS-CoV-2. This causes “cut and paste” editing of the genome. I compare the resulting actions on DNA to changing a Rembrandt into a Jackson Pollock.

SARS-CoV-2 MAY OR MAY NOT WRITE ITSELF INTO YOUR DNA, BUT IT IS ALMOST CERTAINLY CUTTING/PASTING YOUR GENES, WRITING THEM BACK "WRONG" INTO YOUR DNA. LINE-1 ELEMENTS MUST BE TESTED IN ALL THOSE WITH COVID.

Retrotransposons (also called Class I transposable elements or transposons via RNA intermediates) are a type of genetic component that copy and paste themselves into different genomic locations (transposon) by converting RNA back into DNA through the process reverse transcription using an RNA transposition Retrotransposons can be further subdivided into two subclasses: those with Long-Terminal Repeats (LTR) and those without (non-LTR). LTR elements, also known as endogenous retroviruses (ERVs), comprise ~8 % of the human genome. LTR ) elements are thought to be inactive in the human lineage. That is, until SARS-CoV-2 activates them. This is why the HERV-K protein has never before been seen circulating in the body.

Type 2 Diabetes, Schizophrenia and Dementia patients all have disfunctioning Retrotransposons. As has been previously believed, SARS-CoV-2 accelerates pathogenic processes.

According to recent epidemiological studies, the human population also displays very unusual inter-individual variations in terms of its susceptibility to several adult-onset diseases, including cancer, diabetes, obesity, and mental illness. Even in twins, life choices can cause retrotransposons to cause damage in one and not the other.

If we take Retrotransposons as a sole source of pathogenesis we can look at Alstrom Syndrome. Does this sound familiar? Hallmarks of ALMS that develop in early childhood include truncal obesity, significant insulin resistance, hyperinsulinemia, type 2 diabetes mellitus (T2DM), and hypogonadism in both male and female patients. Dilated cardiomyopathy (DCM) and congestive heart failure (CHF) may develop suddenly in infants, whereas the gradual onset of restrictive cardiomyopathy can occur during adolescence or adulthood. Multi-organ fibrosis ultimately leads to major organ failure and premature death.

SARS AND RETROTRANSPOSONS: DIABETES, SCHIZOPHRENIA, DEMENTIA, CANCER, OBESITY
https://wmcresearch.org/sars-and-retrotransposons-diabetes-schizophrenia-dementia-cancer-obesity/

I wrote the above April 25^th of 2021.

A paper published April 4^th of this year proves that Retrotransposons are indeed being expressed and almost certainly contributing to COVID pathogenesis.

Endogenous retroviruses (ERVs) derived from the long terminal repeat (LTR) family of transposons constitute a significant portion of the mammalian genome, with origins tracing back to ancient viral infections. Despite comprising approximately 8% of the human genome, the specific role of ERVs in the pathogenesis of COVID-19 remains unclear. In this study, we conducted a genome-wide identification of ERVs in human peripheral blood mononuclear cells (hPBMCs) and primary lung epithelial cells from monkeys and mice, both infected and uninfected with SARS-CoV-2. We identified 405, 283, and 206 significantly up-regulated transposable elements (TEs) in hPBMCs, monkeys, and mice, respectively. This included 254, 119, 68, and 28 ERVs found in hPBMCs from severe and mild COVID-19 patients, monkeys, and transgenic mice expressing the human ACE2 receptor (hACE2) and infected with SARS-CoV-2. Furthermore, analysis using the Genomic Regions Enrichment of Annotations Tool (GREAT) revealed certain parental genomic sequences of these up-regulated ERVs in COVID-19 patients may be involved in various biological processes, including histone modification and viral replication. Of particular interest, we identified 210 ERVs specifically up-regulated in the severe COVID-19 group.

Notably, TEs constitute nearly 50% of the human genome, whereas coding genes make up only 2% (10, 11). TEs encompass various elements such as endogenous retroviruses (ERVs), which are part of the long terminal repeat (LTR) family, long interspersed nuclear elements (LINEs), short interspersed nuclear elements (SINEs), and DNA transposons. Over millions of years, TEs have played a significant role in shaping the size and structure of our genome due to their transposition abilities. Many TEs have undergone mutations leading to loss of function during evolution (15). Consequently, numerous TEs may no longer generate the necessary proteins for complete transposition. Remarkably, some TEs capable of retrotransposition could insert sequences into new locations within the host genome. If integrated into or near coding gene exons, these elements may exert unforeseen effects on host gene regulation (17, 18). Consequently, abnormal TE expression may contribute to the pathogenesis of various diseases, including infectious diseases, autoimmune disorders, and cancers.

Identification and characterization of endogenous retroviruses upon SARS-CoV-2 infection
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1294020/full

As I have repeatedly stated: COVID is NOT the FLU. Even if you experience an extremely mild case of the disease, it is still almost certainly causing long term damage to us all – in the form of accelerated aging. And all the disease and deterioration that accompanies advancing age.

The reason the activation of these TEs must be paid attention to is that, in and of itself, it represents an entire form of aging. This is known as the Transposon Theory of Aging.

The transposon theory of aging hypothesizes the activation of transposable elements (TEs) in somatic tissues with age, leading to a shortening of the lifespan. It is thought that TE activation in aging produces an increase in DNA double-strand breaks, contributing to genome instability and promoting the activation of inflammatory responses.

The difference in the average lifespan between gypsy permissive and non-permissive flies supports the idea that gypsy activation could be involved in the shortening of lifespan (Above Figure). Significantly, a shorter lifespan has been described in Ago2 mutations, which disrupt the somatic TE control mechanism and increase expression of the retrotransposons gypsy and R2 in brain. It has also been described that lines exhibiting earlier gypsy transposition events showed a shorter lifespan, while those with later transposition events showed a longer lifespan [17]. All of these results are in agreement with the hypothesis of the involvement of TE activation in reducing the lifespan.

Retrotransposons Down- and Up-Regulation in Aging Somatic Tissues
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8750722/

In essence, even a mild case of COVID induces the activation of TEs, which is something that normally occurs in the later stages of life. Once again, we define another mechanism by which SARS-CoV-2 and its Spike Protein may shorten our lifespans.

And, yes, the Spike Protein itself triggers these TEs. Even in healthy individuals (infer as you wish).

Exposure to SARS-CoV-2 recombinant trimeric spike protein triggers HERV-W ENV protein production in PBMC in a subgroup of heathy individuals

SARS-CoV-2 awakens ancient retroviral genes and the expression of proinflammatory HERV-W envelope protein in COVID-19 patients
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10079620/

Like the medieval torture of slowly piling weights to crush a victim to death, the SARS-CoV-2 virus refuses to let its victim go.

We have every intention of stopping that through continual research into truly safe and effective therapeutics. Thank you for your support, readership and dialog.