logo
NOVEL IMMUNOLOGIC SURVEILLANCE STUDY PROVIDES NEW INSIGHTS INTO POST-PANDEMIC RETURN OF RESPIRATORY VIRUSES

NOVEL IMMUNOLOGIC SURVEILLANCE STUDY PROVIDES NEW INSIGHTS INTO POST-PANDEMIC RETURN OF RESPIRATORY VIRUSES

Yahoo5 hours ago
Ongoing clinical research study in US children documents the rebound of endemic respiratory viruses, builds foundation for expediting future vaccines and treatments
AURORA, Colo., Aug. 7, 2025 /PRNewswire/ -- The first paper from a multi-year clinical research study has been published in The Lancet Infectious Diseases: Dynamics of Endemic Virus Re-emergence in Children in the USA Following the COVID-19 Pandemic (2022-2023): A Longitudinal Immunoepidemiologic Surveillance Study and demonstrates how the approach can improve modeling to better predict future outbreaks.
The paper shares findings from a multicenter clinical research study, one of many studies that are part of the recently launched PREMISE (Pandemic Response Repository through Microbial and Immune Surveillance and Epidemiology) program, led by Dr. Daniel Douek at the National Institutes of Health's (NIH) Vaccine Research Center (VRC). Data collected during the first year of the PREMISE study, 2022-2023, shows for the first time how non-pharmaceutical interventions such as masking and distancing targeted towards SARS-CoV-2 during the pandemic also decreased circulation rates of and population immunity to common respiratory pathogens in children. The study provides new evidence-based insight into what was driving the large post-pandemic rebound in these diseases and enables more accurate predictions for the future.
This study is a partnership between PREMISE and clinical research sites at academic institutions led by principal investigator Kevin Messacar, MD, PhD, infectious disease specialist at Children's Hospital Colorado, at the central site at University of Colorado Anschutz Medical Campus and Children's Hospital Colorado with additional study sites at University of North Carolina, Weill Cornell Medicine and the University of Alabama at Birmingham.
The PREMISE study conducted immunologic surveillance on children younger than 10 years old, by enrolling them and following them for over a year. Through repeat blood sampling, the team could determine what children at varying young ages had immunity to and what they were susceptible to. Through respiratory sampling during illness, researchers were able to determine what infections they experienced. The data showed that most younger children lacked immunity to many normal respiratory viruses during the pandemic, suggesting they had not been exposed, as they typically would have, due to prevention measures in place. Following the lifting of pandemic measures, the level of immunity rose across all pathogens studied, reflective of the unprecedented widespread resurgence of these viruses in children after the end of the pandemic.
While most research studies target a specific disease, samples from PREMISE were tested for many common and emerging respiratory viruses, including RSV, influenza and enterovirus D68 (EV-D68), which can cause the polio-like illness, acute flaccid myelitis. The data allowed experts to recreate past circulation patterns and model predictions for future outbreaks with greater accuracy and precision. They showed that PREMISE data from 2022-23 could be used to accurately predict the subsequent wave of disease of the emerging pathogen EV-D68 that occurred in 2024.
"Four cohorts of almost 1,000 children have provided an invaluable bank of samples and data," said lead author Hai Nguyen-Tran, MD, infectious disease specialist at Children's Hospital Colorado and assistant professor at University of Colorado School of Medicine. "These are being used to develop 'on the shelf' medical countermeasures, such as antibody treatments and vaccines, for pathogens of interest. Instead of starting from scratch, this study gives us a head start to understand, predict and prepare for future pandemics."
Samples and data from the PREMISE study will also be used to learn which parts of viruses the human immune system attacks to become immune, so teams can better design new antibody treatments and effective vaccines to mimic this response.
"In the future, this type of immune surveillance can be used to better understand the impact of public interventions on population immunity and future waves of disease," said Dr. Messacar, who is also a professor at University of Colorado School of Medicine. "PREMISE is a great example of a successful research partnership between NIH scientists and clinical researchers in academia, leading to concrete deliverables such as vaccine candidates and monoclonal antibodies that can directly impact public health."
This study is fully funded by a subcontract with Frederick National Laboratory for Cancer Research (FNLCR), currently operated by Leidos Biomedical Research, Inc. through Agreement 21X192QT1. FNLCR funding was provided by the NIH Vaccine Research Center within NIAID. The total project funding is $7.98 million over five years. No financing for this project was supplied by nongovernmental sources.
ABOUT CHILDREN'S HOSPITAL COLORADOChildren's Hospital Colorado is one of the nation's leading and most expansive nonprofit pediatric healthcare systems with a mission to improve the health of children through patient care, education, research and advocacy. Founded in 1908 and ranked among the best children's hospitals in the nation as recognized by U.S. News & World Report, Children's Colorado has established itself as a pioneer in the discovery of innovative and groundbreaking treatments that are shaping the future of pediatric healthcare worldwide. Children's Colorado offers a full spectrum of family-centered care at its urgent, emergency and specialty care locations throughout Colorado, including an academic medical center on the Anschutz Medical Campus in Aurora, hospitals in Colorado Springs, Highlands Ranch and Broomfield, and outreach clinics across the region. For more information, visit www.childrenscolorado.org or connect with us on Facebook, Instagram and YouTube.
Media Contact: Rachael Fowler, Children's Hospital Colorado 24/7 media line: 303-890-8314media@childrenscolorado.org
View original content to download multimedia:https://www.prnewswire.com/news-releases/novel-immunologic-surveillance-study-provides-new-insights-into-post-pandemic-return-of-respiratory-viruses-302523817.html
SOURCE Children's Hospital Colorado
Orange background

Try Our AI Features

Explore what Daily8 AI can do for you:

Comments

No comments yet...

Related Articles

RFK Jr.'s anti-vaccine fixation is a menace to public health
RFK Jr.'s anti-vaccine fixation is a menace to public health

New York Post

time14 minutes ago

  • New York Post

RFK Jr.'s anti-vaccine fixation is a menace to public health

Robert Kennedy Jr. is trying to convince Americans that vaccines will hurt them. No matter what superficial throwaway statements he offers the public to the contrary, that's the obvious goal. In the newest front in his cause, the secretary of Health and Human Services has canceled $500 million in mRNA research, an effort President Donald Trump once called a 'modern-day miracle.' Advertisement The HHS head, who in 2023 said no vaccine was 'safe and effective,' says he still supports 'safe, effective vaccines.' Yet he has canceled 22 research projects focused not only on COVID vaccines but also on influenza, respiratory syncytial virus and other communicable ailments. It should be noted that new research often leads scientists to unexpected results and uses, as well. Advertisement However, Kennedy contends that 'mRNA technology poses more risks than benefits for these respiratory viruses.' How does he know? Maybe the technology that uses fragments of the genetic code to manipulate the body to defend itself against infection and disease won't produce any significant breakthroughs. But RFK Jr. wants Americans to believe that RNA, a molecule in every living cell, isn't just ineffective but dangerous. Advertisement Of course, the real purpose of the cancellation is to preemptively undermine the credibility of this vaccine research — which will almost surely continue, if the private sector sees value in it. In the past, Kennedy argued for the need for greater research to understand vaccines before recommending them — yet in this case, he demands less research. The pattern is clear. Advertisement Example: After visiting Texas children who were needlessly struggling with measles earlier in the year, Kennedy also visited 'two extraordinary healers' named Dr. Richard Bartlett and Dr. Ben Edwards, who 'have treated and healed some 300 measles-stricken Mennonite children using aerosolized budesonide and clarithromycin.' The purpose of the juxtaposition was to create the impression that alternative medicine is enough. It's not. If you want to use that therapy, go for it, I guess. As far as I can tell, there's no evidence that inhaled steroids such as budesonide or oral antibiotics like clarithromycin are effective in treating measles; many doctors think it's junk science. Bartlett was disciplined by the Texas Medical Board in 2003 for 'unusual use of risk-filled medications' of this variety. Get opinions and commentary from our columnists Subscribe to our daily Post Opinion newsletter! Thanks for signing up! Enter your email address Please provide a valid email address. By clicking above you agree to the Terms of Use and Privacy Policy. Never miss a story. Check out more newsletters But RFK Jr., you'll notice, didn't bother to wait for the research to praise those doctors or their methods. A quack who once claimed that the polio vaccine causes cancer that killed 'many, many, many, many, many more people' than polio itself, and lied about the connection between autism and vaccines long after the hoax had been exposed — grossly comparing it to a 'holocaust' — doesn't give one whit about any inquiry that proves or disproves the efficacy of vaccines, live attenuated or inactivated or mRNA. Advertisement He's reflexively against them. Not long ago, RFK Jr. fired the entire Advisory Committee on Immunization Practices and replaced its members with his people, to create the impression that he had more fairly represented the scientific debate over vaccines. 'A clean sweep is needed to re-establish public confidence in vaccine science,' was Kennedy's reasoning. Advertisement The former committee members, he argued, had too many 'conflicts of interest,' a euphemism for working or advising 'Big Pharma.' Imagine creating an advisory board for an industry without including people who understand how it works. Granted, I'm a layman. But I don't believe COVID mRNA vaccines are detrimental (as a lot of people seem to think). Nor does it seem that they are miraculous, as proponents claim. Advertisement My problem with the COVID-vaccine regime was the compulsion — not the efforts to mitigate a pandemic, nor the development of new technology that might head off future ones. Pharma companies can't compel you to inject anything. Only the state can do that. And the Luddite demonization of pharma, which saves and improves millions of lives, is still one of the big mysteries of the modern age. Now, the same people who claim that public health institutions can't be trusted believe everything the new head of HHS tells them. Advertisement It's a shame that so many groups like the American Medical Association, which went all-in on the authoritarian COVID regime, have burned the public's trust and goodwill. However — and it needs to be stressed whenever possible — RFK Jr. is no better than the hacks who undermined our trust in science under former President Joe Biden. In some ways, he is worse. David Harsanyi is a senior writer at the Washington Examiner. Twitter: @davidharsanyi

80-year-old ‘SuperAger' brain operates like that of a 50-year-old. Here's why
80-year-old ‘SuperAger' brain operates like that of a 50-year-old. Here's why

Yahoo

time2 hours ago

  • Yahoo

80-year-old ‘SuperAger' brain operates like that of a 50-year-old. Here's why

The human brain shrinks as it ages, affecting the ability to remember — it's part of life. Yet there are a lucky few, called 'SuperAgers,' who possess a brain that fights back. For these people, memories stay as sharp as they were 30 or more years in the past. Carol Siegler, who lives in the Chicago suburb of Palatine, is a SuperAger. At 82, she won the American Crossword Puzzle Tournament for her age group, which she said she entered 'as a gag.' 'I've auditioned twice for 'Jeopardy!' and did well enough on it to be invited to the live auditions. Then Covid hit,' Siegler told me in 2022, when she was 85. Today, Siegler is still going strong, well on her way to her 90th birthday, said Tamar Gefen, an associate professor of psychiatry and behavioral sciences at the Mesulam Institute for Cognitive Neurology and Alzheimer's Disease at Northwestern University in Chicago. Gefen conducts research at Northwestern's SuperAging Program, which is currently studying 113 SuperAgers. Over the past 25 years, however, 80 SuperAgers have donated their brain tissue to the program, which has led to some fascinating discoveries. CNN spoke to Gefen about those decades of work. She is a coauthor of a new analysis of the research that was published Thursday in Alzheimer's & Dementia, the journal of the Alzheimer's Association. This interview has been lightly edited and condensed for clarity. CNN: How do you define a SuperAger, and what have you found out about their behavior over the years? Tamar Gefen: To be a SuperAger in our program at Northwestern, a person must be over 80 and undergo extensive cognitive testing. Acceptance in the study only occurs if the person's episodic memory — the ability to recall everyday events and past personal history — is as good or better than cognitively normal people in their 50s and 60s. We have screened close to 2,000 individuals who think they may be a SuperAger and less than 10% meet the criteria. Over the past 25 years, we have studied about 300 SuperAgers — a number of whom have donated their brain for research. One key trait of SuperAgers is that they seem to be highly social people. They value connection and are often active in their communities. This is interesting because we know isolation is a risk factor for developing dementia, and so staying socially active is a known protective feature. Another common thread in all SuperAgers is a sense of autonomy, freedom and independence. They're making decisions and living their lives the way that they want to live. I feel very strongly that successful aging is not just about sociability. If a person feels trapped, tethered or burdened, especially in a vulnerable state like poor health or older age, I think it can encroach on their entire psychosocial being. But as far as healthy behaviors, SuperAgers run the gamut. We have SuperAgers with heart disease, diabetes, who aren't physically active, who don't eat any better than their similar age peers. There is one SuperAger who drinks four beers every night. He laughs and says, 'Maybe it's done me wrong, but I'll never know.' He doesn't have an identical twin to compare his behavior to, so would he have lived to 108 instead of 98? We don't know. CNN: Many of your most intriguing discoveries have come from studying donor brain tissue. What have you discovered about the memory center of the SuperAger brain? Gefen: Our studies have shown that an area of the brain that is responsible for attention, motivation, and cognitive engagement — known as the cingulate cortex — is thicker in SuperAgers, even compared with those of people in their 50s and 60s. In the hippocampus, the memory center of the brain, we found SuperAgers have three times fewer tau tangles when compared to their 'normal' peers. Abnormal formations of tau proteins are one of the key signs of Alzheimer's. In Alzheimer's disease, tau also targets the neurons of the primary neurons of the cholinergic system — which is responsible for sustaining our attention in daily life. But that doesn't happen in the brain of a SuperAger. Therefore, the cholinergic system appears to be stronger, and likely more plastic and flexible for reasons that we're not sure about. That's interesting, because I see SuperAgers as focused. They can pay close attention, engage and actively listen. How else could they recall 13 out of 15 random words after 30 minutes? I picture them engraving the words on their cortex with a chisel. SuperAger brains also have bigger, healthier cells in the entorhinal cortex, an area essential for memory and learning, that has direct connections to the hippocampus. The entorhinal cortex, by the way, is one of the first areas of the brain to get hit by Alzheimer's disease. In another study we examined every layer of cells within the entorhinal cortex of SuperAgers, and we painstakingly measured the size of the neurons. We found that in layer two, which is the layer that is most important for information transmission, SuperAgers had humongous, plump, intact, beautiful, gigantic entorhinal cortex neurons. It was an incredible finding, because their entorhinal neurons were even larger than those in individuals who are much younger, some even in their 30s. That told us there is a structural integrity component at play — like the architecture, the bones, the skeleton of the neuron itself is sturdier. We're expanding the studies of these neurons to understand their biochemical signatures, determine what makes them special, and see if these signatures are found in other types of neurons in the brain of SuperAgers. Are these same neurons particularly vulnerable in those with Alzheimer's disease, and if so, how and why? CNN: What have you learned from your research about how the brain of a SuperAger reacts to injury, disease and stress? Gefen: We're looking at the inflammatory system in the brain of SuperAgers, with the goal of understanding how the immune cells in their brain respond to disease and adapt to stress. Inflammation, once it crosses a certain threshold, is a major component of cell loss in Alzheimer's disease and nearly all other neurodegenerative diseases. Compared with the brain of same-age peers, SuperAgers have fewer activated microglia, the resident immune cells of the brain, in their white matter. White matter is the brain's super highway, transporting information from one part of the brain to another. Here's how it works: Microglia are activated because there is some kind of antigen or disease, typically something destructive in the brain. In some cases, however, microglia and other immune cells become hyperactive and go into overdrive, thus causing inflammation and possible damage. The brain of a SuperAger, however, has fewer activated microglia. In fact, the levels of microglia were on par with people in their 30s, 40s and 50s. That could mean there is less junk or disease in the brain of a SuperAger so the microglia have no need to be active. Or it could mean microglia are responding efficiently to in clearing out disease or toxins, and because they are more plastic and adaptable, the microglia are able to activate, respond and then calm down. All of this is fascinating — it may be that at the cellular level, the immune system of a SuperAger brain could be stronger or more adaptive, much like the layers of cells we found in the entorhinal cortex. CNN: Whether or not you were born with the right genes to protect your brain sounds like the luck of the draw. What does that mean for the future? Gefen: Genetics are tricky. It's not just whether you have a gene or not, it about how your internal and external environment works together to influence how a gene is 'turned on,' or expressed — some may be more highly expressed, some will have lower expression. This is the epigenetic part of the puzzle. There is a list of candidate genes that we are starting to study very carefully, these are genes that also have a role in aspects of longevity, senescence, cell repair and cognitive reserve to name a few. I'm excited about that, not only for the genetics that are heritable from parents, but also genetics at the cell level, that enable each neuron or immune cell to carry out its respective job within the brain. With the technology that's advancing so rapidly, I'm certain we're going to get to a point where prevention or modification at the genetic level will be part of the playbook. Clearly, there is not a one target resolution for Alzheimer's disease. I know we all want that one easy fix but it's just simply not going to happen. It's going to take many teams and many specialists to come together and create a kind of personalized cocktail for prevention or treatment. I think it's possible, but it's going to take time. Solve the daily Crossword

How a simple cold could bring cancer back
How a simple cold could bring cancer back

National Geographic

time3 hours ago

  • National Geographic

How a simple cold could bring cancer back

In mice, common respiratory infections reactivated dormant cancer cells. Early evidence suggests the same may happen in humans, with big implications for long-term cancer risk. This colored transmission electron micrograph shows SARS-CoV-2 virus particles (gold) inside endosomes of infected olfactory epithelial cells. New research suggests that when respiratory viruses like COVID-19 reach the lungs, they may trigger the reactivation of dormant breast cancer cells. Micrograph by National Institute of Allergy and Infectious Diseases/National Institutes of Health/Science Photo Library Some cancer cells don't die—they go dormant. Long after remission, these 'sleeping' cells can linger silently in the body, tucked alongside stem cells in organs like the lungs, liver, or brain. For years, scientists have puzzled over what, if anything, might wake them. Now, a new study published in Nature suggests that common respiratory illnesses like the flu and COVID-19 may do precisely that. 'They could sit there for years and decades, and we don't really fully understand what awakens them,' says James DeGregori, a researcher at the University of Colorado Anschutz Medical Campus. 'And so what we asked was, could an infection of the lungs awaken such cells? And we found that they could, in a pretty dramatic fashion.' The findings raise big questions for cancer survivors. Could a cold or the coronavirus infection quietly trigger cancer's return? And what role does the immune system play in all of it? Here's what scientists are discovering—and why the answer may lie in how the body fights viruses. How COVID and the flu may trigger cancer's return DeGregori and a robust team of doctors and researchers found that the flu and COVID-19 can awaken dormant cancer cells in the lungs, at least in mice. A separate accompanying survey of tens of thousands of cancer patients from the COVID-19 pandemic showed that the same thing might be occurring in humans. Previous studies have already linked inflammation caused by bacterial infections or cigarette smoke to the reactivation of dormant cancer cells in the lungs. So the team wanted to know if respiratory illnesses might have the same effect. To test this, the researchers gave the flu and SARS-CoV-2 to mice that had been genetically engineered to have breast cancer. In response, dormant cancer cells that had quietly spread to the lungs began to wake up. (A new blood test can tell if cancer has returned months before a scan.) For about a week and a half, the cells stayed awake, but in most cases, fell dormant again once the infection was gone. 'The respiratory virus infection causes outgrowth of these cells over a couple week period, but then they go back to sleep.' DeGregori says. 'But now they've expanded out on the order of 100-fold.' So, even though many of the mice didn't immediately get lung cancer, during the infection period, their risk of once again developing cancer increased drastically as dormant cancer used the time to multiply rapidly. The culprit behind this reawakening was interleukin-6, or IL-6—a protein the immune system uses to coordinate its response to infection. 'It's basically just a protein that normally travels between cells,' DeGregori explains. 'It can normally be a healthy thing within your body to help clear out an infection, for example.' But when IL-6 meets up with dormant cancer cells, that's a problem. 'So when the dormant cells are present, they take advantage of that inflammatory environment, and it's used to help them expand, to help them grow out and awaken and create now, a situation where you have a far greater metastatic burden. The cancer cells are usurping a mechanism that would normally be used to get rid of the virus and move on with your life,' DeGregori says. Could the same thing happen in humans? Scientists don't know if this is the same situation that happens when human cancer survivors get respiratory illnesses, but early evidence suggests it's possible. An analysis of two databases of cancer patients revealed a significant association between cancer-related death and metastasis in the lungs following a coronavirus infection. Data from the UK Biobank showed that cancer-related deaths in patients diagnosed with cancer at least five years before the pandemic were almost double in patients who contracted COVID-19. In another group of specifically breast cancer patients, their risk of lung cancer increased by nearly 50 percent with a positive coronavirus diagnosis. (Why cancer rates are rising in young women—and what to do about it.) One reason dormant cells often escape treatment is that they behave differently from typical tumor cells, says Julio A. Aguirre-Ghiso, the director of the Cancer Dormancy Institute, who was involved in the study. That's why, even in patients in remission, dormant cancer cells can linger. 'The therapies that we have are conceptualized to target dividing cells, and these dormant cancer cells that are sleeping are not dividing,' he says. Still, many patients, even those who contract a respiratory illness, can live the rest of their lives with dormant cancer cells that never reawaken, Aguirre-Ghiso says. 'Some patients may be at this threshold where they were about to reactivate, or they have more advanced disease, and then the inflammation pushes them all the way to symptomatic disease and lethal in some cases.' he says. 'But there may be many patients that undergo many infections but may not fully engage in a total reactivation mechanism that brings them to lethality or symptomatic disease.' Regardless, if what happened in mice is similar to human responses to respiratory illness, contracting the flu or the coronavirus could be a significant risk factor for cancer patients in remission. Inflammation could be giving dormant cells the leeway to multiply, which can severely increase future risk, even if they fall dormant again after just a few weeks. (When should you get screened for breast cancer—and how often?) Even though doctors don't know for sure how many cancer patients develop dormant cells, based on the association between COVID-19 infection and lung-related cancer deaths, taking precautions to avoid respiratory illness may be beneficial for cancer patients to prevent sleeping cells from waking up. 'It's a no-brainer that people, especially people who have had treatment for cancer and have may have long-term effects on their immune system, should continue to be up to date on their current vaccinations,' says Edwin Ostrin, a pulmonologist at MD Anderson Cancer Center in Texas who was not involved in the study.

DOWNLOAD THE APP

Get Started Now: Download the App

Ready to dive into a world of global content with local flavor? Download Daily8 app today from your preferred app store and start exploring.
app-storeplay-store