Jan 19, 2025
TSRNOSS, p 494.
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TSRNOSS, p 494.
SARS-CoV-2 attacks nearly every organ system of the body including the blood vessel wall linings (endothelial cells), causing inflammation that may lead to blood clots blocking blood flow and causing a particular disease - a key to multi-organ complications of Covid and Long Covid, published in the Science journal on November 28, 2024.
https://www.science.org/doi/10.1126/science.add2962
Leading Edge
Protein called SAM68 plays a key role in blood vessel wall cell (endothelium) interaction with the extracellular matrix regulating cell remodelling and migration
Read the published research paper here
Image from work by Zeinab Rekad and colleagues
Université Côte d'Azur, CNRS, INSERM, iBV, Nice, France
Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)
Published in eLife, August 2023
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The fight against coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 infection is still raging. However, the pathophysiology of acute
COVID-19 is deemed as a (micro)vascular and endothelial disease. Of translational relevance, several candidate drugs which are endothelial protective have been shown to improve clinical manifestations of COVID-19 patients. The purpose of this review is to provide a latest summary of biomarkers associated with endothelial cell activation in COVID-19 and offer mechanistic insights into the molecular basis of endothelial activation/dysfunction in macro- and micro-vasculature of COVID-19 patients.
Repel and Repair
Mustering a balanced response to unwelcome news isn’t always easy. In the body, responding to an infection with an appropriate level of outrage is key too: too little and the invader will run rampant, but an overzealous response can cause more harm than the infection itself. A study has investigated this balance in the lungs of mice. Tracking gene activity in cells of mouse lung blood vessel linings (pictured, with lining cells in green and other lung cells in red) researchers discovered two distinct cell types, ‘immune’ and ‘development’ endothelial cells, key to the immune response and subsequent regeneration respectively. Their differences in gene activity became more pronounced when responding to infection or stress, and maintaining the balance between immune defence and growth is key to successfully repelling and recovering from a threat. Being able to intervene when that balance is skewed could lead to new treatments for lung conditions.
Written by Anthony Lewis
Image by Jalees Rehman Lab
University of Illinois College of Medicine, Chicago, IL, USA
Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)
Research published in JCI Insight, May 2022
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A new potential biomarker raises concerns over the current standard for treating COVID-19 induced blood clots with high dose blood thinners.
An interesting read. I wanted information regarding what induces hemorrhaging in those patients that had adverse affects from covid delta variant, and thought it might be similar to the behavior of Ebola (EVD).
It may be similar, due to ebola virus causing blood clots to form in the bloodstream, is as well similar to covid virus disrupting homeostasis in the vascular system. The blood clots force internal bleeding, but the data regarding covid is inconclusive, as it is with ebola. With covid, I would first study if abrasions form within the endothelial layer of the vascular tract - this seems to the the primary tissue the virus likes to nest in and reproduce within.
Again, much of the information I post her is speculative. I write hypotheses regarding how the virus behaves, and what medical science will eventually conclude on. We are still documenting this disease and the variants it produces.
That said, the topic of bleeding seemed to support a theory I had regarding the potential hostile affects a delta infection had, if the recipient had a prior covid original infection - note that those who had covid original and had a ‘mild’ case, endured an aggressive attack from the delta variant. Those patients (without vaccination) became sicker, some perished, and others suffered hemorrhaging. But I do not have enough information to speculate if this is accurate, it is speculation.
This passage did interest me:
“Research has found that patients with COVID-19 are prone to serious blood clotting. This is why many patients receive high dose anticoagulants as part of their treatment.
But a new study in Scientific Reports, led by senior author Daniel Lawrence, Ph.D., a Professor of Basic Research in Cardiovascular Medicine at Michigan Medicine, found that aside from this heightened clotting risk, some COVID-19 patients have an unbalanced ability to break down clots as well, which is linked to a potential clinical biomarker seen in later stages of the disease.
This abnormal process of breaking down clots can contribute to a high bleeding risk, raising concerns about the current practice of giving COVID-19 patients high dose anticoagulants throughout the duration of their disease course. “
The latter passage has intrigued me, because I did speculate the reason hospitals and doctors resisted all insistence (AND LEGAL THREATS) by family and friends to supply hydroxychloroquine to those distressed by advance covid, was because C18H26ClN3O is also an anticoagulant.
Aside from depressing the immune system and the autoimmunity inflammation of those that take C18H26ClN3O - thus priming individuals for potential risk of contracting covid- hydroxychloroquine could likewise induce internal bleeding of those who already struggled with the cytokine storm - this inflammation attack on the internal organs seeded by covid traces.
In some case studies, the results remained inconclusive if C18H26ClN3O was really effective as a medication to alleviate covid crash. But the fact that doctors and the medical field overall suspected it could do more harm than good in some candidates, does elaborate why the resistance.
However, hydroxychloroquine is still studied as a treatment for some patients. That is done so under doctors supervision and with medical intervention available, to prevent vaers due to the administration of this medication. As with other anticoagulants, to prevent blood clotting as induced by covid infection.
“So, why do COVID-19 patients have such high levels of tPA in the first place?
Lawrence’s team suspects the source of these high levels of tPA in COVID-19 patients, and the subsequent clotting issues, is because of damage to endothelial cells, which are cells that line blood vessels. If badly damaged, the blood vessels can actually break and cause bleeding.
The theory is that a hallmark symptom of COVID-19 ARDS, when fluid builds up in the lungs and causes trouble breathing and low oxygen levels in the blood, may trigger endothelial cell activation, which consequently promotes the release of tPA.“
In COVID-19 ARDS, activated neutrophils—one type of white blood cell—can aggregate in small vessels of lung and form inflammatory sticky spider web like structures that further activate and damage endothelial cells” says Zuo. “This process increases the release of tPA/PAI-1 in very sick COVID-19 patients.”“
What I understand from this passage, is due to the internal damage of the endothelial cells from covid, it triggers the body to generate blood clotting - I need to really research this to make certain if I fully grasp this material. But the abrasion from cell destruction (laced with covid), triggers blood clotting to amend the vascular tissue - but the production goes overboard, causing the long-covid affects in some. In response, the body produces a ‘clot buster’ called Tissue Plasminogen Activator (tPA) - the anticoagulant protein.
This is actually pretty optimistic information. I had speculated that long-haulers were caused by one of two issues - individuals who had bone marrow damage induced by covid, or endothelial damage. The bone marrow damage is more difficult to heal from, and could have aggressive affects later if the individual does not heal entirely from a covid infection.
However, if the endothelial is damaged, then there is a better chance with healing, with appropriate therapy and care, and vaccination for those eligible. Especially, if the formerly infected is able to prevent future infection. Especially, since several variants of covid circulate, and each of them is an endothelial disease at its core.
Laying Pipes
A thriving community can’t move into a brand new building until a full network of plumbing is in place. The same applies in tissue engineering. To support cell growth at a useful scale in a supportive hydrogel environment, the structures need rapid vascularisation – the formation of vessels to transport nutrients and other materials. A new approach encourages this at two scales, creating both large open channels and dense clusters of microcapillaries (tiny vessel networks) with a new bio-ink called gelatin-norbornene, which is compatible with standard 3D bioprinting methods. It enables cells that form connective tissue and vessel linings to assemble into shape (pictured, with red connective cells bridging across channels to allow green vessel lining cells to migrate across). This combination of a new bio-ink with cell biology and custom structural designs can help engineer vascularised tissues, essential for developing tissue engineering to ultimately help patients in need.
Written by Anthony Lewis
Image from work by Bram G. Soliman and colleagues, Light Activated Biomaterials (LAB) Group
Department of Orthopaedic Surgery and Musculoskeletal Medicine, University of Otago Christchurch, Christchurch, New Zealand
Image supplied and copyright held by the original authors
Research published in Advanced Healthcare Materials, January 2022
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You have no idea how alarming it is to listen to people talk about their covid experience, and just casually mention, “Yeh, I lost my sense of smell and taste.”
Because when people hear that, and run with this presumption of misinformation that this is somehow a disease comparable to a flu or mild cold - based on clinical symptoms associated with any infection, whether it be viral or bacterial - they think this is totally normal. They have a false perception that this is very normal symptoms, because everyone loses their sense of smell or taste with any old rhino virus or flu bug.
The problem is much more grim. Because doctors and medical publications do note that the loss or smell and taste, or hypo and parosmia, is a neurological dysfunction associated with brain activity, not damage to the olfactory lining itself. link stuff )
That is why when covid recoveries manage to pass over that threshold, they can still have limited to no return of their smell or taste.
Yesterday I was browsing through the comments on a youtuber’s community feed, because they tested positive for covid, everyone gives their account of the experience. One comment did catch my attention.
One viewer expressed a weird metallic taste in their mouth. Like they could taste it vividly, but they experienced hyposmia and parosmia.
And that is VERY concerning. It is one thing to have auditory or visual hallucinations, but its another thing entirely to experience a vivid ‘hallucinated’ taste. It’s usually an indication of something wrong with the connections of the neurons of the brain.
But on the flip side, hallucinated food and taste is not a driving nail in the coffin. Sometimes hormonal shifts can make people experience those sensations. But because it came with covid association, I am concerned for that individual.
As well, there were reports by those who experienced VAERS from their covid vaccine, and reported a ‘metallic’ taste about 10 minutes following injection. I do not believe the youtube viewer had any associationn with these individuals, or viewed the VAERs reports. What would the point be? The topic of vaccines was not on the table, so why make a vague association between vaccines and covid symptoms?
The main takeaway from this is, be wary. The brain is very ‘plasticity’ or whatever they refer to it. Losing a portion of it, or a section becoming damaged is not the end of the world. Plasticity, to my understanding, means it adapts to damage. The neurons in the brain have the capacity to repair themselves, but based on age and health, they may not be as strengthened or correct. The concern I have right now is individuals who don’t ‘get it’ when it comes to covid, and do not take necessary precautions going forward.
So you had covid once o r twice, of five times. Your immune system is shit. The causes of death due to covid complications is vast, based on our current grasp of the virus.
It causes neurological dysfunctions
It can deal extensive and unknown damage to the vascular system
The cardiovascular system has a harder time adapting
Blood clots
Stroke
People are pushing that these new variants such as Omicron and whatever that new bitch is, are benign and something like a rhino virus.
IT
IS
NOT
This is a virus that has found its niche and success in survival, by not murdering its reservoir species. But inevitably in those who court this virus, their bodies run out of reserves and capillaries and blood to feed it. When you are no longer of use to this disease, then you perish.
People have had covid before and then caught one of the other variants a year or two later, and died. If it doesn’t kill you, then it will seriously give you a fuck over.
Stay safe. Wear a mask. Distance from others when you can. Stay up to date with vaccines if you are eligible.