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.
Autoimmunity does not mean the same thing as immunocompromised. When you are immunocompromised, your immune system is under-performing. If you are immunocompromised, you have a weakened immune system with a reduced ability to fight infections and other diseases. Autoimmune diseases are usually associated with an overactive immune system that mistakenly attacks healthy cells. COVID can cause both immunocompromised conditions and autoimmunity diseases. “COVID-19 itself shares some similarities with systemic autoimmune rheumatic diseases, which could be a challenge for diagnostics.”
The matched cohort study Incident autoimmune diseases in association with a SARS-CoV-2 infection found:
Incident autoimmune diseases in association with a SARS-CoV-2 infection
“We found a 42.63% higher likelihood of acquiring autoimmunity for patients who had suffered from COVID-19.”
Conclusions SARS-CoV-2 infection is associated with an increased risk of developing new-onset autoimmune diseases after the acute phase of infection.
The study, titled “Iron Dysregulation and Inflammatory Stress Erythropoiesis Associated with Long-Term Outcome of COVID-19,” reveals that Long-COVID is linked to elevated levels of C-reactive protein and prolonged elevation of cytokines compared to healthy controls. Iron dysregulation is a common occurrence after infections, as the body swiftly moves iron out of the bloodstream to prevent it from becoming a potential breeding ground for harmful bacteria. The study suggests that defects in iron homeostasis, dysregulated erythropoiesis, and immune dysfunction resulting from COVID-19 may contribute to inefficient oxygen transport, inflammatory imbalances, and persistent symptoms. The information on autoimmune diseases emphasizes that an excessive release of cytokines, which are signaling molecules involved in immune responses, can lead to an exaggerated inflammatory response. This heightened inflammation has the potential to damage tissues and contribute to autoimmune diseases, where the immune system mistakenly attacks healthy cells.
SARS-CoV-2 and the results of COVID-19 cause long-term immune system dysfunction. That is to say COVID results in a compromised immune system.
* SARS-CoV-2 infection weakens immune-cell response
The magnitude and quality of a key immune cell’s response to vaccination with two doses of the Pfizer-BioNTech COVID-19 vaccine were considerably lower in people with prior SARS-CoV-2 infection compared to people without prior infection, a study has found. In addition, the level of this key immune cell that targets the SARS-CoV-2 spike protein was substantially lower in unvaccinated people with COVID-19 than in vaccinated people who had never been infected. Importantly, people who recover from SARS-CoV-2 infection and then get vaccinated are more protected than people who are unvaccinated. These findings suggest that the virus damages an important immune-cell response.
* Dysfunctional Kynurenine Pathway
“Targeted and untargeted metabolomics analyses identified altered tryptophan metabolism into the kynurenine pathway, which regulates inflammation and immunity.”
* Down Regulating 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.”
* Up Regulating 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.
* Rogue Antibodies
Autoantibodies are antibodies (immune proteins) that mistakenly attack a person’s own healthy tissues and organs. 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.
* Dysregulation of the innate immune system, i.e. “cytokine storm”
It is important to note that the severity of disease in humans is not determined only by virus replication but also by the host immune response to the infection, which may lead to dysregulation of the innate immune system, i.e. “cytokine storm” (Omicron SARS-CoV-2 can infect faster and better)
* Reinfection Greater Risks & Exacerbates Underlying Conditions
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 heal<th, musculoskeletal and neurological disorders
* 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.”
* Elevated Cytokines and Low Iron
Defects in iron homeostasis, dysregulated erythropoiesis contribute to inefficient oxygen transport, inflammatory imbalances, and persistent symptoms. The information on autoimmune diseases emphasizes that an excessive release of cytokines, which are signaling molecules involved in immune responses, can lead to an exaggerated inflammatory response. This heightened inflammation has the potential to damage tissues and contribute to autoimmune diseases, where the immune system mistakenly attacks healthy cells.
* 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.
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.”
About 4 weeks after my second dose of Moderna, I noticed my NAD+ symptoms resolved (diarrhea, headaches, fatigue, soreness, temperature regulation, night sweats, etc.) Even after stopping the Niacin treatment, all of the NAD+ downregulation appears to be “back to normal”.
Finally being NAD+ symptom free, I was able to discover my IDO upregulation symptoms (tinnitus, feels like a cold in the ears, sinus pressure, vertigo, brain fog, etc.) Within 90 days of my second jab, all these symptoms improved dramatically. Now, the only time I feel any effects is going from low pressure to high pressure. The symptoms are very mild compared to last summer.
My conclusion is one of two things.:
1) after 23 moths, my damaged cells died. This is unlikely since the average life of a cell is nine years.
2) or more likely, the vaccine caused my immune system to clear the long-COVID damage.
Get vaccinated. Less likely to get COVID in the first place. Might fix your long-COVID if you have it.
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.
