In February of 2020, I contracted SARS-CoV-2. By May of 2020, I recognized a pattern of recurring symptoms including: difficulty breathing, congestion, cough, stomach aches, diarrhea, loss of taste and smell, temperature deregulation, night sweats, nightmares, vivid dreams, dizziness, brain fog, headaches, muscle aches, earaches, and peripheral neuropathy.
Over the next year, I was able to treat most of these symptoms with nicotinic acid; however, reducing the niacin dosage yielded increased symptoms. It was only after becoming fully vaccinated in 2021 (post-infection vaccination) that I appear to have been cured of most of the above symptoms. Approximately ninety days after my second dose of the COVID vaccine I was able to reduce my niacin dosage with no ill side effects.
If you have had COVID, I highly recommend a medical physical and complete blood work. Though only 10% of people “present with symptoms”, it appears COVID will impact 99% of survivors in the long-term.
With vaccination, medication, and diet, I have been able to control all of my known conditions.
1) SARS-CoV-2 can live in organs for an indefinite period of time. Even after testing negative for weeks, the virus can be active in the brain, heart, blood, etc.
2) There appear to be dozens of epigenetic modifications. The changes are not uniform across the population due mainly to preexisting conditions and/or predispositions (eg family history).
In my case, it is likely I had both conditions. The persistent COVID-19 was causing most of my readily apparent symptoms. The niacin helped treat the NAD+ deficiency but did not help clear the virus. It was only after I was fully vaccinated that I was able to clear the virus.
On the other hand, the epigenetic changes appear to be of a permanent nature. My genes are now programmed for increased hypertension, blood sugars, and cholesterol. Unfortunately, it is quite likely I have other undetected epigenetic modifications. I am looking to my family history and being extra diligent on cancer and other health screenings.
The BBC has produced a documentary entitled The long haul of long Covid that talks about COVID induced: cognitive impairment, fatigue, lactic acid, metabolic dysfunction, micro clots, hypertension, blood sugar, diabetes, asthma, allergies, overactive immune system, muscle and joint pain, arthritis, migraines, shortness of breath, and other chronic problems.
Three years after the official declaration of a pandemic, 65 million people – one in 10 who had Covid-19 – still have symptoms. Some are so ill they are yet to return to work.
The Economist’s health editor, Natasha Loder, examines the science behind long Covid and hears about the challenges as researchers try to unravel the cause behind a condition associated with around 200 symptoms.
Natasha gains insights about the disease from Dr Walter Koroshetz, co-director of the long Covid Recover study in the United States, pulmonologist Dr Lancelot Pinto in Mumbai, India, and long Covid expert Dr Waasila Jassat in Johannesburg, South Africa.
She also meets Dr Emma Wall at London’s Francis Crick Institute to hear about the UK’s long Covid drug trial and Dr Maria Teresa Ferretti, from the Women’s Brain Project, discusses why women are twice as likely to get long Covid than men.
* The evidence shows that reinfection further increases risks of death, hospitalization and damage to multiple organ systems
* COVID exacerbates underlying conditions including pulmonary, cardiovascular, hematological, diabetes, gastrointestinal, kidney, mental health, musculoskeletal and neurological disorders
First infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with increased risk of acute and postacute death and sequelae in various organ systems. Compared to no reinfection, reinfection contributed additional risks of death, hospitalization, and sequelae including pulmonary, cardiovascular, hematological, diabetes, gastrointestinal, kidney, mental health, musculoskeletal and neurological disorders. The risks were evident regardless of vaccination status. The risks were most pronounced in the acute phase but persisted in the postacute phase at 6 months. Compared to noninfected controls, cumulative risks and burdens of repeat infection increased according to the number of infections. Limitations included a cohort of mostly white males. The evidence shows that reinfection further increases risks of death, hospitalization and sequelae in multiple organ systems in the acute and postacute phase. Reducing overall burden of death and disease due to SARS-CoV-2 will require strategies for reinfection prevention.
In three separate studies of the kidneys, heart, and brain, COVID-19 has been found to act as an aging accelerant.
“Some of the theories for what may be causing long-COVID symptoms include the persistence of the virus. So, instead of the virus coming and going, it sticks around causing inflammation, auto-immune problems and changes in the microbiome,” Dr. Michael Peluso, an infectious disease specialist at the University of California, San Francisco said.
“You can start thinking about getting COVID as almost an accelerant to aging. The viral infection accelerates the aging process in people,” said Dr. Ziyad Al-Aly, director of the Clinical Epidemiology Center at Washington University in St. Louis and the chief of research and education service at Veterans Affairs St. Louis Health Care System.
Dr. Al-Aly researched data from millions of people across the country. The studies on kidney outcomes in long COVID, long COVID in the brain and long COVID in the heart had similar patterns.
“We have seen that people are losing about three to four percent kidney function in the year following that infection. That usually happens with three to four years of aging,” Al-Aly said.
A symptom of long COVID may be the reason you feel exhausted after a workout — “long COVID may reduce exercise capacity, measured by how much oxygen your body can use and how your heart and lungs function during exercise.”
In January of 2024, a study found long-COVID patients have muscle abnormalities that resulted in cell death after exercise. “It’s really confirming that there is something inside the body going wrong with the disease,” said Dr Rob Wüst, an author of the study at Vrije Universiteit (Free University) Amsterdam.
In the report Cardiopulmonary Long COVID-19 Symptoms found “exercise capacity was reduced by 4.9 mL/kg/min among individuals with symptoms consistent with LC compared with individuals without symptoms more than 3 months after SARS-CoV-2 infection. Findings among individuals with exertional intolerance suggest that deconditioning, dysfunctional breathing, chronotropic incompetence, and abnormal peripheral oxygen extraction and/or use may contribute to reduced exercise capacity.”
“This decline in oxygen peak rate would roughly translate to a 40-year-old woman with an expected exercise capacity of 9.5 METs, dropping to 8.1 METs, the approximate expected exercise capacity for a 50-year-old woman,” says Dr. Matt Durstenfeld, an author on the study and assistant professor of medicine at the University of California, San Francisco.
The press release “Feeling winded after your workout? Long COVID may claim another symptom” states:
The findings suggest that the long COVID cohort in this subgroup may have reduced oxygen extraction in the muscles, irregular breathing patterns, and a lesser ability to increase heart rate during exercise to match cardiac output. In addition, there was evidence of deconditioning, which occurs to some extent after most physical illnesses that result in inactivity, the researchers noted. Importantly, not all the findings could be attributed to deconditioning.
Exercise tests were conducted at least three months following SARS-CoV-2 infection and involved cardiopulmonary exercise testing (CPET), in which oxygen and carbon dioxide were measured, together with other indices of heart and lung function, while the participant used a treadmill or stationary bike.
Doubles Tennis, Lap Swims May Be Too Strenuous for Those With Long COVID
In comparing exercise tolerance, the researchers found the long COVID group’s peak rate of oxygen was 4.9 ml/kg/min lower than the recovered group. According to first author Matthew S. Durstenfeld, MD, MAS, of the UCSF Department of Medicine and of the Division of Cardiology at Zuckerberg San Francisco General Hospital, this difference is equivalent to 1.4 metabolic equivalent of tasks (METs), a measure of energy consumed during physical activities. “This decline in oxygen peak rate would roughly translate to a 40-year-old woman with an expected exercise capacity of 9.5 METs, dropping to 8.1 METs, the approximate expected exercise capacity for a 50-year-old woman,” he said.
Another way of looking at it, Durstenfeld said, is that a doubles tennis player might need to transition to playing golf with a cart or stretching exercises, and those who swim laps may find that low-impact aerobics is a better match.
A distinctive symptom of patients with long COVID is post-exertional malaise (malaise is a general feeling of discomfort, illness, or uneasiness whose exact cause is difficult to identify), which is associated with a worsening of fatigue and pain-related symptoms after acute mental or physical exercise, but its underlying pathophysiology is unclear. We show that skeletal muscle structure is associated with a lower exercise capacity in patients, and local and systemic metabolic disturbances, severe exercise-induced myopathy and tissue infiltration of amyloid-containing deposits in skeletal muscles of patients with long COVID worsen after induction of post-exertional malaise.
Patients with long COVID displayed a markedly lower exercise capacity, which related to skeletal muscle metabolic alterations and a shift towards more fast-fatigable fibers. The pathophysiology of post-exertional malaise includes an acute exercise-induced reduction in skeletal muscle mitochondrial enzyme activity, an increased accumulation of amyloid-containing deposits in skeletal muscle, signs of severe muscle tissue damage, together with a blunted exercise-induced T-cell response in skeletal muscle. Collectively, these findings help to decipher the underlying physiology of fatigue and a limited exercise capacity from the development of post-exertional malaise in patients with long COVID.
Viral infections can alter mitochondrial function, and multiple studies have shown that residual SARS-CoV-2 protein presence is associated with long COVID. It is unknown if the full virus is present, or only protein remnants. Because the spike protein is located on the exterior of the virus, this protein may have different proinflammatory/coagulatory effects compared with the nucleocapsid protein. The higher skeletal muscle infiltration of CD68+ macrophages and CD3+ T-cells suggests a locally disturbed immune response in patients with long COVID.
In conclusion, this study reveals that local and systemic metabolic disturbances, severe exercise-induced myopathy, infiltration of amyloid-containing deposits, and immune cells in skeletal muscles of long COVID are key characteristics of post-exertional malaise. While these explain the symptomatology of post-exertional malaise in long COVID, the molecular pathways underlying these alterations in patients suffering from post-exertional malaise remain to be determined.
The risk of older people (over 65) developing Alzheimer’s disease over a one-year period nearly doubled following a COVID-19 diagnosis. The same researchers had previously found that individuals with dementia had a greater risk of contracting COVID-19 and being hospitalized and dying from the disease than those without dementia.
“Many people believe that for Alzheimer’s disease there is a combination of factors that work together to give you the cognitive impairment, and we were concerned that the kinds of things that happened during COVID-19 — the intense inflammation, and perhaps the kinds of direct action on the brain of the of the virus — might be a risk factor,” Dr. Davis, the study’s co-author, said. “So we went looking for that in our study.”
“We can say that they are associated, but we cannot infer causality,” she stressed.
“First, the pandemic presented serious delays for individuals seeking out medical diagnoses like Alzheimer’s disease, meaning these results could be driven by those who already had Alzheimer’s disease when they were infected but had not yet sought out a formal diagnosis,” Dr. Snyder, vice president of medical and scientific relations at the Alzheimer’s Association, explained.
“Alternatively, COVID-19 infection — which is linked to immune changes, including inflammation — may impact the onset of brain changes that are linked to Alzheimer’s disease and other dementia,” said Dr. Snyder. “However, because this study only showed an association through medical records, we cannot know what the underlying mechanisms driving this association are without more research.”
Part I: What is a persistent virus? (The Chronic Infection Hypothesis)
Persistent viruses are not cleared but remain in specific cells of infected individuals. Persistent infections may involve stages of both silent and productive infection without rapidly killing the host. Diseases caused by persistent virus infections include acquired immune deficiency syndrome (AIDS), AIDS-related complexes, chronic hepatitis, Epstein-Barr (the virus that causes most cases of cases of mononucleosis), subacute sclerosing panencephalitis (chronic measles encephalitis), chronic papovavirus encephalitis (progressive multifocal leukoencephalopathy), several herpesvirus-induced diseases, and COVID-19.
“Some of the theories for what may be causing long-COVID symptoms include the persistence of the virus. So, instead of the virus coming and going, it sticks around causing inflammation, auto-immune problems and changes in the microbiome,” Dr. Michael Peluso, an infectious disease specialist at the University of California, San Francisco said.
“You can start thinking about getting COVID as almost an accelerant to aging. The viral infection accelerates the aging process in people,” said Dr. Ziyad Al-Aly, director of the Clinical Epidemiology Center at Washington University in St. Louis and the chief of research and education service at Veterans Affairs St. Louis Health Care System.
Dr. Al-Aly researched data from millions of people across the country. The studies on kidney outcomes in long COVID, long COVID in the brain and long COVID in the heart had similar patterns.
“We have seen that people are losing about three to four percent kidney function in the year following that infection. That usually happens with three to four years of aging,” Al-Aly said.
Long-term SARS-CoV-2 Found in Multiple Organs
COVID has been found to persist for months in individuals even if their case was mild. The virus continues to infect multiple organs including the brain. The U.S. National Institutes of Health said they found the pathogen is capable of replicating in human cells beyond the respiratory tract and can infect all organs.
In 2024, researchers from Helmholtz Munich and Ludwig-Maximilians-Universität (LMU) found the SARS-CoV-2 spike protein can persist in the brain’s protective layers (the meninges) and the skull’s bone marrow indefinitely, potentially triggering chronic inflammation and increasing the risk of neurodegenerative diseases. The team, led by Prof. Ali Ertürk, Director at the Institute for Intelligent Biotechnologies at Helmholtz Munich, also found that mRNA COVID-19 vaccines significantly reduce the accumulation of the spike protein in the brain.
A Connecticut patient had/has COVID for 471 Days (and still going as of July 02, 2022) that has evolved into 3 new lineages. She currently has three types of persistent COVID at the same time. Two of the mutations were created by the patient and will likely develop into more mutations. “The chronic infection hypothesis for novel SARS-CoV-2 variant emergence is increasingly gaining credence following the appearance of Omicron. Here we investigate intrahost evolution and genetic diversity of lineage B.1.517 during a SARS-CoV-2 chronic infection lasting for 471 days (and still ongoing) with consistently recovered infectious virus and high viral loads. During the infection, we found an accelerated virus evolutionary rate translating to 35 nucleotide substitutions per year, approximately two-fold higher than the global SARS-CoV-2 evolutionary rate. This intrahost evolution led to the emergence and persistence of at least three genetically distinct genotypes suggesting the establishment of spatially structured viral populations continually reseeding different genotypes into the nasopharynx.” (Accelerated SARS-CoV-2 intrahost evolution leading to distinct genotypes during chronic infection)
The chronic infection hypothesis is important work. Ziyad Al-Aly, director of the clinical epidemiology center at the Veterans Affairs St. Louis Health Care System in Missouri, who has led separate studies into the long-term effects of COVID-19 says, “For a long time now, we have been scratching our heads and asking why long-COVID seems to affect so many organ systems. This paper sheds some light, and may help explain why long-COVID can occur even in people who had mild or asymptomatic acute disease.”
The virus lives for an undetermined amount of time after you test negative. These autopsies were performed on people up to 230 days after asymptomatic and mild cases of COVID.
“We show that SARS-CoV-2 is widely distributed, even among patients who died with asymptomatic to mild COVID-19, and that virus replication is present in multiple pulmonary and extrapulmonary tissues early in infection. Further, we detected persistent SARS-CoV-2 RNA in multiple anatomic sites, including regions throughout the brain, for up to 230 days following symptom onset. Despite extensive distribution of SARS-CoV-2 in the body, we observed a paucity of inflammation or direct viral cytopathology outside of the lungs. Our data prove that SARS-CoV-2 causes systemic infection and can persist in the body for months.”
“One patient in the autopsy study was a juvenile who likely died from unrelated seizure complications, suggesting infected children without severe COVID-19 can also experience systemic infection.”
In yet another study, Gastrointestinal symptoms and fecal shedding of SARS-CoV-2 RNA suggest prolonged gastrointestinal infection, scientists found COVID in people’s stool up to 7 months after they tested negative for COVID. “The extended presence of viral RNA in feces, but not in respiratory samples, along with the association of fecal viral RNA shedding with GI symptoms suggest that SARS-CoV-2 infects the GI tract and that this infection can be prolonged in a subset of individuals with COVID-19.”
PART II: What does it mean? (SARS-CoV-2 and Your Kids)
Is SARS-CoV-2 being a persistent virus and the risks associated with persistent viruses. Here are a couple examples:
Chicken pox and Shingles. “Shingles is caused by varicella zoster virus (VZV), the same virus that causes chickenpox. After a person recovers from chickenpox, the virus stays dormant (inactive) in their body. The virus can reactivate later, causing shingles.”
Mononucleosis, Multiple Sclerosis, and Epstein-Barr. The Epstein-Barr virus is a persistent virus linked to causing Mononucleosis (Mono) and Multiple Sclerosis (MS). Studies have also found “people who developed shingles had four times the risk of being diagnosed with MS within the following year.”
Persistent viruses often cause long term health problems, a decreased quality of living, and a shortened lifespan. Some of these chronic conditions will become apparent immediately. Some of the chronic conditions, cancers, and other ailments may not present themselves for years. Research has shown, “Associations between gut microbiota composition, levels of cytokines and inflammatory markers in patients with COVID-19 suggest that the gut microbiome is involved in the magnitude of COVID-19 severity possibly via modulating host immune responses. Furthermore, the gut microbiota dysbiosis after disease resolution could contribute to persistent (long-COVID) symptoms.” Good gut bacteria is a critical component of the human immune system.
Where is COVID Lurking in the body?
The problem with studying persistent viruses is you typically need to do an autopsy to obtain the tissue. A new technique can be used on live volunteers by performing a PET (Positron Emission Tomography) scan. The scan can find persistent virus locations in the body of the HIV virus. They are also applying this technique to find where the persistent SARS-CoV-2 is lurking in long-COVID patients.
This BBC episode of Science In Action “A medical scan which reveals where HIV and other viruses hide in the body” explains:
Protect Children
Unfortunately, I have seen many of my friends posting about their children having COVID. These kids now have a forever health risk. It may be many years before we know all the consequences; however, we already are seeing that COVID elevates the severity of conditions one is predisposed to, such as, a pre-diabetic that gets COVID turning into a diabetic. This is one of the reasons so many children are being diagnosed for COVID when hospitalized for other conditions. COIVD is triggering other ailments. “Persons aged <18 years with COVID-19 were more likely to receive a new diabetes diagnosis >30 days after infection than were those without COVID-19 and those with prepandemic acute respiratory infections,” said the CDC’s Morbidity and Mortality Report.
One should do everything possible to avoid exposure to their children. There is zero (0) evidence of prolonged immunity through infection. So, there is no (none, zip, nadda) benefits of infection. There is a 99% chance of a negative outcome from infection.
Persistent viruses are not cleared but remain in specific cells of infected individuals. Persistent infections may involve stages of both silent and productive infection without rapidly killing the host. Diseases caused by persistent virus infections include acquired immune deficiency syndrome (AIDS), AIDS-related complexes, chronic hepatitis, subacute sclerosing panencephalitis (chronic measles encephalitis), chronic papovavirus encephalitis (progressive multifocal leukoencephalopathy), spongioform encephalopathies (caused by prions), several herpesvirus-induced diseases, and COVID-19. The mechanisms by which persistent infections are maintained involve both modulation of virus and cellular gene expression and modification of the host immune response.
COVID has been found to persist for months in individuals even if their case was mild. The virus continues to infect multiple organs including the brain. The U.S. National Institutes of Health said they found the pathogen is capable of replicating in human cells beyond the respiratory tract and can infect all organs.
There are many questions about Long-COVID (also known as Long Haulers Syndrome.)
Long-COVID is the condition most people develop after recovering from the SARS-CoV-2 virus. Between 40 and 70% of recovered COVID cases report lingering symptoms, but it is quite likely 99.9% of recovered individuals have silent conditions. COVID-19 makes a multitude of changes to the human genome. Some of the changes result in noticeable symptoms, such as, brain fog, fatigue, soreness, night sweats, diarrhea, and loss of taste. There are also many changes to the genome that may go unnoticed, such as, an increase risk of cancer, rogue antibodies, and blood clotting.
The epigenetic changes that cause Long-COVID are very similar to having HIV.
The Journal Nature reports in the article HIV infection alters the human epigenetic landscape, “Early in 2010, a study on the DNA methylation status of B lymphoma confirmed that HIV infections may induce novel epigenetic changes, including DNA methylation status alteration of specific functional sites.”
“Immune dysregulation during HIV infection can increase anemia risk through red blood cell destruction (hemolysis) or ineffective red blood cell production,” according to BMC Infectious Diseases. This is similar to symptoms in some Long-COVID patients. Long-COVID is known to result in a variety of blood issues.
“HIV enters its genetic information into helper T cells to make copies of itself. When this happens, the helper T cells die. This severely disrupts the immune response. Low levels of helper T cells mean killer T cells and other white blood cells do not receive as much information about pathogens in the body,” as reported in Medical News Today. Long-COVID is also suspected of interfering with T cells and the immune system. Long-COVID causes an upregulation in 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.
In December 2021, typical seasonal viruses’ severity was up suggesting recovery from COVID results in a compromised immune system. T cells may lose effectiveness against any pathogen. It is estimated half of the U.S. population has had a COVID infection. Hospitals are seeing a sharp rise in Flu, RSV, and other viral infections. It is also likely infants and younger children are contracting the viruses due to their parents compromised immune systems.
The epigenetic changes caused by both Long-COVID and HIV compromise the immune system.
“This is remarkably important work,” said Ziyad Al-Aly, director of the clinical epidemiology center at the Veterans Affairs St. Louis Health Care System in Missouri, who has led separate studies into the long-term effects of COVID-19. “For a long time now, we have been scratching our heads and asking why long COVID seems to affect so many organ systems. This paper sheds some light, and may help explain why long COVID can occur even in people who had mild or asymptomatic acute disease.”
To date, there is zero (0) evidence that contracting the original strain of COVID gives you any immunity to re-infection — natural immunity. On the other hand, there are a multitude of examples of re-infection.
Natural immunity to the original strain lasts on average from 60 days to 6 months; however, there does not appear to be any natural immunity to the variants.
In India’s recent wave, 1 in 4 Delta cases were re-infections. “Antibodies against Sars-CoV-2 — the virus that causes Covid-19 — were found in about 27% of the 91 participants at a time when the second wave was raging in the country, researchers at the Institute of Genomics and Integrative Biology, National Centre for Disease Control and the Cambridge University, said.” — Hindustan Times
“During the Novavax vaccine trials in South Africa, the study found an overall primary efficacy of 49.4% in 4,400 participants, meaning about half of the patients vaccinated and later infected did not experience symptoms. Genomic analyses revealed that about a third of the 4,400 were previously positive for infection, meaning the South African variant was then and is now capable of reinfection, evading neutralizing antibodies in a similar capacity to the Brazilian variant.”
“The study also showed that prior infection with an earlier version of the virus did not reduce the risk of COVID-19 caused by the South African variant among people who got placebo shots.” — Reuters
“Among Kentucky residents infected with SARS-CoV-2 in 2020, vaccination status of those reinfected during May–June 2021 was compared with that of residents who were not reinfected. In this case-control study, being unvaccinated was associated with 2.34 times the odds of reinfection compared with being fully vaccinated.” — CDC
“Our case series shows that reinfection with different strains is possible, and some cases may experience more severe infections with the second episode. The findings also suggest that COVID-19 may continue to circulate even after achieving herd immunity through natural infection or vaccination, suggesting the need for longer-term transmission mitigation efforts.” — Journal of Investigative Medicine
Vaccines do not appear to be much more effective against the Delta variant than natural immunity through infection. The increase of breakthrough cases has been increasing in lock-step with the increase spread of the Delta variant. “Fewer than 10% of new coronavirus infections occurred in fully vaccinated people in the weeks before June, but the rate increased this summer. In the first four weeks of August, roughly 30% of infections were in fully vaccinated individuals.” — The Star Tribune
A study by the CDC found vaccine efficacy dropped from roughly 90% to 66% as the Delta variant emerged. “This report updates vaccine effectiveness (VE) estimates including all COVID-19 vaccines available through August 14, 2021, and examines whether VE differs for adults with increasing time since completion of all recommended vaccine doses.” — CDC
Another CDC study that compared natural immunity to vaccination has found — “Among COVID-19–like illness hospitalizations among adults aged ≥18 years whose previous infection or vaccination occurred 90–179 days earlier, the adjusted odds of laboratory-confirmed COVID-19 among unvaccinated adults with previous SARS-CoV-2 infection were 5.49-fold higher than the odds among fully vaccinated recipients of an mRNA COVID-19 vaccine who had no previous documented infection.”
CONCLUSION PART I
There is a need for longer-term transmission mitigation efforts. Because reinfection is likely, vaccines efficacy is not high enough, and new variants are emerging, herd immunity is not achievable. Humans can not learn to live with the virus. Mitigation efforts must be made to stop community spread.
CONCLUSION PART II
COVID causes an immune dysfunction. When a person become infected, the SARS-CoV-2 virus alters your genes in order to infect you. “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.” — Nature
When a person recovers from the virus, they are left with multiple gene alterations to there immune system. It is impossible for natural immunity to be feasible in an individual with an immune system that is compromised by a COVID-19 infection.
COVID survivors are left with a severe NAD+ deficiency, and an upregulation of IDO (which suppresses your T and NK cells.) Short term this makes your immune system dysfunctional. This means your antibodies can’t function properly and have little to no memory. Long term it makes you more likely to have heart, blood, respiratory, and neurological disorders. You are at high risk of developing dementia. In addition, you have reduced P53 genes (tumor suppression genes) putting you at higher risk of cancer. — The Membrane Domain
I strongly advise against contracting COVID.
OMICRON UPDATE
December 4, 2021
A study out of South Africa, “Increased risk of SARS-CoV-2 reinfection associated with emergence of the Omicron variant in South Africa,” found that individuals who recently recovered from the Delta variant were afforded little to no protection from the Omicron variant. “Population-level evidence suggests that the Omicron variant is associated with substantial ability to evade immunity from prior infection. This finding has important implications for public health planning, particularly in countries like South Africa with high rates of immunity from prior infection.”
As stated above, everybody is advised to:
* speak to your doctor
* get vaccinated
* wear an N95 mask
* stay socially distanced
UPDATE June 2022: No Immune Boost From Omicron
“If you were infected during the first wave, then you can’t boost your immune response if you have an Omicron infection,” said Prof Rosemary Boyton, of Imperial College London, a co-author of the study. “When Omicron started flying around the country, people kept saying that’s OK, that will improve people’s immunity,” said Boyton. “What we’re saying is it’s not a good booster of immunity.”
“It’s actually worse than that, because the adaptations that the spike [protein] has now are actually inducing a kind of regulation or shutdown of immune response,” Prof Danny Altmann, another author of the study, adding that while the study looked at responses to the BA.1, similar findings were likely for other subvariants of Omicron.
by Daniel Brouse
August 23, 2021
help@membrane.com
Q: Why are there so many breakthrough cases of COVID in the vaccinated?
A: There are several reasons why there are breakthrough cases with any vaccine; however, COVID is different. Many of the vaccinated people getting COVID already had COVID prior to being vaccinated. This is the second time they have contracted the virus.
Once you have had COVID, your immune system is compromised. You should consider yourself immune compromised. The vaccine will not fully compensate for that fact. COVID damages your immune system. The virus makes your antibodies dysfunctional. The virus suppresses your memory T cells. The virus does a lot more to thwart an immune response. So though you may have the antibodies, maybe even lots and lots of antibodies, you’ve got Nobody’s At Home Syndrome. There is little to no immune response regulation nor coordination. This is also why natural immunity through infection is impossible. COVID erases the memory from your memory cells, so to speak. It can’t even remember itself.
Q: Is this a hallmark of the virus? I mean is this finding in all post COVID cases?
A: Yes. Severity of illness does not appear to be a factor (mild cases to severe all exhibit similar compromises to the immune system.) The exception is asymptomatic cases. We still don’t know about asymptomatic cases. The evidence is pointing to all cases that progress past the nasal passage result in immunocompromised individuals. There also is a small percentage (1 in 100,000) of people that appear to evade impact.
The scientific community is looking for ways to cure the problems. So far, there is only some success in treating the symptoms. There is nothing else to really compare to long-COVID. A similar condition happens to some measles survivors that bares a slight resemblance in T cell response, but it is not same. “Measles induces immune suppression through a process called immune amnesia. Studies in non-human primates revealed that MV actually replaces the old memory cells of its host with new, MV-specific lymphocytes. As a result, the patient emerges with both a strong MV-specific immunity and an increased vulnerability to all other pathogens.” COVID appears to use a different process that involves T cell suppression. There is also some similarity to HIV. “HIV attacks a specific type of immune system cell in the body. It’s known as the CD4 helper cell or T cell. When HIV destroys this cell, it becomes harder for the body to fight off other infections.” Again, COVID appears to use a different mechanism to suppress T cells.
Q: What do we know about the immune system post-COVID?
A: We know at least two important pieces of the puzzle:
1) The SARS-CoV-2 causes gene expressions in the host that result in dysfunctional NAD+. The virus makes it harder for the body to create NAD+ and also increases the breakdown in 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
2) The SARS-CoV-2 causes gene expressions in the host that result in 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.’ (Wikipedia)
Q: How long do these gene expressions (epigenetics) last? How long does long haulers syndrome last?
A: We don’t know how long post-COVID cases will suffer with a compromised immune system. Long-COVID patients from January of 2020 are still immune compromised. It is possible the genetic changes will never revert.
Exercise aggravates long-COVID symptoms. COVID causes changes to your genes making it harder to create NAD+ and quicker to consume NAD+. Normally, exercise helps boost your NAD+. Not with long-COVID. The inflammation caused by exercise, anxiety, or exertion causes a rapid depletion of NAD+ aggravating long-COVID symptoms and perpetuating the downward cycle in NAD+ levels. So, Long Haulers should limit their activity until their NAD+ deficiency is under control.
What other factors can impact the severity of your long-COVID symptoms? We know anything that depletes NAD+ will cause problems. Aging, Hypertension, Obesity, Type 2 Diabetes, and other ailments result in suboptimal NAD+. But, what about your environment?
I have been conducting research and development on two other environmental factors — elevation and temperature.
ELEVATION I — Change in Atmospheric Pressure
Elevation is the number of feet above sea level on which you stand. The bio-hacker experiment I’ve been conducting takes me from 400 feet above sea level to 1,400 feet above sea level. The more rapid the change from higher elevations to lower elevation, then the worse my long-COVID symptoms. All systems feel an impact; however, the middle ear takes the brunt of the punishment. Brain fog, dizziness, tinnitus, ear aches, vertigo, and pressure in the ears are all amplified in their severity. I just did a 24 hour experiment and am beginning to think it has to do with pressure. Perhaps O2 (oxygen in the blood) as well, but more to do with “atmospheric pressure and sea level.” The symptoms seem to lag behind the increase in pressure.
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.”
“IDO (Indoleamine 2,3-dioxygenase) 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)
It is possible that changes in the weather that cause changes in atmospheric pressure (Lows and Highs) may result in the same problems. This happened to me with weather systems over the weekend (August 22, 2021.) A very low pressure system (hurricane Henri) passed by followed by a high pressure system. The following 2 days I suffered from brain fog, dizziness, tinnitus, ear aches, vertigo, and pressure in the ears.
COVID causes a decrease in the “rate of oxygen uptake into the lung to the oxygen gradient between the capillary blood and the alveoli.” Dr. Ade Wentzel said, “We know that the Lung Diffusion co-efficient is increased [by optimizing NAD+ levels].”
TEMPERATURE
The sweet spot is between 50-70 degrees Fahrenheit. The further below 50 degrees the more severe the symptoms. Lower temperatures appear to be a linear relationship. On the other hand, temperatures above 70 degrees appear to have an exponential relationship. That is to say, if 80 degrees causes symptoms to be twice as bad, 90 degrees causes symptoms to be four times as severe.
CONCLUSION
Mountain hiking in 90 degree temperatures (exercise at higher elevations in the heat) causes unnecessary stress on your system and dramatically increases your chances of a negative outcome.
