Mitochondrial dysfunctions cause telomere attrition, while telomere damage leads to the reprogramming of mitochondrial biosynthesis and mitochondrial dysfunctions, which have important implications in aging and diseases. #BoxOfNails #BagOfBeans #Spiroplasma #AirborneAIDS
Mitochondrial & telomere are mostly studied independently. However, SARS Let'er R.I.P. has made clear that there are intimate links between mitochondria, telomeres, and telomerase subunits. There's an erratic looping mechanism when one of these goes wrong. en.wikipedia.org/wiki/MRNA_surv…
We know senescent cells contribute to body dysfunction (ageing). We know telomere shortening is a recognized cause of cellular senescence. Several conditions associated with normal ageing are precipitated by accelerated telomere dysfunction. #BagOfBeans ncbi.nlm.nih.gov/pmc/articles/P…
When you are reading papers or studies about cancer, inflammation, cellular senescence, stem cell exhaustion, mitochondrial dysfunction, genomic instability, telomere dysfunction and cellular aging - it is important to look for references AFTER 2009.
Prior to 2009, the dominant theory was free radicals coming from mitochondria processing of oxygen (ROS) created a feedforward loop linking telomere dysfunction, mitochondrial dysfunction and more oxidative stress pathways, resulting in ageing. Not all theories are right.
That theory only partially explains the age-related increase in the inflammatory response seen in the aged population. It doesn't explain the cooperation between cell-intrinsic telomere dysfunction-driven molecular pathways and the microbiome in driving the inflammatory response.
These competing theories are, both right.
After 2009 we were able to understand how both theories are "symptoms" of another process involved in telomere shortening where we still don't have a complete understanding of the causation of the feedback loop. sciencedirect.com/science/articl…
After 2009, we understood how human chromosomes can be copied in a complete way during cell divisions while they are protected against degradation using Nonsense-mediated mRNA decay (NMD). en.wikipedia.org/wiki/Nonsense-…
We solved a major problem in biology: the cure against aging is found in the ends of the chromosomes – the telomeres – and in an enzyme that forms them – telomerase. The process of detecting aberrant transcripts occurs during the translation of the mRNA.
That discovery of such a fundamental mechanism in the cell has stimulated the development of gut biome therapeutic strategies but it's also enabled us to characterize the causation of certain metabolic diseases.
This is a great graphic to understand CoVs #BoxOfNails flawed reproduction process. The initial infected cells are epithelium, but secondary infection adjacent cells can be any type of cells.
“The effect is more pronounced for the N protein of wild-type SARS-CoV-2 than that of the Omicron variant and other human coronaviruses.” This study only applied research for lung epithelium cells so if there’s persistent GI infection then this effect will occur with Omikron.
The infected epithelium cells are prevented from signalling danger and undergoing apoptosis (natural cell death) is delayed. The infected cell is held hostage to throw more boxes of nails from the roof (reproduction). #SARSsexSlaves
We are in the opposite of harm reduction - we are implementing Let’er R.I.P. (Re-Infection Policy) where even vaccination strategies are being abandoned.
This pathogen still has a CFR of just under 10% and 30% are suffering long term symptoms. That’s 40% of those infected who go invisible to society each wave.
The young will not die. They will not experience severe long term illness until later.
The “cure” not to die during acute phase SARS infection, is to have either full blown AIDS or already be persistent infected with SARS (both acquired lymphocytopenia)
There’s still going to be an accelerated aging of the immune system (immunosenescence) but death will be “WITH” mysterious and spontaneous LongSARS/#PASC and not death “FROM” SARS.
We discovered survivors of SARS infection had persistent infection well too late to really help improve their health and reverse immunity damage being caused by persistently infected renal epithelium cells.
Autopsies have previously evidenced SARS viral persistence in gastrointestinal tissues including ocular tissues. This study detected SARS RNA in ocular fluids/tissue in 61% of cases; cornea 42%, horoid/sclera 50%, lens 53%, retina 35%, optic nerve 59%. ajp.amjpathol.org/article/S0002-…
What new with these autopsies results?
SARS experts have long known there’s viral persistence leading to #LongCovid
The viral reservoir was always thought to produce non-viable SARS
Previously, SARS was a “temporary” 2- year viral persistence.
This is why physicians don’t have the ability to conduct most testing that could clinically determine SARS viral persistence. If the pre-determined set of flow charts end with “must be in the patient’s head”, the physician must argue with the insurance companies.
That “insurance form” game is rigged in favour of the insurance companies. The limitations of the game are set by government agencies where the scientific process is politically manipulated. Public Health scientist’s research funding is determined by politicians.
The elite who don’t need their physician to work within restricted cookie cutter solutions will receive the full scale, unnecessary but not invasive diagnosis and treatment.