October 24, 2021
A CLEAR AND PRESENT DANGER: SARS-CoV-2 AND PRE-CLINICAL MASSIVE TELOMERE/DNA DAMAGE: REPLICATION CATASTROPHE AND CYTOKINE STORMS
Doesn’t this make sense? Think of the vast panoply of pathologies associated with COVID. It is all due to “broken” cells. A realization” The observed systemic senescence in COVID-19 is not a direct result of the virus. It is a result of the body desperately trying to protect its genome.
A paper (written a mile from my home) from UVM found that WITHIN 48 HOURS of SARS-CoV-2 infection there was a MASSIVE loss of telomere length and a profound activation of the ATR DNA damage response.
The authors posit that the telomere shortening is a result of the DNA damage response and that the purpose is to somehow aid in the replication of the virus. I believe they have it backwards. The DNA damage response is a result of the immense telomere shortening. Indeed, in a study of Saudi colorectal patients it was discovered that the ATR DNA damage response was upregulated in relation to shortened telomeres due to the present cancer.
A paper from March 2021 predicts that S2 spike RNA treated AEC2 will produce less telomerase activity in a peak of 24h. It appears to be the case that the spike protein immediately and silently gets to work at reducing the lifespan of the host. Of course, no natural virus would engage this particular strategy. A shortened host’s life does not benefit the virus.
If you look more deeply, you will notice that ATR is involved with keeping a protein called RPA from being depleted. If RPA is depleted, then double stranded DNA breaks occur with impunity, leading to a “shattered factory” of cell replication.
Isn’t that EXACTLY what we are seeing in Long COVID? A “shattered” collection of biological systems?
The paper noted that after 48 hours the levels of ATR decrease. It would be important to continue to observe the levels of ATR, as the virus and/or spike may be depleting ATR, leading to the depleation of RPA. Inhibition of ATR or Chk1 triggers unscheduled firing of dormant origins, leading to a progressive RPA depletion, exposure of unprotected ssDNA, and massive DNA breakage.
It could be that ALL OF COVID IS RELATED TO THIS INITIAL ASSAULT ON THE GENOME VIA TELOMERES. Surprisingly, a study from the Harvard School of Public Health found, in 2014, that at any follow-up time, each incremental ng/mL increase in plasma CRP concentration was associated with a decrease in telomere length of −2.6×10−2 (95%CI: −4.3×10−2, −8.2×10−3, p = 0.004) units. Similarly, the estimate for the negative linear association between SAA and telomere length was −2.6×10−2 (95%CI:−4.5×10−2, −6.1×10−3, p = 0.011). No statistically significant associations were observed between telomere length and plasma concentrations of pro-inflammatory interleukins, TNF-α, and VEGF.
All of this happens very quickly. Within 48 hours of infection. Before symptoms appear.
The Relationship between Inflammatory Biomarkers and Telomere Length in an Occupational Prospective Cohort Study
SARS-CoV-2 Spike and Telomerase RNAs Compared to Arrive at an Explanation for Increased Ageing in Alveolar Cells in Severe COVID-19
Shorter telomere lengths in patients with severe COVID-19 disease
ATR Prohibits Replication Catastrophe by Preventing Global Exhaustion of RPA
The expression of telomere-related proteins and DNA damage response and their association with telomere length in colorectal cancer in Saudi patients
Dysfunctional telomeres activate an ATM-ATR-dependent DNA damage response to suppress tumorigenesis
DNA Damage Sensing by the ATM and ATR Kinases
SARS-CoV-2 triggers DNA damage response in Vero E6 cells