* 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.”
Good gut bacteria are the microorganisms (bacteria and archaea) that live in the digestive tract. The gut microbiota produces fermentation of non-digestible substrates like dietary fibres and endogenous intestinal mucus.
“Approximately 100 trillion micro-organisms (most of them bacteria, but also viruses, fungi, and protozoa) exist in the human gastrointestinal tract — the microbiome is now best thought of as a virtual organ of the body. he human genome consists of about 23 000 genes, whereas the microbiome encodes over three million genes producing thousands of metabolites, which replace many of the functions of the host, consequently influencing the host’s fitness, phenotype, and health,” according to the Role of the Gut Microbiota in Nutrition and Health. “Gut microbes are key to many aspects of human health including immune, metabolic, and neurobehavioural traits.”
Research published in the Journal Nature states, “The human oral and gut commensal microbes play vital roles in the development and maintenance of immune homeostasis.”
In the study, Gut microbiota composition reflects disease severity and dysfunctional immune responses in patients with COVID-19, it was reported:
Although COVID-19 is primarily a respiratory illness, there is mounting evidence suggesting that the GI tract is involved in this disease. Gut microbiome composition was significantly altered in patients with COVID-19 compared with non-COVID-19 individuals. Moreover, this perturbed composition exhibited stratification with disease severity concordant with elevated concentrations of inflammatory cytokines and blood markers such as C reactive protein, lactate dehydrogenase, aspartate aminotransferase and gamma-glutamyl transferase. SARS-CoV-2 primarily infects the respiratory tract, however, pathophysiology of COVID-19 can be attributed to aberrant immune responses in clearing the virus.
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, highlighting a need to understand how gut microorganisms are involved in inflammation and COVID-19.
With growing evidence that COVID-19 can persist in the body, especially the gut, and cause systemic effects, researchers are calling for greater awareness, ongoing monitoring, and expanded health support — not just for those with long COVID, but for the broader public as well.
Originally, COVID-19 was thought to be a respiratory infection. It didn’t take long to discover that SARS-CoV-2 quickly enters the heart, blood stream, and can infect every organ.
Now we know that SARS-CoV-2 causes micro bloodclots that do not necessarily clear the system.
Resta Pretorius, a South African scientist, says, “When we speak about long COVID and microclots, I think we should just step back a second and speak about acute COVID. We have noted – we and others have noted that the vascular system and clotting is not working properly during acute COVID. So the dilemma with long COVID is that the percentage of individuals, up to 30%, never really get over the presence of these clotting abnormalities or physiological abnormalities when they are not infective anymore – so when they get over the normal five to 10 days of acute COVID. So during long COVID, these clots then just continue to be present.”
“Inside the microclots that are present in these individuals’ blood in circulation, there are various entrapped molecules, inflammatory molecules, that actually prevent the breakdown of the microclots. So although the body’s trying very hard to break down these clots with the normal physiological processes, molecules entrapped in the microclots actually prevent it from breaking down.”
“Now, that is a massive issue because if these microclots are in circulation, it damages the vasculature, or your blood vessels, and in that process, prevents the cells to receive enough oxygen, causing then a failure of the coagulation system of oxygen to your cells. And that can be linked to all of the lingering symptoms that have been noted in long COVID.”
The Results of Persistent clotting protein pathology in Long COVID/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased levels of antiplasmin: We show that plasma samples from Long COVID/PASC still contain large anomalous (amyloid) deposits (microclots). We also show that these microclots in both acute COVID-19 and Long COVID/PASC plasma samples are resistant to fibrinolysis (compared to plasma from controls and T2DM), even after trypsinisation. After a second trypsinization, the persistent pellet deposits (microclots) were solubilized. We detected various inflammatory molecules that are substantially increased in both the supernatant and trapped in the solubilized pellet deposits of acute COVID-19 and Long COVID/PASC, versus the equivalent volume of fully digested fluid of the control samples and T2DM. Of particular interest was a substantial increase in α(2)-antiplasmin (α2AP), various fibrinogen chains, as well as Serum Amyloid A (SAA) that were trapped in the solubilized fibrinolytic-resistant pellet deposits.
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.
The most common symptoms were loss of smell (43%), weakness (40%), fatigue (38%), loss of taste (37%), muscle pain (25%), depression (23%), headache (21%), and anxiety (16%). The researchers also identified major but less common neurologic disorders such as ischemic stroke (1.9%), hemorrhagic stroke (0.4%), and seizures (0.06%).
Among the few nonhospitalized COVID-19 patients with mild illness in the dataset, neurologic and psychiatric symptoms were still common, with 55% reporting fatigue, 52% loss of smell, 47% muscle pain, 45% loss of taste, and 44% headache.
In a University College London news release, lead study author Jonathan Rogers, BChir, said his team had expected neurologic and psychiatric symptoms to be more common in severe COVID-19. “But instead we found that some symptoms appeared to be more common in mild cases,” he said. “It appears that COVID-19 affecting mental health and the brain is the norm, rather than the exception.”
“Months after a bout with COVID-19, many people are still struggling with memory problems, mental fog and mood changes. One reason is that the disease can cause long-term harm to the brain. The current catalog of COVID-related threats to the brain includes bleeding, blood clots, inflammation, oxygen deprivation and disruption of the protective blood-brain barrier. And there’s new evidence in monkeys that the virus may also directly infect and kill certain brain cells,” From blood clots to infected neurons, how COVID threatens the brain
“It’s very clear in our monkey model that neurons are infected,” says Morrison, who presented some of the research at the Society for Neuroscience meeting.
In a 2022 study, the University of Oxford found “Increased risk of some neurological and psychiatric disorders remains two years after COVID-19 infection” even if you have been vaccinated. (Neurological and psychiatric risk trajectories after SARS-CoV-2 infection: an analysis of 2-year retrospective cohort studies including 1,284,437 patients) “New diagnoses of disorders including psychosis, dementia, seizures and ‘brain fog’ remain commoner two years after 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.
COVID-19 can cause psychological problems including loss of smell and taste, long-lasting memory, speech, and language impairments, and psychosis. Here, we provide the first report of prosopagnosia following symptoms consistent with COVID-19. Annie is a 28-year-old woman who had normal face recognition prior to contracting COVID-19 in March 2020. Two months later, she noticed face recognition difficulties while experiencing symptom relapses and her deficits with faces have persisted.
