by Daniel Brouse
August 25, 2021
help@membrane.com
Post Acute Covid Syndrome 19 (PACS19), long-COVID, and Long Haulers Syndrome are names for the condition that an individual has after recovering from the SARS-CoV-2 virus. Long-COVID is actually a combination of several conditions and syndromes including changes to your genetics, an accelerant to aging, and the persistence of the virus in multiple organs for long periods of time.
The CDC Panel Report Long COVID Panel Survey found:
* 81% of adults with ongoing symptoms of COVID lasting three months or longer — or four out of five adults — are experiencing limitations in their daily activities compared to before they had the virus. (Economic implications include work force participation and long-term health care costs.)
* Young adults between ages 18 and 29 had the highest share of people currently with long COVID who have trouble performing daily tasks, at 86.3%. What will the long-term costs and quality of life be when these people are in their 50’s,60’s, and if they get to live into their 70’s?
There are over 60 proteins involved in the epigenetic response to COVID. So far out of these 60 proteins, three long-COVID epigenetic syndromes have been identified. There are likely many more. (The epigenetic changes are in addition to the organ damage caused by the virus.)
COVID-19 also causes other long term damage that we are still discovering.
Vaccines Help Prevent Secondary Complications
A study shows you are less likely to develop long-COVID Myocardial Infarction and Ischemic Stroke after a COVID-19 Infection if you ARE VACCINATED. Many people may not even know that COVID causes an increased risk of thrombosis. Vaccines can prevent secondary complications.
Rogue Antibodies
Autoantibodies are antibodies (immune proteins) that mistakenly attack a person’s own healthy tissues and organs. A study published in Nature found “rogue antibodies involved in almost one-fifth of COVID deaths. The self-targeting antibodies attack type 1 interferons that play a key role in fighting infection. Antibodies that turn against elements of our own immune defences are a key driver of severe illness and death following SARS-CoV-2 infection in some people, according to a large international study. These rogue antibodies, known as autoantibodies, are also present in a small proportion of healthy, uninfected individuals — and their prevalence increases with age, which may help to explain why elderly people are at higher risk of severe COVID-19.”
Up to three percent of the population already has faulty genes that create these autoantibodies. Of those between the ages of 18 and 69, 0.18% had existing autoantibodies against type 1 interferon. “Autoantibodies were present in around 1.1% of 70- to 79-year-olds, and 3.4% of those over the age of 80.”
A follow up study, “New-onset IgG autoantibodies in hospitalized patients with COVID-19,” found “Coronavirus Disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection, is associated with many different clinical features that are commonly found in autoimmune diseases, including arthralgias, myalgias, fatigue, sicca, and rashes. Less common manifestations of autoimmunity have also been observed in COVID-19 patients, including thrombosis, myositis, myocarditis, arthritis, encephalitis, and vasculitis. These clinical observations, and the increasing proportion of “recovered” patients with persistent post-COVID-19 symptoms (so-called “long haulers”, or “long COVID”) suggest that inflammation in response to SARS-CoV-2 infection promotes tissue damage in the acute phase and potentially some of the long-term sequelae. A subset of autoantibodies targeting traditional autoantigens or cytokines develop de novo following SARS-CoV-2 infection.”
“The team also found that individuals with genetic mutations that disrupt the activity of type 1 interferons are at higher risk of life-threatening disease” suggesting COVID causes changes to the genes resulting in the creation of rogue autoantibodies.
In a study of healthcare workers, all had persistent autoantibodies, including ones that can cause chronic inflammation and injury of the joints, skin and nervous system. “We would not normally expect to see such a diverse array of autoantibodies elevated in these individuals or stay elevated for as long six months after full clinical recovery,” said Susan Cheng of the Cedars-Sinai Smidt Heart Institute in Los Angeles. (As reported in Paradoxical sex-specific patterns of autoantibody response to SARS-CoV-2 infection)
“We don’t yet know how much longer, beyond six months, the antibodies will stay elevated and/or lead to any important clinical symptoms,” Cheng said. “It will be essential to monitor individuals moving forward.” The team is investigating autoantibody elevations and their relationship to persistent symptoms in people with long-COVID.
NAD+ Deficiency
COVID both increases the breakdown of NAD+ and decreases the production of NAD+. “NAD regulates the inflammatory response in immune and non-immune cells through Sirtuins. Epigenetic regulation of histones and non-histone proteins is induced by sirtuins and is essential for the development, reprogramming, and differentiation of the immune system and its related pathologies. A deregulation of the NAD+ levels has been associated with metabolic diseases and aging-related diseases, including neurodegeneration, defective immune responses, and cancer.” — NAD-immune-system
The NAD+ deficiency results in a compromised immune system. The body can not properly metabolize vitamins nor mount a proper immune response. The NAD+ deficiency also resembles an autoimmune disease where the immune system appears to be attacking a healthy body. Without NAD+ regulating the immune system, the immune response becomes dysfunctional.
Though there is no cure for the NAD+ Deficiency Syndrome (CISP — COVID-19 Induced Secondary Pellagra), the symptoms can be treated with Niacin (Nicotinic Acid).
Upregulation of IDO
Indoleamine 2,3-dioxygenase (IDO) is an immune checkpoint molecule in the sense that it is an immunomodulatory enzyme produced by alternatively activated macrophages and other immunoregulatory cells. IDO is known to suppress T and NK cells, generate Tregs and myeloid-derived suppressor cells, and also supports angiogenesis.
Memory T cells are crucial for the immune system to remember how to fight pathogens. IDO is also related to the viscosity of body fluids and membrane function. Brain fog, dizziness, tinnitus, ear aches, vertigo, and pressure in the ears are some of the symptoms associated with epigenetic changes in the upregulation of Indoleamine 2,3-dioxygenase.
Dr. Ade Wentzel said, “The epigenetic upregulation of IDO will determine the amount of quinolinic acid. Quinolinic acid comes from the kynurenine pathway. If the viscosity of the whole middle ear is increased then the ability to equalize will be less… same as having a cold. So, the ear isn’t equalizing correctly on increasing pressure. The same as when you land in a plane. If the viscosity in the semicircular canals is increased, the otoliths may well be lagging causing the vertigo. The otoliths usually “Float” in the semicircular canal and trigger tiny sensory hairs that allow you to detect position.”
Coronavirus Transforms Pancreas Cell Function
When COVID infects cells, it impairs cell activity and can also change their function. When insulin-producing beta cells in the pancreas become infected with the virus, they produce much less insulin than usual, and also start to produce glucose and digestive enzymes. “We call this a change of cell fate,” said study leader Dr. Shuibing Chen, who described the work in a presentation at the annual meeting of the European Association for the Study of Diabetes.
It is not clear whether the changes are long-lasting, or if they might be reversible, the researchers reported in Cell Metabolism, “SARS-CoV-2 infection induces beta cell transdifferentiation“. “Single-cell RNA sequencing and immunostaining from ex vivo infections confirmed that multiple types of pancreatic islet cells were susceptible to SARS-CoV-2, eliciting a cellular stress response and the induction of chemokines. Upon SARS-CoV-2 infection, beta cells showed a lower expression of insulin and a higher expression of alpha and acinar cell markers, including glucagon and trypsin1, respectively, suggesting cellular transdifferentiation. Trajectory analysis indicated that SARS-CoV-2 induced eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that could be reversed with trans-integrated stress response inhibitor (trans-ISRIB). Altogether, this study demonstrates an example of SARS-CoV-2 infection causing cell fate change, which provides further insight into the pathomechanisms of COVID-19.”
ALSO SEE: COVID: Insulin Reduction, Diabetes, High Cholesterol, Heart Disease and Stroke
Increased Risk of Cancer
In the case of cancer and tumor suppression, COVID chooses people that have reduced P53 (the tumor suppression gene.) It is also possible that COVID further reduces functional P53 genes. “Mutations in p53 are found in most tumor types, and so contribute to the complex network of molecular events leading to tumor formation.” — The p53 tumor suppressor protein
COVID also suppresses NK cells. “A type of immune cell that has granules (small particles) with enzymes that can kill tumor cells or cells infected with a virus. A natural killer cell is a type of white blood cell. Also called NK cell and NK-LGL.” — Natural Killer Cell
A study “Cancer Prevention with Resistant Starch” (conducted over the last 30 years) shows that resistant starch reduces your risk of cancer. The resistant starches produce good bacteria that reduces a type of acid that promotes changes to your DNA. The changes to your DNA increase the risk of many types of cancer. The discovery may also explain in part why COVID increases your risk of cancer. COVID is known to destroy good gut bacteria.
“Dr Betty Raman, from the University of Oxford and one of the lead investigators on the study, says it is clear that those living with long-COVID symptoms are more likely to have experienced some organ damage.”
The biggest impact was seen on the lungs, where MRI scans were 14 times more likely to show abnormalities. Scans were also three times more likely to show abnormalities in the brain, and twice as likely in the kidneys, among people who had severe COVID.
The article Multiorgan MRI findings after hospitalisation with COVID-19 in the UK (C-MORE): a prospective, multicentre, observational cohort study was published September 22, 2023 in The Lancet Respiratory Medicine.
After hospitalisation for COVID-19, people are at risk of multiorgan abnormalities in the medium term. Our findings emphasise the need for proactive multidisciplinary care pathways, with the potential for imaging to guide surveillance frequency and therapeutic stratification.
ABOUT LONG-COVID
Long-standing multiorgan impairment following SARS-CoV-2 infection has been a major concern for individuals recovering from severe disease and is thought to be caused by a multitude of factors, including direct viral cytotoxicity, chronic inflammation, ischaemic injury, acute reactivation of other viruses, metabolic derangements, and acute treatment effects (especially invasive ventilation). Numerous reports of delayed organ complications such as myocarditis, stroke, and pulmonary emboli have led to speculations that the multiorgan dysfunction caused by COVID-19 might be responsible for impaired recovery and ongoing symptoms in individuals, a condition referred to as long COVID.
Long COVID Update:3 Years of Living With It
