Qatari researchers find SARS-CoV-2 accelerates biological ageing

Since 2021, Walter Chestnut has been investigating whether SARS-CoV-2’s spike protein causes accelerated biological ageing.

On Monday, researchers from Qatar published a paper that explored and summarised research on biological ageing markers in covid patients.  This paper confirmed Chestnut’s hypothesis that the spike protein induces accelerated ageing.

The hallmarks of ageing are a set of biological processes that contribute to the ageing process and are characterised by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. These hallmarks were first proposed by Carlos López-Otín and his colleagues in 2013 and have since been widely accepted as a framework for understanding the molecular basis of ageing.

There are nine hallmarks of ageing.  The Qatari researchers focused on two: epigenetic alterations and telomere attrition.

Epigenetic alterations are changes in gene expression that occur without altering the underlying DNA sequence, which can lead to altered cellular function and behaviour. Telomere attrition is the shortening of telomeres, the protective caps on the ends of chromosomes, which can lead to cellular senescence and genomic instability.

The Qatari researchers found “multiple studies utilising different epigenetic clocks unveiled epigenetic age acceleration and telomere shortening in covid-19 patients, particularly in severe cases.”

Yesterday, Chestnut published an article about the newly published study, comparing it to his own research.  While both the Qatari researchers and Chestnut focus on SARS-CoV-2, we should bear in mind that covid injections induce cells in the bodies of recipients to produce the spike protein that is found on the surface of the SARS-CoV-2 virus.

Confirmation of My 2021 Hypothesis that the Spike Protein Induces Accelerated Aging

By Walter Chestnut

In November 2021, I published a post on Twitter (now X) demonstrating how the Spike Protein of SARS-CoV-2 induces all nine “hallmarks of ageing” as defined in the classic paper by Carlos López-Otín et al.

I had formed the hypothesis in early 2021 and by November enough had been published to prove it in theory. The paper published yesterday proves it in fact.

Here is my post from November 2021: ‘Hallmarks of Ageing and the Spike’.

The findings published yesterday focus on two of the nine hallmarks of ageing that the spike protein induces. These are epigenetic alterations by methylation and telomere attrition.

Let’s first look at DNA methylation.

A study conducted by Mongelli et al. determined the Biological Age (bAge) of 117 individuals who had recovered from COVID-19 (referred to as post-COVID-19) and 144 healthy participants using pyrosequencing focusing on CpG islands that have previously been identified as reliable indicators of bAge developed by Beckaert et al. The results indicate an increase in bAge among the post-COVID-19 group with an acceleration of DeltaAge by approximately 5.25 years, beyond the normal range (26, 46).

The calculated EAA showed a significant DNAm age acceleration across different clocks including Horvath, Hannum, PhenoAge, and GrimAge clocks in severe COVID-19 patients (48). Similarly, non-severe COVID-19 cases exhibited significant DNAm age acceleration in the Horvath, Hannum, skin&blood, and GrimAge clocks. Further analysis of epigenetic age dynamic acceleration across each COVID-19 disease phase revealed an acceleration from the initial phase, which was partly reversed in later phase.

The impact of COVID-19 on “biological ageing”, Frontiers Immunology, 10 June 2024

As I wrote in November 2021, the spike protein induces this:

Viral Protein: Spike protein
Host Machinery: ACE2R
Epigenetic Change: Methylation at CpG site

An immune epigenetic insight to COVID-19 infection, National Library of Medicine, 9 March 2021

The other aspect of biological ageing that yesterday’s paper focused on is telomere shortening.

In a prospective study, telomere length in hospitalized COVID-19 patients revealed a significantly higher proportion of COVID-19 patients with shorter telomeres when compared to the control cohort. Telomere attrition was associated with a higher risk of critical disease, defined as admission to the intensive care unit (ICU) or death without ICU (59). In another study on COVID-19 survivors, significant telomere shortening was observed following absolute human telomere length measurement (26). A similar finding was reported by Sanchez-Vazquez et al. where telomeres in severe COVID-19 cases were observed to be shorter than those in patients with mild COVID-19 symptoms (53, 60).

The impact of COVID-19 on “biological ageing”, Frontiers Immunology, 10 June 2024

Once again, as I wrote in November 2021, the spike protein alone induces telomere shortening.

We predict that S2 spike RNA treated AEC2 will produce less telomerase activity in this peak of 24h. The reduction in the activity can be quantified with G-quadruplex-intercalating porphyrin telomerase inhibitor. Further, the telomerase activity can also be quantified with PCR based Telomere Repeat Amplification Protocol (TRAP).

SARS-CoV2 Spike and Telomerase RNA’s Compared to Arrive at an Explanation for Increased Ageing in Alveolar Cells in Severe COVID-19, Journal of Bacteriology and Parasitology

What concerns me is that the forest is not being seen, only the trees. Isn’t it clear? Repeated exposures to the spike protein will almost certainly continually induce these effects. Three exposures? Thank you very much for fifteen years of your life! Capisce?

If there is a silver lining in all of this, it is that since we understood the fundamentals correctly here, it is much more likely that the therapeutics we have been discussing are perhaps more likely to ameliorate these conditions. I will keep working. As always.

Source:  https://expose-news.com/2024/06/13/sars-cov-2-accelerates-biological-ageing/

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