Tag: epigenetic

bookmark_borderIntroduction to COVID-19: Understanding the Long-Term Impact

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Author: Daniel Brouse

COVID Science Updates

COVID-19, caused by the SARS-CoV-2 virus, has left an indelible mark on global health, demonstrating not only its immediate threat but also the potential for enduring consequences. This article explores the profound and lasting impact of COVID-19, delving into the virus’s role in chronic conditions and its ability to leave a lasting imprint on various aspects of health.

Long-Term Complications and Excess Deaths

A COVID-19 infection often leads to persistent complications that significantly diminish both the quality of life and life expectancy. Shockingly, 10% of excess deaths can be directly attributed to COVID itself, while the remaining 90% are attributed to what can be considered COVID’s silent killers. Individuals who have experienced COVID may face a diminished quality of life and an increased risk of premature death. Dr. Rob Wust underscores this by stating, “There is something inside the body going wrong with the disease.”

Long-COVID: A Looming Reality

For those who have contracted COVID, the probability of developing chronic conditions, known as Long-COVID, is a staggering 99%. This alarming statistic underscores the pervasive and lasting impact of the virus on an individual’s health.

Key Insights into COVID-19’s Long-Term Effects

  1. Direct Impact on Organs:
    • COVID-19 has been responsible for millions of deaths and has caused long-term damage to vital organs, leaving many survivors permanently disabled.
  2. Persistent Viral Presence:
    • SARS-CoV-2 can persist in the body for months or even years, causing chronic infections and leaving behind viral proteins associated with Long-COVID. This persistence is comparable to other viruses like Chicken Pox leading to Shingles or Epstein-Barr virus contributing to Mononucleosis and Multiple Sclerosis.
  3. Compromised Immune System and Autoimmune Risks:
    • Post-COVID individuals often experience a compromised immune system and an increased risk of autoimmune diseases. Local immune responses may be disturbed by both mental and physical exertion in long-COVID patients.
  4. Genetic and Epigenetic Changes:
    • SARS-CoV-2 induces genetic and epigenetic alterations to DNA, resulting in a compromised immune system, elevated risks of diabetes, hypertension, cancer, and damage to neurological, circulatory, and cardiovascular systems. Predisposed conditions are likely to escalate to more advanced stages.
  5. Complexity of Long-COVID:
    • Long-COVID is likely a multifaceted condition involving persistent virus presence, residual viral proteins, and lasting epigenetic and genetic changes, potentially lasting indefinitely.
  6. Increased Risks with Reinfection:
    • Reinfection with COVID amplifies the risks of death, hospitalization, and multi-organ damage, exacerbating underlying conditions across various bodily systems.

Understanding the epigenetic changes induced by COVID, including the downregulation of NAD+ and the impact on tryptophan, sheds light on the physical and mental health challenges faced by individuals. The deficiency in niacin, zinc, and vitamin D is a common consequence. It is crucial to recognize that COVID’s epigenetic changes may vary widely based on an individual’s genetic makeup, requiring tailored treatments for optimal outcomes.

COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderCOVID: Excess Deaths and Quality of Life

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by Daniel Brouse
December 14, 2023

COVID=19

Long-COVID, or post-infection COVID, appears to affect the majority of the population. For individuals that “recover” from COVID-19, they can expect a decreased quality of life and a premature death.

Decrease in Quality of Life
Known chronic conditions resulting from a COVID infection include: Permanent Organ Damage, Persistent SARS-CoV-2 RNA in multiple organs and throughout the brain, Destruction of Good Gut Bacteria Resulting in a Compromised Immune System, Epigenetic Modifications (Changes to DNA), Change in Cell Fate, Tryptophan Deficiency, Dysfunctional Kynurenine Pathway, Neurological Damage, New-Onset Alzheimer’s Disease, Exertional Intolerance, Oxygen Extraction, Reduced Exercise Capacity, Down Regulating NAD+, Up Regulating IDO, Rogue Antibodies, Insulin Reduction, Diabetes, High Cholesterol, Heart Disease and Stroke, Increased Risk of Cancer, Blood Clots, Hypertension, Vascular Disorders, Myocarditis and Heart Disease, Multisystem Inflammatory Syndrome in Children (MIS-C), and Dysregulation of the innate immune system, i.e. “cytokine storm”.

Decrease in Life Expectancy
In epidemiology, the excess deaths or excess mortality is a measure of the increase in the number deaths.

On October 26, 2023, Insurance News Network reported, “Excess mortality is the difference between the total number of deaths for a specific time period and the number that would have been expected. The numbers were naturally forecast to climb during the pandemic, but some industry and health authorities are concerned the rates haven’t greatly diminished as COVID infection rates have declined.”

In November of 2023, the SOA Research Group released Group Life COVID-19 Mortality Survey Report finding the 39-month period of April 2020 through June 2023 showed the following Group Life mortality results:
• Estimated reported Group Life claim incidence rates were up 13.2% on a seasonally-adjusted basis compared to 2017–2019 reported claims.
• Estimated incurred Group Life incidence rates were 12.2% higher than baseline on a seasonally-adjusted basis. As noted above, the incurred incidence rates in May and June 2023 are based on fairly incomplete data, so they are subject to change and should not be fully relied upon at this point.

90% of these excess deaths were caused by post-COVID conditions. 10% of the excess deaths are attributed to the COVID virus.

A Boston University study identified a total of 1,179,024 excess deaths from March 2020 through February 2022, including an estimated 634,830 excess deaths from March 2020 to February 2021, and 544,194 estimated excess deaths from March 2021 to February 2022.

Causes
A decrease in life expectancy, quality of life, or death after a COVID infection is usually caused by complications from the infection, persistent virus (chronic infection), and/or epigenetic changes.

COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderCOVID: Insulin Reduction, Diabetes, High Cholesterol, Heart Disease and Stroke

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by Daniel Brouse
March 11, 2023

COVID=19

Post-COVID patients are at an increased risk of developing or exacerbating diabetes.

In addition, the American Heart Association (AHA) states that diabetes often lowers HDL (good) cholesterol levels and raises triglycerides and LDL (bad) cholesterol levels.

Both blood sugar and cholesterol increase the risk for heart disease and stroke.

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 (though individuals have been impacted more than 3-years after infection), the researchers reported in Cell Metabolism in August 2021, 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.”

Diabetes Risk Rises After COVID
A March 2022 study published in the Journal Nature found, “Even mild SARS-CoV-2 infections can amplify a person’s chance of developing diabetes, especially for those already susceptible to the disease. People who get COVID-19 have a greater risk of developing diabetes up to a year later, even after a mild SARS-CoV-2 infection, compared with those who never had the disease.”

A study published in February of 2022 in JAMA, Diabetes After COVID-19 Infection, found COVID-19 Omicron infection is linked to new-onset diabetes. COVID-19 Omicron survivors may be at a greater than 60% risk of new-onset type 1 or 2 diabetes (a potential precursor of heart attack and stroke.)

A Cedars-Sinai news release said that data trends and patterns suggest that COVID-19 may act as a disease accelerator, amplifying the risk of an illness that may have come later in life. “So, it could be that instead of being diagnosed with diabetes by age 65, a person with preexisting risk for diabetes might—after a COVID-19 infection—be more likely to develop diabetes by age 45 or 55.”

The Pennsylvania State University meta-analysis Association of COVID‑19 with Diabetes included eight studies on new-onset type 1 or 2 diabetes in COVID-19 survivors published from December 2019 to October 2022. COVID-19 was tied to a 66% higher risk of new-onset diabetes regardless of age or sex. “Given the extraordinary number of COVID-19 survivors globally, the modest increase in diabetes risk could correspond to a drastic rise in the number of people diagnosed with the disease worldwide,” the authors wrote.

Cholesterol Levels
The study Risks and burdens of incident dyslipidaemia in long COVID found people with a prior COVID infection had a 24% increased risk for high cholesterol levels.

“These are people who never had cholesterol problems before,” said Dr. Ziyad Al-Aly, an author of the study and a clinical epidemiologist at Washington University in St. Louis. “Now, all of a sudden, they started having problems weeks and months after Covid-19.”

In June of 2023, the study Incidence of Diabetes in Children and Adolescents During the COVID-19 Pandemic was published in the Journal Nature and found COVID is linked to surge in child and teen diabetes.

Increased Risk of Heart Disease and Stroke
The Centers for Disease Control says, “High blood cholesterol is a major modifiable risk factor for heart disease, the leading cause of death in the United States. A 10% decrease in total blood cholesterol levels can reduce the incidence of heart disease by as much as 30%,” and “Over time, high blood sugar can damage blood vessels and the nerves that control your heart. People with diabetes are also more likely to have other conditions that raise the risk for heart disease.”

COVID: Hypertension, Heart-disease Risk Soars

Long COVID Update: Living With It

COVID in Your Genes

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderLong-COVID: What We Know About Long Haulers Syndrome

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COVID=19
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.

Association Between Vaccination and Acute Myocardial Infarction and Ischemic Stroke After COVID-19 Infection (Vaccines Help Prevent Long-COVID 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.

Permanent Organ Damage

“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

COVID-19 Chronic Conditions

COVID in Your Genes

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderCOVID in Your Genes

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by Daniel Brouse
email help@membrane.com
May 30, 2021

COVID gets into your genes and makes alterations. Anybody that has “Long Haulers” (Post Acute COVID-19 Syndrome) can tell you about some of the resulting symptoms. COVID-19 Induced Secondary Pellagra (CISP) is one of the outcomes. CISP occurs when COVID changes your genome to chronically increase the breakdown of NAD+ and simultaneously decrease the production of NAD+ (nicotinamide adenine dinucleotide). NAD+ is in every cell and is involved in cell creation, maintenance, metabolism, and regulating cell processes. Without the ability to maintain NAD+ levels, the body’s immune system is severely compromised. For instance, you can not properly metabolize Vitamin C, Vitamin D, and zinc without NAD+. No matter how large of a megadose you take, it will not be metabolized; therefore, it will not be utilized in your immune response to any pathogen.

Not only will inadequate NAD+ levels impact your immune response, lack of NAD+ causes significant symptoms due to lack of cell regulation. A COVID NAD+ deficiency can cause a lack of serotonin regulation resulting in a lack of body temperature regulation. Dr. Ade Wentzel added, “NAD+ deficiency causes a lack of Tryptophan which is used for serotonin production and hence temperature…” Lack of cell and cytokine regulation also causes headaches, brain fog, anxiety, stress, loss of taste or smell, dizziness, fatigue, muscle aches, dermatitis, diarrhea, dementia, and death. Any activity that causes inflammation or a demand for NAD+ will result in more acute symptoms. Exercise and exertion of any kind exacerbates the condition.

The types of COVID-19 genome modifications are known as epigenetics. “Unlike genetic changes, epigenetic changes are reversible and do not change your DNA sequence, but they can change how your body reads a DNA sequence,” explains the CDC. At this time, we do not how many many genome modifications COVID makes nor how long the modifications will last.

Thousands of CISP patients have been treated successfully with a modified pellagra therapy; however, after a year of treatment, NAD+ production has not returned to normal for most patients.

In addition to genome modifications to NAD+, COVID also makes other changes. 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 (IDO). “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.’ (Wikipedia)

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.”

It is possible that changes in the weather that cause changes in atmospheric pressure (Lows and Highs) may result in the same problems.

There are many other Epifactors and Transcription Factors caused by COVID. “Using integrative analyses of gene co-expression networks and de-novo pathway enrichment, we characterize different gene modules and protein pathways enriched with Transcription Factors or Epifactors relevant for SARS-CoV-2 infection. We identified EP300, MOV10, RELA, and TRIM25 as top candidates, and more than 60 additional proteins involved in the epigenetic response during viral infection that has therapeutic potential. Our results show that targeting the epigenetic machinery could be a feasible alternative to treat COVID-19.” (Nature)

“We found that exposure to the SARS-CoV-2 spike protein alone was enough to change baseline gene expression in airway cells,” said Evans who is based in the laboratory of Sharilyn Almodovar, Ph.D., at the Texas Tech University Health Sciences Center.

“This suggests that symptoms seen in patients may initially result from the spike protein interacting with the cells directly.”

The researchers analyzed expression in genes with functions related to oxidative and osmotic stress, cell death, the inflammatory response, and DNA damage, among others. They found that expression of CCL2, IL1A, IL1B, and MMP9 showed up to two-fold changes in expression after recovery.

All of these genes play a role in inflammation. CCL2 levels are increased in neuroinflammatory disorders such as epilepsy and Alzheimer’s, as well as in some autoimmune diseases like psoriasis, whereas MMP9 is needed for wound healing and recovery from lung damage.

IL1A and IL1B are part of the interleukin family of cytokines and directly produce inflammation and promote fever, as well as playing a regulatory role in the greater immune response. —
— Clinical OMICs

Structural analyses have elucidated hot spots in viral binding domains, mutations, and specific proteins in the host such as the receptor angiotensin-converting enzyme 2 (ACE2) and the transmembrane protease serine 2 (TMPRSS2) to be implicated in cell entry and viral infectivity. Furthermore, epigenetic changes that regulate chromatin structure have shown a major impact in genome stabilization and maintenance of cellular homoeostasis and they have been implicated in the pathophysiology of the virus infection. Epigenetic research has revealed that global DNA methylation along with ACE2 gene methylation and post-translational histone modifications may drive differences in host tissue-, biological age- and sex-biased patterns of viral infection. Moreover, modulation of the host cells epigenetic landscape following infection represents a molecular tool used by viruses to antagonize cellular signalling as well as sensing components that regulate the induction of the host innate immune and antiviral defence programmes in order to enhance viral replication and infection efficiency.
— Epigenetic mechanisms regulating COVID-19 infection (NIH)

“Viral proteins encoded by SARS-CoV-2 disrupt critical components of human cells’ molecular machinery and disable responses to infection. Researchers in the US describe how specific viral proteins bind to human RNAs involved in RNA splicing, protein translation, and protein trafficking, and in doing so suppress the host cell’s coordination of a key antiviral defense known as the type I interferon response.”
— SARS-CoV-2 Disables Key Components of Human Cells’ Defense System

“[COVID-19] interferes with protein trafficking to the cell membrane upon infection. Disruption of each of these essential cellular functions acts to suppress the interferon response to viral infection. Our results uncover a multipronged strategy utilized by SARS-CoV-2 to antagonize essential cellular processes to suppress host defenses.
— SARS-CoV-2 Disrupts Splicing, Translation, and Protein Trafficking to Suppress Host Defenses

COVID-19 genetic changes have been found to cause Reverse-transcribed SARS-CoV-2 RNA.

Prolonged detection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA and recurrence of PCR-positive tests have been widely reported in patients after recovery from COVID-19, but some of these patients do not appear to shed infectious virus. We investigated the possibility that SARS-CoV-2 RNAs can be reverse-transcribed and integrated into the DNA of human cells…
— Reverse-transcribed SARS-CoV-2 RNA can integrate into the genome of cultured human cells and can be expressed in patient-derived tissues (PNAS)

How many different modifications to your genes does COVID-19 make? How long will the alterations last? We don’t know.

“Not all epigenetic changes are permanent. Some epigenetic changes can be added or removed in response to changes in behavior or environment.” Most of a person’s lifetime epigenetic changes have to do with aging. Infections and behaviors, like smoking, also can cause epigentic changes. Most of a smoker’s epigenetic changes revert back after a year of not smoking. Perhaps the COVID epigentic changes will go away over time. Unfortunately, COVID also does insertions. Insertions can not be reverted. The biggest unknown for COVID is the possibility — “if the insertion is in a tumor suppressor, for example, and disrupts that gene, then cancer can be a concern.”

Most experts are of the opinion that “the preexisting state may well determine the final outcome when there is genetic upregulation. COVID is choosing those that may well already have some subclinical symptoms of upregulated pathways.” In the case of cancer and tumor suppression, it appears COVID chooses people that have reduced P53 just like other coronavirus do (P53 is the tumor suppression gene.) Therefore, COVID is unlikely to cause insertions into the gene and be an additional cancer risk.

We do know there is upregulation of genes by COVID and these genes are related to abnormal T-cell, macrophage function, and abnormal humoral immunity. The epigenetic changes related to NAD+ have reverted in some cases after 13 months of treatment. The longer one has left it before getting help the harder and longer it takes for the epigenetics to revert. Currently, we are monitoring cases of epigenetic reversion as more people reach 12 months of treatment.

Post–COVID-19 Associated with Immune Cell Infiltration and Altered Gene Expression
COVID causes long-term immune dysfunction. “These findings indicate that T cell–mediated inflammation persists in the olfactory epithelium long after SARS-CoV-2 has been eliminated from the tissue, suggesting a mechanism for long-term post–COVID-19 smell loss.”

COVID-19 Chronic Conditions

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus