Researchers discovered that cells in the nasal lining of children have a better defense against the SARS-CoV-2 virus, which might explain why they usually have milder symptoms.
Cells in the nasal lining of children have a better defense against the SARS-CoV-2 virus
In Short
Children are less affected by the Covid-19 virus than older adults
The reason lies in the nasal cells that have a better defense mechanism against SARS-CoV-2
Although children rarely get very sick from Covid-19, older people still face high risks, researchers said
The Covid-19 pandemic may have indiscriminately affected people of all age groups but the most vulnerable candidates were the elderly. The reason why children were less severely infected than the senile population above the age of 60, was because of their nasal cells.
A recent study by University College London and the Wellcome Sanger Institute discovered that cells in the nasal lining of children have a better defense against the SARS-CoV-2 virus, which might explain why they usually have milder symptoms.
Scientists grew nasal cells from three age groups: children under 12, adults aged 30 to 50, and people over 70. Then, they exposed these cells to the Covid-19 virus.
The results, published in Nature Microbiology, showed that children’s nasal cells fought off the virus quickly, while this ability weakened with age.
The nasal epithelial cells (NECs) from older adults had more virus and showed more damage.
Although children rarely get very sick from Covid-19, older people, especially those over 60, still face high risks, even with vaccines and better treatments.
This study highlights the importance of considering age when studying and treating infectious diseases.
Although children rarely get very sick from Covid-19, older people, especially those over 60, still face high risks, even with vaccines and better treatments.
“Our research shows how age affects our nasal cells’ ability to fight off SARS-CoV-2. This could help develop treatments and prevention strategies tailored to different age groups, especially for older adults who are at higher risk of severe illness,” said Dr Claire Smith, who led the project at UCL.
Children infected with SARS-CoV-2 rarely progress to respiratory failure, but the risk of mortality in infected people over the age of 85 remains high, despite vaccination and improving treatment options.
“By carrying out SARS-CoV-2 infections of epithelial cells in vitro and studying the responses with single cell sequencing, we get a much more detailed understanding of the viral infection kinetics and see big differences in the innate immune response between cell types,” said co-senior author Dr Kerstin Meyer (Wellcome Sanger Institute).
The team suggest that future research should consider how ageing impacts the body’s response to other viral infections.
Four years into the pandemic, many people have had COVID more than once—but the health consequences of repeat infections are not yet clear
The specter of COVID has haunted the globe for four years now—the disease has killed at least seven million people worldwide. Yet the pandemic’s long-term effects are still hazy—because when it comes to a novel virus such as SARS-CoV-2, which causes COVID, scientists still have a lot to learn.
What we do know is that COVID is here to stay—and that catching it doesn’t give people permanent immunity. Four years into the pandemic, researchers and clinicians know that people are racking up multiple infections, but the long-term consequences of repeatedly getting the virus aren’t yet clear. Fortunately, both individuals and governments have strategies to avoid some infections—if they use them.
“However you slice it, whatever long-term health effect you look at, the risk [from reinfection] is not zero,” says Ziyad Al-Aly, a clinical epidemiologist at Washington University in St. Louis. “The truth is that, yes, we’re sick and tired of the virus, we’re sick and tired of the pandemic—but it’s still here. It’s still hurting people.”
In the U.S. alone, more than 1.1 million people have died of COVID since the pandemic began, according to the Centers for Disease Control and Prevention. The agency is no longer tracking infections at the community level, but in mid-January it reported that nearly four percent of deaths nationwide were caused by COVID.
And while the winter wave of infections appears to be waning, the world missed its chance to make COVID disappear. “This ugly guest isn’t going to leave us any time soon,” Al-Aly says. “It’s going to be here probably for decades.”
Early on in the pandemic, scientists hoped that COVID would be the sort of disease for which vaccination or infection creates immunity that lasts for years or a lifetime. But the SARS-CoV-2 virus had other plans. Vaccination and, to a lesser degree, infection make you less vulnerable to catching the virus and having a severe case, but that protection wanes over time.
“One infection does protect you against future infections” but not completely, says Jamie Rylance, a physician on the World Health Organization’s clinical management team. The SARS-CoV-2 virus mutates rapidly, so a person’s immune system can’t necessarily fully fight off a new infection, even if it’s been primed by a recent bout with a different strain. The same holds true for vaccinations: although initial shots and boosters help a person’s immune system respond more effectively to an infection and reduce the odds of a serious COVID case, current COVID vaccines can’t prevent infection completely.
Complicating things further, COVID often triggers asymptomatic infections, which helped the virus continue to spread early in the pandemic even in places where governments established relatively strict containment protocols. And four years into the pandemic, many people are testing for COVID less often and tests miss many asymptomatic cases, making them even harder to identify. So people have likely been infected more times than they know.
“We don’t know how often we’re getting reinfected because we have some protection from vaccination or even past infection,” says Maria Van Kerkhove, interim director of the WHO’s department of Epidemic and Pandemic Preparedness and Prevention. She doesn’t think that’s something to be complacent about, however. “We know that when the virus enters our body, it affects multiple organ systems,” she says
The combination of evidence on COVID and the long-term impacts of other viruses paints a grim picture of what it might mean to experience regular COVID infections.
“Every time you get infected [with COVID], it does harm to the body in some way,” says Avindra Nath, a neurologist at the National Institutes of Health who has led research on long COVID and other postviral conditions. For example, a pulmonary infection can leave scars in the lungs or trigger blood clots. COVID may also interfere with the immune system itself, he says. Nath notes that the protective sheaths of many viruses include regions that can interfere with the immune system. Separately, one study that followed up with participants after a flu infection found that in about 30 percent of people, the immune system remained somewhat impaired two months later.
And because COVID is still relatively new, scientists realistically have no idea what happens 10, 20 or even 30 years after an infection, much less multiple bouts. “What we need to be able to track is the complications of pulmonary function [and] cardiac function five years from now, 10 years from now,” Van Kerkhove says.
Frustratingly, we may never have a clear sense of the damage COVID reinfections are causing, says Sunil Ahuja, an infectious disease specialist at University of Texas Health Science Center at San Antonio. “To ascribe cause and effect is very challenging,” he says of potential long-term consequences of repeated bouts with COVID. During the span of time between infections, “they’ve also had many other things happen to them, too.”
Some viruses can hide out in the body and emerge decades after the initial infection to cause new problems. The virus that causes chicken pox, for example, can trigger shingles many years later. And scientists have recently learned that infection with the common Epstein-Barr virus seriously increases the risk of a person developing the autoimmune disorder multiple sclerosis. “I don’t think we’ve seen the end of this movie yet,” Al-Aly says of SARS-CoV-2’s long-term impacts.
Moreover, COVID has already shown its potential to cause lasting harm in the form of long COVID, which can include debilitating fatigue, breathing problems, difficulty thinking, digestive issues and a wide variety of other symptoms. As of mid-2023 long COVID impacted 11 percent of Americans reporting a previous infection—a notable decline from the previous year. Scientists are still working to determine what triggers long COVID, but it’s clear that people can develop the condition after several infections, not just their first encounter with COVID.
“Each time that you have COVID, you have a chance of having post-COVID condition afterwards,” Rylance says, though he adds that “it’s still fairly unpredictable at an individual level.”
While scientists desperately want more data to better understand the ways COVID could shape a person’s health for years to come, the hints available now are worrying, experts say. “There’s a major concern here that people who are getting repeated infections [could] have long-term consequences,” Nath says. “And the data that is coming out suggests that possibility.”
Although COVID is now endemic and widely circulating, people and societies can both work to minimize the odds of infection, Van Kerkhove and Al-Aly say. For individuals, getting vaccinated and masking in public and crowded spaces remain the most effective strategies for avoiding COVID or reducing the severity of an infection. Unfortunately, just one in five adults in the U.S. had gotten the updated 2023-2024 COVID vaccine as of mid-January, according to the CDC—even though initial analysis of the vaccines shows that they are about 50 percent effective against infections, including by the latest subvariant, known as JN.1. Testing for COVID when feeling unwell and using antiviral medications such as Paxlovid also remain vital tools for reducing disease risk.
WHO’s Van Kerkhove says that government action is key, including ensuring that masks, vaccines, tests and treatments are available and affordable. But she also called on governments to take bolder steps such as strengthening ventilation requirements in buildings and supporting the development of better vaccines, including an oral or nasal vaccine that could more effectively prevent against COVID in the respiratory tract, where the virus enters a person’s body. In addition, Al-Aly says, we need a longer-lasting vaccine that would offer meaningful protection for several years, so people would not need to get vaccinated every year.
“It’s not beyond the might of U.S. medicine to really develop the technology and to deliver those solutions,” Al-Aly says of such next-generation vaccines. He says the investment is particularly important now that we understand that COVID is not a problem we will dispense with quickly—and now that concerns are mounting about the damage of repeated infections.
“Those are going to be the long-term, sustainable solutions,” Al-Aly says. “It isn’t sustainable to ask people to mask for the next 100 years.”
JN.1, a new COVID-19 variant detected in August 2023, has quickly spread worldwide, showing significant evolutionary changes from previous strains. This development calls for ongoing vigilance and adaptation in global health strategies.
The JN.1 COVID-19 variant, emerging in late 2023, marks a significant shift in the virus’s evolution, emphasizing the need for sustained global health efforts.
The World Health Organization (WHO) classified JN.1 as a “variant of interest” in December 2023 and in January strongly stated COVID was a continuing global health threat causing “far too much” preventable disease with worrying potential for long-term health consequences.
JN.1 is significant. First as a pathogen – it’s a surprisingly new-look version of SARS-CoV-2 (the virus that causes COVID) and is rapidly displacing other circulating strains (omicron XBB).
It’s also significant because of what it says about COVID’s evolution. Normally, SARS-CoV-2 variants look quite similar to what was there before, accumulating just a few mutations at a time that give the virus a meaningful advantage over its parent.
However, occasionally, as was the case when omicron (B.1.1.529) arose two years ago, variants emerge seemingly out of the blue that have markedly different characteristics to what was there before. This has significant implications for disease and transmission.
Until now, it wasn’t clear this “step-change” evolution would happen again, especially given the ongoing success of the steadily evolving omicron variants.
JN.1 is so distinct and causing such a wave of new infections that many are wondering whether the WHO will recognize JN.1 as the next variant of concern with its own Greek letter. In any case, with JN.1 we’ve entered a new phase of the pandemic.
Where did JN.1 come from?
The JN.1 (or BA.2.86.1.1) story begins with the emergence of its parent lineage BA.2.86 around mid-2023, which originated from a much earlier (2022) omicron sub-variant BA.2.
Chronic infections that may linger unresolved for months (if not years, in some people) likely play a role in the emergence of these step-change variants.
In chronically infected people, the virus silently tests and eventually retains many mutations that help it avoid immunity and survive in that person. For BA.2.86, this resulted in more than 30 mutations of the spike protein (a protein on the surface of SARS-CoV-2 that allows it to attach to our cells).
The sheer volume of infections occurring globally sets the scene for major viral evolution. SARS-CoV-2 continues to have a very high rate of mutation. Accordingly, JN.1 itself is already mutating and evolving quickly.
How is JN.1 different to other variants?
BA.2.86 and now JN.1 are behaving in a manner that looks unique in laboratory studies in two ways.
The first relates to how the virus evades immunity. JN.1 has inherited more than 30 mutations in its spike protein. It also acquired a new mutation, L455S, which further decreases the ability of antibodies (one part of the immune system’s protective response) to bind to the virus and prevent infection.
The second involves changes to the way JN.1 enters and replicates in our cells. Without delving into the molecular details, recent high-profile lab-based research from the United States and Europe observed BA.2.86 to enter cells from the lung in a similar way to pre-omicron variants like delta. However, in contrast, preliminary work by Australia’s Kirby Institute using different techniques finds replication characteristics that are aligned better with omicron lineages.
Further research to resolve these different cell entry findings is important because it has implications for where the virus may prefer to replicate in the body, which could affect disease severity and transmission.
Whatever the case, these findings show JN.1 (and SARS-CoV-2 in general) can not only navigate its way around our immune system, but is finding new ways to infect cells and transmit effectively. We need to further study how this plays out in people and how it affects clinical outcomes.
JN.1 has some characteristics which distinguish it from other variants.
Is JN.1 more severe?
The step-change evolution of BA.2.86, combined with the immune-evading features in JN.1, has given the virus a global growth advantage well beyond the XBB.1-based lineages we faced in 2023.
Despite these features, evidence suggests our adaptive immune system could still recognize and respond to BA.286 and JN.1 effectively. Updated monovalent vaccines, tests, and treatments remain effective against JN.1.
There are two elements to “severity”: first if it is more “intrinsically” severe (worse illness with an infection in the absence of any immunity) and second if the virus has greater transmission, causing greater illness and deaths, simply because it infects more people. The latter is certainly the case with JN.1.
What next?
We simply don’t know if this virus is on an evolutionary track to becoming the “next common cold” or not, nor have any idea of what that timeframe might be. While examining the trajectories of four historic coronaviruses could give us a glimpse of where we may be heading, this should be considered as just one possible path. The emergence of JN.1 underlines that we are experiencing a continuing epidemic with COVID and that looks like the way forward for the foreseeable future.
We are now in a new pandemic phase: post-emergency. Yet COVID remains the major infectious disease causing harm globally, from both acute infections and long COVID. At a societal and an individual level we need to re-think the risks of accepting wave after wave of infection.
People are advised to continue to take active steps to protect themselves and those around them.
For better pandemic preparedness for emerging threats and an improved response to the current one it is crucial we continue global surveillance. The low representation of low- and middle-income countries is a concerning blind spot. Intensified research is also crucial.
Without preparedness, the WHO warned, a pandemic from Disease X could cause much more damage than COVID, which has killed more than 7 million worldwide.
Story at a glance
At the recent World Economic Forum, the World Health Organization warned that the world could face a pandemic 20 times worse than COVID-19 in the future.
Scientists use the term Disease X to refer to the hypothetical new pandemic, which they say would most likely be a respiratory virus.
The WHO has already begun some initiatives to protect against a future pandemic, including efforts to support technology sharing and boost disease surveillance between countries.
At the recent World Economic Forum, the World Health Organization issued a warning to world leaders, saying the world could face a pandemic 20 times worse than COVID-19 in the future.
Scientists call it Disease X, a term that recognizes the next global pandemic could come as the result of an unknown pathogen rather than the spread of a currently recognized disease.
Scientists with the WHO held a session last week calling on world leaders to work together to develop strategies to prevent or manage a Disease X pandemic in the future.
Disease X is not real. It is the name given to a hypothetical pathogen that is being used to help plan for future health crises. Global healthcare experts on Wednesday spoke on a WEF panel called “Preparing for Disease X.” The name was coined by the World Health Organization in 2018.
One of the issues raised was developing better communication strategies to reduce misinformation and conspiracy theories, even as some took to X, formerly known as Twitter, to call the session itself a conspiracy against freedom.Ukrainian soldiers developing ‘mouse fever’
Scientists say the most likely culprit for Disease X would be a respiratory virus, possibly one already circulating in animals that hasn’t yet made the jump to humans.
Without preparedness, the WHO warned, a pandemic from Disease X could cause much more damage than COVID, which has killed more than 7 million worldwide.
The WHO has already begun some initiatives to protect against a future pandemic, including efforts to support technology sharing and boost disease surveillance between countries.
While Disease X was the focus of the session, it’s not the only illness that concerns epidemiologists. Other viruses that could potentially cause a pandemic include Ebola, Marburg, Crimean-Congo hemorrhagic fever, Lassa fever, SARS, MERS, Nipah virus, Rift Valley Fever, Zika virus and new evolutions of COVID-19.
A new variant of the COVID-causing virus SARS-CoV-2 is behind the latest surge in infections this winter, but it doesn’t appear to cause more severe disease
It’s winter, that cozy season that brings crackling fireplaces, indoor gatherings — and a wave of respiratory illness. Nearly four years since the pandemic emerged, people are growing weary of dealing with it, but the virus is not done with us.
Nationally, a sharp uptick in emergency room visits and hospitalizations for covid-19, influenza, and respiratory syncytial virus, or RSV, began in mid-December and appears to be gaining momentum.
Here are a few things to know this time around:
What’s Circulating Now?
The covid virus is continually changing, and a recent version is rapidly climbing the charts. Even though it appeared only in September, the variant known as JN.1, a descendant of omicron, is rapidly spreading, representing between 39% to half of the cases, according to pre-holiday stats from the Centers for Disease Control and Prevention.
Lab data indicates that the updated vaccines, as well as existing covid rapid tests and medical treatments, are effective with this latest iteration. More good news is that it “does not appear to pose additional risks to public health beyond that of other recent variants,” according to the CDC. Even so, new covid hospitalizations — 34,798 for the week that ended Dec. 30 — are trending upward, although rates are still substantially lower than last December’s tally. It’s early in the season, though. Levels of virus in wastewater — one indicator of how infections are spreading — are “very high,” exceeding the levels seen this time last year.
And don’t forget, other nasty bugs are going around. More than 20,000 people were hospitalized for influenza the week ending Dec. 30, and the CDC reports that RSV remains elevated in many areas.
“The numbers so far are definitely going in the not-so-good direction,” said Ziyad Al-Aly, the chief of the research and development service at the Veterans Affairs St. Louis Healthcare System and a clinical epidemiologist at Washington University in St. Louis. “We’re likely to see a big uptick in January now that everyone is back home from the holidays.”
But No Big Deal, Right?
Certainly, compared with the first covid winter, things are better now. Far fewer people are dying or becoming seriously ill, with vaccines and prior infections providing some immunity and reducing severity of illness. Even compared with last winter, when omicron was surging, the situation is better. New hospitalizations, for example, are about one-third of what they were around the 2022 holidays. Weekly deaths dropped slightly the last week of December to 839 and are also substantially below levels from a year ago.
“The ratio of mild disease to serious clearly has changed,” said William Schaffner, a professor of medicine in the division of infectious diseases at Vanderbilt University School of Medicine in Nashville, Tennessee.
Even so, the definition of “mild” is broad, basically referring to anything short of being sick enough to be hospitalized.
While some patients may have no more than the sniffles, others experiencing “mild” covid can be “miserable for three to five days,” Schaffner said.
How Will This Affect My Day-to-Day Life?
“Am I going to be really sick? Do I have to mask up again?” It is important to know the basics.
For starters, symptoms of the covid variants currently circulating will likely be familiar — such as a runny nose, sore throat, cough, fatigue, fever, and muscle aches.
So if you feel ill, stay home, said Marcus Plescia, chief medical officer of the Association of State and Territorial Health Officials. “It can make a big difference.”
Dust off those at-home covid test kits, check the extended expiration dates on the FDA website, and throw away the ones that have aged out. Tests can be bought at most pharmacies and, if you haven’t ordered yours yet, free test kits are still available through a federal program at covid.gov.
Test more than once, especially if your symptoms are mild. The at-home rapid tests may not detect covid infection in the first couple of days, according to the FDA, which recommends using “multiple tests over a certain time period, such as two to three days.”
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With all three viruses, those most at risk include the very young, older adults, pregnant people, and those with compromised immune systems or underlying diseases, including cancer or heart problems. But those without high-risk factors can also be adversely affected.
While mask-wearing has dropped in most places, you may start to see more people wearing them in public spaces, including stores, public transit, or entertainment venues.
Although a federal mask mandate is unlikely, health officials and hospitals in at least four states — California, Illinois, Massachusetts, and New York — have again told staff and patients to don masks. Such requirements were loosened last year when the public health emergency officially ended.
Such policies are advanced through county-level directives. The CDC data indicates that, nationally, about 46.7% of counties are seeing moderate to high hospital admission rates of covid.
“We are not going to see widespread mask mandates as our population will not find that acceptable,” Schaffner noted. “That said, on an individual basis, mask-wearing is a very intelligent and reasonable thing to do as an additional layer of protection.”
The N95, KN95, and KF94 masks are the most protective. Cloth and paper are not as effective.
And, finally, if you haven’t yet been vaccinated with an updated covid vaccine or gotten a flu shot, it’s not too late. There are also new vaccines and monoclonal antibodies to protect against RSV recommended for certain populations, which include older adults, pregnant people, and young children.
Generally, flu peaks in midwinter and runs into spring. Covid, while not technically seasonal, has higher rates in winter as people crowd together indoors.
“If you haven’t received vaccines,” Schaffner said, “we urge you to get them and don’t linger.”
Aren’t We All Going to Get It? What About Repeat Infections?
At the same time, repeat infections are common. Fifteen percent of respondents to a recent Yahoo News/YouGov poll said they’d had covid two or three times. A Canadian survey released in December found 1 in 5 residents said they had gotten covid more than once as of last June.
Aside from the drag of being sick and missing work or school for days, debate continues over whether repeat infections pose smaller or larger risks of serious health effects. There are no definitive answers, although experts continue to study the issue.
Two research efforts suggest repeat infections may increase a person’s chances of developing serious illness or even long covid — which is defined various ways but generally means having one or more effects lingering for a month or more following infection. The precise percentage of cases — and underlying factors — of long covid and why people get it are among the many unanswered questions about the condition. However, there is a growing consensus among researchers that vaccination is protective.
Still, the VA’s Al-Aly said a study he co-authored that was published in November 2022 found that getting covid more than once raises an “additional risk of problems in the acute phase, be it hospitalization or even dying,” and makes a person two times as likely to experience long covid symptoms.
The Canadian survey also found a higher risk of long covid among those who self-reported two or more infections. Both studies have their limitations: Most of the 6 million in the VA database were male and older, and the data studied came from the first two years of the pandemic, so some of it reflected illnesses from before vaccines became available. The Canadian survey, although more recent, relied on self-reporting of infections and conditions, which may not be accurate.
Still, Al-Aly and other experts say taking preventive steps, such as getting vaccinated and wearing a mask in higher-risk situations, can hedge your bets.
“Even if in a prior infection you dodged the bullet of long covid,” Al-Aly said, “it doesn’t’ mean you will dodge the bullet every single time.”
Symptoms of VEXAS syndrome, first discovered in 2020, are highly variable and nonspecific.
Some vaccinated and COVID-infected people are reportedly being diagnosed with a new type of disease called VEXAS syndrome—an autoinflammatory disease discovered in 2020.
Many people are familiar with autoimmune diseases, often caused by dysfunction among the adaptive immune cells, while problems within the innate immune system often cause autoinflammatory diseases.
VEXAS syndrome—short for vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic syndrome—is caused by mutations in the innate immune cells, a somatic mutation in the UBA1 gene found on the X chromosome.
Somatic mutations cannot be inherited, meaning individuals acquire this mutation later in life.
The mutation affects the stem cells in the bone marrow. The cells mature into specialized immune cells that circulate within the bloodstream.
Immune cells carrying the UBA1 mutation are highly inflammatory, and once enough of them accumulate, patients start developing symptoms.
In April 2023, a French paper reported on a 76-year-old man diagnosed with VEXAS syndrome following COVID vaccination.
Three days after receiving the Pfizer COVID vaccine, the man developed tender bumps under the skin, rashes, and purple spots on his limbs. Skin problems are commonly reported in VEXAS patients. He was later determined to have the UBA1 mutation.
“The rare incidence of VEXAS syndrome and the short delay of 3 days between vaccination and onset of symptoms were very suggestive of the vaccine role as a trigger,” authors from Drôme Nord Hospitals wrote.
Another VEXAS syndrome diagnosis occurred in a 72-year-old patient. He developed fever, fatigue, deep vein thrombosis, and a cough after a COVID-19 infection.
For months, clinicians misdiagnosed him as having long COVID. However, the patient was diagnosed with VEXAS syndrome upon detecting the UBA1 mutation.
Some doctors say there may be a link but an indirect one.
“In my experience, it is unlikely that VEXAS syndrome could have been triggered by an infection or COVID-19 vaccination,” Dr. Sinisa Savic, immunologist and associate clinical professor at the University of Leeds, told The Epoch Times.
“We know that as people age, they develop all sorts of mutations in the bone marrow … That is why VEXAS is largely found in the elderly population,” he added.
VEXAS syndrome tends to manifest in older men over 50.
However, infections and vaccinations can trigger or worsen symptoms in people already on track to develop VEXAS syndrome, Dr. Savic said.
“Anything that triggers an immune response can cause temporary worsening symptoms; I don’t think there’s any particular argument about that.”
An Italian study reported a VEXAS syndrome patient who developed blood clots after COVID infection. Blood clots are common in both VEXAS syndrome and COVID-19.
Immune Reactions Worsen Autoinflammatory Diseases
Among the specialized immune cells, only the innate immune cells have been found to carry the mutation. The adaptive immune cells, forming what is known as the “third” or last line of defense, have not been found to carry this mutation.
Dr. Savic said it is possible that adaptive immune cells—T and B cells—would be unable to survive long enough to become specialized if they carry the UBA1 mutation, while specialization of innate immune cells appears to be less affected by the UBA1 mutation.
All infections and vaccinations trigger immune responses necessary for the immune system to react and form immune memory to the pathogen.
However, for patients suffering from autoinflammatory diseases, any immune reaction can cause an imbalance in an already precarious system, potentially worsening the patient’s conditions, according to Dr. Savic.
“This is the case with any autoimmune or inflammatory condition because the immune system tries to control itself, but if you’re then challenged by something else, then that level of control may be reduced,” he said.
During an immune response, the body produces more immune cells; in patients with VEXAS syndrome, this could mean more mutated innate cells.
Innate immune cells are also the first line of defense; they are the first immune cells to activate.
“Cells that carry the mutation are much easier to trigger an inflammatory response,” Dr. Savic added.
Symptoms Highly Variable, Could Potentially ‘Cause Damage to Everything’
VEXAS syndrome was first detected in 2020. Researchers from the National Institutes of Health (NIH) recruited over 2,500 patients suffering from various inflammatory diseases and studied their genes for shared mutation.
Three patients were found to have UBA1 mutation, which the authors linked to their inflammatory manifestation. Since then, hundreds of people with VEXAS syndrome have been identified by the NIH and around the world.
Symptoms of VEXAS syndrome are highly variable and nonspecific, Dr. Savic said.
Patients may develop weight loss, fever, malaise, skin rashes, and joint and tissue inflammation. Since the disease affects immune cells in the blood, many people may have anemia and insufficient immune cells in circulation.
In the bone marrow, mutated stem cells produce specialized yet mutated immune cells with vacuoles that look “completely disorganized” under the microscope. They also “produce quite significant amounts of inflammatory chemicals,” Dr. Savic said.
These specialized immune cells then enter into the circulation, inducing inflammation in the body.
As the disease progresses, different organs become inflamed and impaired and may start to fail, causing death.
It has not been proven without a doubt, Dr. Savic said, but “there is certainly an agreement in opinion that most of the organ inflammation is caused by these mutated cells infiltrating the organ and causing damage to everything.”
Many patients also develop progressive bone marrow failure, which can also lead to death if untreated.
However, the prognosis of patients varies; some decline rapidly, while others with similar biometrics may survive for many years.
Limited Treatment for VEXAS Syndrome
Since the disease was only recently discovered, researchers have not found many viable long-term treatments.
Patients usually respond well to anti-inflammatory steroids, but steroids are harmful if used for prolonged periods.
Patients at risk of bone marrow failure may be considered for allogeneic stem cell transplant. In this procedure, the body’s stem cells are destroyed using chemo and radiation therapy and replaced with another person’s stem cells.
Autologous transplants, meaning transplantation of the person’s own healthy stem cells, are often not considered out of concern that mutated cells may be transplanted.
However, Dr. Savic said that there have been cases of successful autologous transplants where the patient with VEXAS syndrome was cured. These transplantations, however, took place before the patient was diagnosed with VEXAS syndrome.
While clinicians have not found better treatments for their patients, they at least have a clearer idea of what not to give them.
“In the past, many of these patients would have been on treatments that are so-called traditional DMARDs (disease-modifying antirheumatic drugs), which are to a degree bone marrow toxic, and in these circumstances certainly wouldn’t be the conditions you would want to use,” Dr. Savic explained.
Many patients found not to have the UBA1 mutation still have symptoms that look very similar to those of VEXAS syndrome.
People who were injected with “vaccines” for the Wuhan coronavirus (COVID-19) are increasingly being diagnosed with a new type of disease they are calling VEXAS syndrome, an autoinflammatory ailment that was first discovered in 2020 around the time Operation Warp Speed was launched by the Trump regime.
VEXAS syndrome, short for vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic syndrome, is said to be caused by mutations in the innate immune cells, as well as a somatic mutation in the UBA1 gene found on the X chromosome. Most inflammatory diseases, by the way, are caused by dysfunction that arises in adaptive immune cells.
“Somatic mutations cannot be inherited, meaning individuals acquire this mutation later in life,” explains The Epoch Times about the disease. “The mutation affects the stem cells in the bone marrow. The cells mature into specialized immune cells that circulate within the bloodstream.”
“Immune cells carrying the UBA1 mutation are highly inflammatory, and once enough of them accumulate, patients start developing symptoms.”
(Related: Be careful of the World Health Organization [WHO], which wants to control and rule over the world under the guise of protecting the world against COVID and other “threats.”)
Autoinflammation caused by COVID jabs
Back in April, French scientists reported on the case of a 76-year-old man who almost immediately after getting jabbed for COVID with Pfizer’s mRNA (modRNA) variety was diagnosed with VEXAS syndrome. His symptoms included tender bumps under the skin, rashes and purple spots on his limbs.
Skin problems are commonly reported among VEXAS patients, and the man was no exception. He was later determined by specialists to have the UBA1 mutation inherent to the disease.
“The rare incidence of VEXAS syndrome and the short delay of 3 days between vaccination and onset of symptoms were very suggestive of the vaccine’s role as a trigger,” the study authors, from Drôme Nord Hospitals, wrote.
Another patient, 72, developed similar symptoms, as well as a fever, fatigue, a cough and deep vein thrombosis. He was initially misdiagnosed with “long COVID,” only to later also show evidence of the same UBA1 mutation as the first patient.
“In my experience, it is unlikely that VEXAS syndrome could have been triggered by an infection or COVID-19 vaccination,” commented Dr. Sinisa Savic, an immunologist and associate clinical professor at the University of Leeds. “We know that as people age, they develop all sorts of mutations in the bone marrow … That is why VEXAS is largely found in the elderly population.”
Typically, VEXAS syndrome occurs in men over the age of 50. Both infections and vaccinations can trigger or worsen symptoms in people who are already on track to develop VEXAS syndrome.
“Anything that triggers an immune response can cause temporary worsening symptoms,” Dr. Savic added. “I don’t think there’s any particular argument about that.”
Among specialized immune cells, only innate immune cells have been found to carry the UBA1 mutation. Adaptive immune cells, meanwhile, form what is known as the “third” or last line of defense against disease, and these cells have not been found to carry the UBA1 mutation.
Dr. Savic believes that adaptive immune cells, including T and B cells, probably cannot survive long enough to become specialized if they carry the UBA1 mutation. Specialization of innate immune cells, conversely, appear to be less affected by the UBA1 mutation.
Both infections and vaccinations trigger responses in the immune system that are supposed to (in theory for vaccinations, anyway) form immune memory. This process does not occur in people with autoinflammatory conditions – in fact, an immune reaction can cause an imbalance that actually worsens a patient’s condition.
“This is the case with any autoimmune or inflammatory condition because the immune system tries to control itself, but if you’re then challenged by something else, then that level of control may be reduced,” Dr. Savic said.
It is well established that cardiovascular disease was associated with more severe outcomes during the first wave of COVID-19, including an increased risk of hospitalisation and death. New research suggests that this may have also applied to people with an elevated 10-year cardiovascular risk score, even in the absence of overt disease. This group has not previously been identified as a risk group for severe COVID-19.
The observational study, which has not yet been peer reviewed, was led by researchers from the London School of Hygiene and Tropical Medicine (LSHTM), University College London and the University of Bristol, and will be presented at this year’s European Congress of Clinical Microbiology & Infectious Diseases (ECCMID), to be held in Lisbon, Portugal on April 23-26.
Study Details
The team used linked electronic health record data from almost a million adults aged 40-84 years registered at GP practices across England during the first wave of the pandemic in 2020. They calculated the incidence and risk of laboratory-confirmed SARS-CoV-2 and related deaths, intensive care unit admissions, and hospitalisations among adults at raised and low cardiovascular risk based on QRISK3 scores. These scores combine a range of factors, including body mass index, smoking history, blood pressure, cholesterol, age, social deprivation, and ethnicity. A score of 10% or greater, meaning a 10% or higher chance of a heart attack or stroke within the next 10 years, was classed as denoting raised risk, and a score of less than 10% deemed low risk.
Among the initial sample of 949,973 individuals, 113,142 (12%) had existing CVD, 303,558 (32%) were classed as being at raised risk of CVD, and 533,273 (56%) at low risk.
Between March 12 and September 29, 2020, SARS-CoV-2 was confirmed in 4017 participants (average age 58 years, 50% male), giving an adjusted incidence of 5.5 per 1000 (95% CI 5.3 to 5.7). Incidence was similar among the 1144 individuals with raised cardiovascular risk, at 4.9 per 1000 (95% CI 4.6 to 5.1), as among the 1819 people with low cardiovascular risk, at 4.5 per 1000 (95% CI 4.3 to 4.7).
Among those with COVID-19, outcomes included:
Hospitalisation 414.4 /1000 (95% CI390.6 to 439.8) (n=1091)
ICU admission 60.4/1000 (95% CI 51.7 to 70.6) (n=159)
Mortality 218.8 /1000 (95% CI 201.6 to 237.4) (n=576)
Occurrence of Severe Outcomes ‘Far Higher’ in People with Elevated Risk
Rates of all of these adverse outcomes were substantially higher in those with raised cardiovascular risk compared with those at low risk:
Hospitalisation 607.2 [552.5 to 667.4] versus 169.3 [149.1 to 192.3]/1000
ICU admission 97.4 [77.0 to 123.4] vs 35.7 [27.1 to 47.1]/1000
Mortality 310.7 [272.2 to 354.6] vs 23.6 [16.8 to 33.2]/1000
These rates were adjusted for additional sociodemographic and clinical confounders that are not included in the QRISK3 score calculation, including alcohol intake, primary care attendance frequency, prescription of antiplatelets, prescription of anticoagulants, chronic liver disease, chronic respiratory disease, asthma, dementia, chronic neurological disease, cancer, and immunosuppression.
After adjustment, hazard ratios (HR) in those with raised cardiovascular risk were:
Hospitalisation HR 2.78 [2.24-3.45]
ICU admission HR 2.99 [1.80-4.96]
Mortality HR 6.84 [4.18-11.19]
People with elevated cardiovascular risk “showed a substantially greater risk of severe outcomes”, the team concluded.
Author Jennifer Davidson, a PhD student in public health research at the LSHTM said: “Although the risk of contracting COVID-19 infection appears similar among individuals with raised and low cardiovascular risk, the occurrence of severe outcomes is far higher in those at elevated risk.”
She added: “Our study is one of the largest population-based studies with a comprehensive measure of cardiovascular risk.”
Expecting Similar Results with Larger Dataset
The authors noted that this is an observational study, so no firm conclusions can be drawn about cause and effect, and they cannot rule out the possibility that other unmeasured factors may have affected the results. However they suggested that investing in strategies to improve cardiovascular health could reduce the severity of COVID-19 across the population.
Senior author Dr Charlotte Warren-Gash, associate professor of epidemiology and honorary consultant in public health at the LSHTM, said: “Because many of the cardiovascular risk factors associated with more severe consequences from COVID-19 are potentially modifiable, clinicians and policy makers should consider that strategies which improve cardiovascular health may also improve outcomes for people following COVID-19.”
The researchers are currently updating their findings with a dataset of over 6 million individuals to confirm the initial results. This will be presented at the meeting and then submitted for a peer-review publication.
Ms Davidson told Medscape UK that their analysis of the larger dataset is still in progress and they do not yet have results to share. However: “At this point we do not anticipate the results of the larger dataset will be materially different to our initial analysis.”
Oral lesions may be a sign of reactivated viruses and fungal infections due to a more vulnerable immune system.
Little girl with band aid on the shoulder from the injection. Vaccinated in the arm. Prevention of children diseases through vaccination. Health care and medicine concept. Focus on shoulder.
Multiple studies have reported oral and facial lesions occurring after COVID vaccinations and infections, with one review pointing out an observational study that found 70 percent to 100 percent of COVID-19 patients have reported some oral manifestations following infections.
Internal medicine physician Dr. Keith Berkowitz expressed that he is not surprised that patients are reporting ulcers, dry mouth, and various other orofacial manifestations.
“Any immune suppression can cause ulcers,” he told The Epoch Times, adding that oral lesions may be a sign of reactivated viruses and fungal infections due to a more vulnerable immune system.
Integrative medicine practitioner Dr. Yusuf Saleeby said that with the more recent COVID variants, he started noticing a change in the symptomology among his patients and also himself. Ulcers in and around the mouth became more prominent.
“Blistering, like lesions on the face, mouth, and ‘herpetic-like’ lesions in the mouth, lips, gums, and on the tongue,” Dr. Saleeby listed. Tooth and gum pain without the usual evidence of bacterial infections like an abscess has also been observed.
“Many infections present clinically in the oral cavity,” Dr. Nicola Cirillo, dentist and professor of dental medicine pathology and pharmacology at the University of Melbourne, told The Epoch Times.
Similar symptoms are observed in vaccinated people.
“Regarding vaccines, I do observe, occasionally, abnormalities in the head and neck region following vaccination—for example, enlarged cervical lymph nodes, swellings, and oral ulcerations,” said Dr. Cirillo.
A Wide Range of Oral Symptoms
Xerostomia
Also known as dry mouth, xerostomia is one of the most common symptoms reported in COVID-19 infections and an adverse event postvaccination.
Dry mouth can be both subjective—meaning the person feels that their mouth is dry—or it can be an objective indication that there is less saliva in the mouth.
Dr. Berkowitz said that, generally, dehydration is a likely cause of dry mouth since viral infections often cause fluid loss. However, dry mouth can also be caused by conditions such as diabetes and Sjogren’s syndrome, an autoimmune disease.
Dehydration is also a common problem for his long-COVID patients and those suffering from vaccine adverse events, Dr. Berkowitz observed. These patients often have trouble regulating fluid balance and need regular hydration therapy.
Mouth and Mucosal lesions
Ulcers and mouth lesions are common occurrences in infections. Studies have shown that the COVID-19 virus can infect the mouth, so some of these symptoms may be due to the virus infecting cells in the oral cavity.
The mucosa, which lines the inside of the oral cavity, has abundant ACE-2 receptors. The SARS-CoV-2 virus uses its surface spike proteins to bind to these receptors and cause infections. The COVID-19 vaccines also induce the body to produce spike proteins, which may similarly infect cells through the same receptors.
However, viruses and fungi may take advantage of the body during an infection and cause opportunistic infections, which can similarly cause painful lesions around and in the mouth. COVID-19 infections and the vaccine have been shown to cause a reactivation of oral herpes, which can cause blisters and cold sores around the mouth and inflamed gums.
Drs. Saleeby and Berkowitz believe that the cases in which vaccinated people report viral or fungal reactivation may be caused by immunosuppression. Candida is a common fungal infection reported in both COVID-19 infections and postvaccination. Patients may develop a painful white coating, known as thrush, on the tongue and other interior surfaces of the mouth. Usually, this white coating can be wiped off, leaving behind a red surface.
Swollen and Inflamed Tongue
COVID-19 infections have been known to cause tongue swelling and loss of taste buds, causing the tongue to look patchy or pink and glossy. This has also been reported as an adverse reaction postvaccine.
An Australian case study reported a 60-year-old woman who developed painful tongue inflammation and dry mouth three days following her first Pfizer vaccine.
“After partial interval improvement, her symptoms progressively worsened after a second vaccination and third booster vaccination,” the authors wrote. During this time, the patient lost nearly 20 pounds due to difficulty eating.
The patient was treated with oral corticosteroids, which helped to reduce the inflammation, and within weeks, her problems were resolved.
Gum Symptoms
Studies have extensively linked gum diseases with COVID-19 infection. People with periodontal disease are more at risk of having a poor prognosis with COVID-19 infection. Likewise, COVID may worsen periodontal disease.
Burning and bleeding gums is a common adverse event reported following COVID-19 vaccinations. One study found that it was the most commonly reported oral adverse event among females.
A Korean study reported a case in an 81-year-old female who reported pain in her tongue and left palate three hours after taking her Pfizer vaccine.
At the appointment, her doctor noticed the area where she reported pain had ulceration and a decline in gum tissue, exposing her root. She was treated with the steroid dexamethasone, nystatin syrup (an antifungal), and chlorhexidine gargle (an antiseptic). A week later, her tongue pain had alleviated, and there were also signs of gum regeneration, though some swelling and redness remained.
Transient and Often Responds Well to Treatment
Most case studies have reported recovery weeks and months after treatments are prescribed.
Dr. Cirillo, one of the first to discuss the link between facial palsy and COVID-19 vaccines, said that “most adverse reactions are transient and self-limiting … some may be serious or life-threatening.”
Since even transient conditions may extend for months or years, Dr. Cirillo said, “it is important to inform vaccine recipients about these possible consequences.”
In a letter to the editor of the journal Oral Diseases, Indian dentists recommended that patients with oral lesions following COVID-19 vaccinations take dexamethasone, a steroid used to reduce swelling and inflammation, along with an antiviral (acyclovir), an antifungal (nystatin syrup), and an antiseptic (chlorhexidine gargle).
If the patient has oral candidiasis, the analgesic clonazepam and fluconazole syrup are recommended.
“All cases were resolved within a varying period of 1 week to 1 month, while some even took up to 2 months. These treatments significantly relieved all symptoms, including tongue pain and ulcerative lesion,” the authors wrote.
For patients with herpes skin reactions, he also adds the antiviral acyclovir, monolaurin, and L-lysine. Monolaurin is a chemical naturally occurring in coconut milk and human breast milk with strong antibacterial and antiviral properties. L-lysine is an essential amino acid needed to produce all amino acids in the body. It has also been shown to help with the recovery of cold sores
Immune-mediated neurologic events may include Guillain-Barre syndrome or
Risk associated with SARS-CoV-2 vaccination and Guillain-Barré syndrome (GBS) — or possibly with Bell’s palsy — is slight and shouldn’t change vaccine recommendations, reviewers concluded.
An analysis of 69 papers on neuro-immunologic disease and COVID vaccines showed that 11 studies specifically assessed relationships with GBS, reported Hans-Peter Hartung, MD, of University Hospital Düsseldorf in Germany, and co-authors in JAMA Neurologyopens in a new tab or window.
Ten of these studies found links between GBS and the adenoviral vector vaccines from Johnson & Johnson (Ad.26.COV2.S) or AstraZeneca (ChAdOx1). One also reported an association between GBS and Pfizer’s BNT162b2 mRNA vaccine (Comirnaty). One study showed no connection between GBS and COVID vaccination.
Of four studies that analyzed the occurrence of Bell’s palsy after vaccination, the relationship was unclear.
GBS is an acquired demyelinating polyneuropathy that often begins in the lower extremities and ascends over time with loss of reflexes, causing muscle weakness, or in the most severe cases, paralysis. Some cases start a few days or weeks after respiratory or gastrointestinal viral infection. Often, GBS is reversible.
“GBS remains the neurological condition with the clearest evidence of a causal link with SARS-CoV-2 vaccination,” Hartung and colleagues wrote. “However, neither SARS-CoV-2 nor adenoviruses have been convincingly associated with GBS pathogenesis.”
“In general, evidence that vaccination is causally significant in the pathogenesis of autoimmune neurological syndromes is rarely validated even by large, well-conducted epidemiological studies,” with the exception being vaccine-associated immune thrombosis and thrombocytopenia (VITT)opens in a new tab or window, a rare, specific complication mainly associated with adenoviral vector vaccines, the researchers noted.
“An increased risk of developing other neurological autoimmune disorders has been extensively sought, but only the very low incidence of GBS following adenoviral vector vaccine administration has been supported by significant evidence,” they pointed out.
An analysis of surveillance data in 2022 from the Vaccine Safety Datalink showed the overall risk of GBS was low, but unusually highopens in a new tab or window after the Johnson & Johnson shot. In May 2023, Johnson & Johnson’s Janssen unit requested the voluntary withdrawalopens in a new tab or window of its emergency use authorization for its adenoviral vector COVID vaccine in the U.S., saying the company did not intend to update the shot to address emerging variants.
Hartung and co-authors evaluated 69 unique articles about neurologic disease occurrence or worsening after SARS-CoV-2 vaccination. Neurologic disease included central and peripheral nervous system complications, including autoimmune diseases. Risks were measured against expected or background rates.
In the 11 studies that examined GBS occurrence, the post-vaccination window spanned from 0 to 42 days. In a retrospective study in Mexicoopens in a new tab or window, an association emerged between GBS and the Pfizer vaccine. A case series analysis in the U.K. and Spain showed no relationship between GBS and either adenoviral vector or mRNA vaccination.
Four studies in the analysis assessed Bell’s palsy risk. The window after vaccination ranged from 1 to 30 days, and the association between COVID vaccines and Bell’s palsy “was unclear,” Hartung and colleagues wrote.
The phase III mRNA vaccine trials identified a numerical imbalance of Bell’s palsy in the vaccinated group compared with placebo, they noted. This concern was investigated in the World Health Organization’s VigiBaseopens in a new tab or window, which showed mRNA vaccines did not have a higher reported rate of facial paralysis compared with other viral vaccines. “This finding of no association was supported by an interim analysis of surveillance dataopens in a new tab or window from 6.2 million individuals in the U.S. vaccinated with 11.8 million doses of mRNA vaccine,” the researchers said.
Hartung’s team also reported that other studies in their analysis found no quantifiable excess risk for myasthenia gravis, multiple sclerosis, or neuromyelitis optica spectrum disorders.
All studies in their review had substantial confounding factors, the researchers acknowledged. “Vaccination of a substantial proportion of the world’s population happened after a year of severe pandemic illness and restricted interperson mixing, with background health and environmental risk substantially modifying health and immune exposures,” they wrote.
“The global search for a vaccine solution was met in many quarters by suspicion and criticism of new technology,” they added. Physicians, the public, and politicians were motivated to report perceived complications, and it’s “very unlikely that the risks of vaccination for any associated condition have been underestimated.”
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