Category: 8. Health

  • Study finds past H1N1 exposure shields animals from deadly H5N1

    Study finds past H1N1 exposure shields animals from deadly H5N1

    Could your previous flu infection protect you from bird flu? Scientists find that immunity to 2009 H1N1 slashes the risk of severe H5N1 illness, even after close contact exposure.

    Study: Preexisting immunity to the 2009 pandemic H1N1 virus reduces susceptibility to H5N1 infection and disease in ferrets. Image Credit: digicomphoto / Shutterstock

    In a recent study published in the journal Science Translational Medicine, a group of researchers tested whether infection-elicited immunity to influenza A virus (IAV) subtypes hemagglutinin 1 neuraminidase 1 (H1N1) or hemagglutinin 3 neuraminidase 2 (H3N2), and the order of exposure, lessens ferret susceptibility to and disease from clade 2.3.4.4b hemagglutinin 5 neuraminidase 1 (H5N1), including after direct contact with a dairy cow isolate.

    Background

    By age five, most people have already encountered IAVs, leaving an immune imprint that shapes their responses to later exposures. Since 2020, clade 2.3.4.4b H5N1 has swept through birds and spilled over into mammals, including an unprecedented outbreak in United States dairy cows, affecting 989 herds in 17 states within a year, and 41 laboratory-confirmed infections in farm workers by June 2025.

    Most human cases have been mild, prompting a key question: can preexisting immunity to seasonal strains blunt H5N1 disease? Understanding the answer matters for workers, clinicians, and pandemic planners.

    Further research is needed to clarify how imprinting and cross-reactive antibodies sustain protection over time.

    About the study

    The researchers used a well-established ferret model because ferrets recapitulate key features of human influenza pathogenesis and transmission. They first induced preexisting immunity by infecting animals with either B/Brisbane/60/2008 influenza B virus (IBV), A/Perth/16/2009 seasonal H3N2 IAV, or A/California/07/2009 pandemic H1N1 IAV.

    In a separate experiment, ferrets received two sequential infections, 90 days apart, to test the effect of immune imprinting. Ninety days after the last seasonal infection, animals were either intranasally challenged with 10² tissue culture infectious dose 50% (TCID₅₀) of an A/mink/Spain/2022 highly pathogenic H5N1 virus or pair housed with a naïve cage mate that had been inoculated with 10¹⁰ TCID₅₀ of the A/dairy cattle/Texas/2024 H5N1 virus to model direct contact exposure.

    Nasal washes were collected every other day and titrated on Madin-Darby canine kidney cells; body weight, clinical scores, and survival were monitored. Serum immunoglobulin G (IgG) binding, neutralizing, and neuraminidase-inhibiting antibodies were quantified by enzyme-linked immunosorbent assay (ELISA), microneutralization, and enzyme-linked lectin assay (ELLA), respectively.

    Predetermined humane endpoints triggered euthanasia. Four ferrets were used per group; the experiments were not randomized or blinded. Statistical comparisons utilized analysis of variance or nonparametric tests as appropriate, and survival was analyzed using the Mantel-Cox test in Prism.

    Study results

    Preexisting immunity mattered, as compared with immunologically naïve or IBV-preimmune ferrets, animals previously infected with the 2009 pandemic H1N1 IAV shed markedly less virus after challenge with the A/mink/Spain/2022 H5N1 strain, maintained body weight, showed no clinical illness, and all survived.

    Seasonal H3N2 IAV immunity offered partial protection: viral titers were intermediate, some animals lost notable weight, but all survived. Only H1N1 pre-immune ferrets mounted robust IgG responses to H1N1, and these antibodies neutralized H1N1 and inhibited the neuraminidase activity of H5N1; they also showed low, non-neutralizing cross-reactivity to H5 hemagglutinin.

    When the team layered infections to probe immune imprinting, the pattern held. Regardless of whether H1N1 came first or second, any group that included the 2009 H1N1 virus shed minimal or no H5N1 and did not develop disease. In contrast, ferrets that experienced two rounds of IBV infection, or the sequence H3N2 followed by IBV, shed high titers, lost at least 15 percent of body weight, and up to half reached humane endpoints. Thus, order mattered less than simply having H1N1 in the infection history.

    Finally, in a direct contact experiment modeling the high-dose exposures seen during dairy milking, naïve donor ferrets infected with a dairy cow H5N1 strain transmitted the virus to 100% of naïve cage mates, causing universally lethal disease. Prior H3N2 immunity did not prevent infection; every contact shed virus, and only half survived. Prior H1N1 immunity substantially raised the bar: only half of contacts had low, transient shedding on a single day, none developed clinical disease, and all survived.

    Together, these data show that infection-elicited immunity to the 2009 H1N1 virus reduces susceptibility to, replication of, and disease caused by contemporary clade 2.3.4.4b H5N1 viruses in ferrets, whereas H3N2 immunity alone confers incomplete and variable protection.

    Mechanistically, H1N1 exposure generated high titers of cross-reactive N1 neuraminidase–binding antibodies that inhibited the dairy cow and mink H5N1 neuraminidases, plus low titers of group 1 hemagglutinin stem-directed antibodies that bound but did not neutralize H5. Nucleoprotein antibodies, a proxy for responses to conserved internal antigens, were comparable between the H1N1 and H3N2 groups, suggesting that the superior protection in H1N1-primed animals likely reflected hemagglutinin or neuraminidase cross-reactivity rather than broader immunity to internal proteins. These immunologic patterns mirror recent human serology against clade 2.3.4.4b H5N1, reported in independent studies.

    Conclusions

    To summarize, preexisting, infection-elicited immunity to the 2009 pandemic H1N1 IAV acted as a strong barrier against clade 2.3.4.4b H5N1 infection, replication, and disease in ferrets, even after high-dose direct contact exposure. Immunity to seasonal H3N2 IAV attenuated but did not reliably prevent infection or illness. The order of earlier infections (immune imprinting) did not erode the protection conferred by H1N1 exposure.

    While the authors acknowledge certain limitations, such as the fixed 90-day infection intervals not reflecting human timelines and an inability to assess cellular immunity, these findings help explain why most recent human H5N1 infections linked to dairy cows have been mild and argue that neuraminidase-focused cross-reactivity should be considered in preparedness strategies, vaccine design, risk assessment, and clinical surveillance policies.

    Journal reference:

    • Restori, K. H., Weaver, V., Patel, D. R., Merrbach, G. A., Septer, K. M., Field, C. J., Bernabe, M. J., Kronthal, E. M., Minns, A., Lindner, S. E., Lakdawala, S. S., Le Sage, V., & Sutton, T. C. (2025). Preexisting immunity to the 2009 pandemic H1N1 virus reduces susceptibility to H5N1 infection and disease in ferrets. Sci. Transl. Med. 17 (808). DOI: 10.1126/scitranslmed.adw4856, https://www.science.org/doi/10.1126/scitranslmed.adw4856

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  • Every Step Counts, But Do You Really Need 10,000?

    Every Step Counts, But Do You Really Need 10,000?

    Good news for the sole: Contrary to popular wisdom, people can get the same health benefits from walking 7000 steps a day as they do from walking 10,000 paces, according to a comprehensive review and meta-analysis published in The Lancet Public Health.

    “For all outcomes, health benefits continued to accrue until around 7000 steps,” said Katherine Owen, PhD, biostatistician at the University of Sydney, Sydney, Australia, who led the review. “After 7000 steps, benefits either plateaued or there were very small additional benefits.”

    Owen and her colleagues reviewed 57 studies and conducted a meta-analysis on 31 of them, examining the relationship between health and physical activity based on daily steps. 

    The researchers looked at nine different health outcomes: all-cause mortality, the incidence of and deaths from cardiovascular disease, dementia, cancer incidence and mortality, the incidence of type 2 diabetes, depressive symptoms, and falls. Every outcome showed improvement as the amount of daily activity increases, but for most people the benefits tapered off at around 5000-7000 steps per day.

    Compared with taking just 2000 steps per day, walking approximately 7000 steps per day reduced all-cause mortality by 47% and decreased the incidence of cardiovascular disease by 25%, of cancer by 6%, of type 2 diabetes by 14%, of dementia by 38%, of depression by 22%, and of falls by 28%.

    The study also highlighted that even modest step counts of around 4000 per day were beneficial compared with lower activity of just 2000 steps. “Every step counts,” Owen said. “All physical activity is beneficial, but increasing daily steps to around 7000 steps is optimal to improve all health outcomes.”

    The conventional wisdom that 10,000 steps per day was the optimal amount has no real basis in fact, said I-Min Lee, MD, epidemiologist at Harvard Medical School, Boston, who was the first to show that the health benefits of daily exercise leveled off after 7500 steps.

    “There are quite a bit of data now showing that fewer than 10,000 steps per day brings health benefits,” she said.

    Lee said that most studies to date have focused on all-cause mortality and cardiovascular health. The new study expands the evidence to other health outcomes, although the data for some conditions, such as diabetes, are relatively sparse.

    Current guidelines for physical activity, such as those from the US Department of Health and Human Services, recommend 150 minutes per week of moderate-to-vigorous physical activity. However, due to lack of evidence at the time of publication, these guidelines do not include daily step targets.

    As step tracking technologies have become more common, and data on step-based activity have improved, Lee wants future guidelines to incorporate step targets. 

    “I don’t believe they should replace time targets, since not everybody wants to track their steps,” she said. “But they should be included.”

    Owen and Lee declared having no competing interests. 

    Brian Owens is a freelance journalist based in New Brunswick, Canada.

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  • Heart attack risk? This heart scan can tell you more than a cholesterol test; but you probably haven’t heard of it |

    Heart attack risk? This heart scan can tell you more than a cholesterol test; but you probably haven’t heard of it |

    When it comes to heart health, most people rely on the usual suspects , cholesterol numbers, blood pressure readings, maybe a stress test if things look off. But what if there’s a scan that could tell you your real heart attack risk long before symptoms show up? There is a quick, painless CT scan that looks for calcium buildup in your arteries (a major red flag for heart disease). It’s way more accurate at predicting future heart attacks than just looking at cholesterol alone. The kicker? Most people have never even heard of it. Whether you’re in your 40s and feeling fine or just curious about your long-term heart health, this scan might be the wake-up call you didn’t know you needed. Here’s what it is, how it works, and why it might just save your life.

    Heart Attack Warning Signs That Women May Confuse With Menopause Symptoms

    What is the Coronary Artery Calcium Test?

    The CAC test is a simple, non-invasive CT scan (a type of X-ray) that looks specifically for calcium deposits in the coronary arteries the blood vessels that supply your heart muscle with oxygen-rich blood. These calcium spots are essentially hardened bits of plaque resulting from the buildup of fats, cholesterol, and other substances in your arteries (a process called atherosclerosis). The presence and amount of calcium in your arteries signal the extent of coronary artery disease (CAD), which is the main cause of heart attacks.

    Poll

    What do you think is the most important factor in assessing heart health?

    Think of it this way: Your cholesterol test gives you clues, but it’s kind of like guessing what’s inside a wrapped gift. The CAC test is like unwrapping it to see if there’s actually something you should worry about inside your arteries.“A coronary calcium scan isn’t for everyone, but it’s the finest way for those who are uncertain about their heart disease risk to make better decisions about treatment and medications,” says Michael Blaha, M.D., M.P.H., director of clinical research at the Ciccarone Center for the Prevention of Heart Disease at Johns Hopkins.

    Why is this test a game changer?

    Many people rely on cholesterol levels (LDL, HDL, total cholesterol) and traditional risk calculators to estimate their heart attack risk. But these don’t always tell the whole story. The CAC test:Detects plaque buildup early often before symptoms appear.Helps predict your actual heart attack risk better than cholesterol numbers alone.Guides decisions on preventative treatment, especially whether or not you should start or continue statin medications (which lower cholesterol).Gives you a clear calcium score, a numeric value that correlates with your risk level — from zero (no calcium, low risk) to over 1,000 (very high risk).

    Who should consider getting a CAC Test?

    The test isn’t for everyone. Various health guidelines suggest considering it if you:

    • Are between 40-80 years old.
    • Have an intermediate risk of heart disease based on risk factors like age, blood pressure, smoking, diabetes, or family history.
    • Are unsure whether to start statin therapy or want to weigh benefits versus possible side effects.
    • Have a family history of early heart disease but otherwise seem low-risk.

    Your healthcare provider can help you decide if this test makes sense for you. It’s not typically recommended if you have low risk or already have known heart disease, because other tests may be better suited then.

    What does the research say?

    Studies in the US consistently highlight how the CAC test improves risk prediction. For example, the MESA study (Multi-Ethnic Study of Atherosclerosis) showed that CAC scoring can better identify those at risk of heart attack who might have been missed by traditional risk calculators. The test also helps avoid unnecessary statin use in low-risk people scoring zero, reducing overtreatment.If you’re worried about your heart health but don’t have clear symptoms, and your cholesterol or risk scores seem “in the middle,” a CAC test can be a powerful eye-opener.Here’s something wild—Johns Hopkins researchers studied nearly 7,000 people to see how well we’re actually predicting heart risk. They looked at two methods: one used the usual risk factors like cholesterol levels, smoking habits, blood pressure, and diabetes. The other added in results from a Coronary Artery Calcium (CAC) scan—that quick CT scan that checks for calcium buildup in your heart arteries. Turns out, adding the CAC scan seriously sharpened the accuracy. According to a 2013 study published in the European Heart Journal, some people who were told they were at very low risk based on traditional factors actually had high calcium scores—15% of them, in fact. That’s a big deal. Even more surprising? Around 35% of people flagged as high risk had zero calcium buildup, meaning they might not be in as much danger as once thought. Bottom line: the CAC test can change how we see and treat heart risk—big time. It’s quick, painless, and offers a peek inside your arteries that cholesterol tests simply can’t. The real value? Knowing your risk can save your life by prompting early treatment or lifestyle changes — or putting your mind at ease if your arteries are clean.Disclaimer: This information is for educational purposes only and is not medical advice. Always consult your healthcare provider before considering a Coronary Artery Calcium test or making heart health decisions. Individual risks vary, and only a qualified professional can provide guidance tailored to your specific needs.


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  • Impact of weight-loss drugs on dating habits revealed in new survey

    Impact of weight-loss drugs on dating habits revealed in new survey

    Shifts in dating behaviour have been reported by people taking weight-loss medication, including more confidence when it comes to asking people out and ex-partners getting back in touch.

    The Kinsey Institute at Indiana University explored how GLP-1 weight-loss drugs are changing how people date.

    A survey of 2,000 single adults in the US found that 8% used a weight-loss drug, and of those, more than half said the medication had at least one effect on their love life.

    The findings showed that:

    • 17% bought new clothing to show off their body
    • 16% said they heard from former partners looking to reconnect
    • 14% reported getting more matches on dating apps
    • 13% felt more confident posting online photos of themselves
    • 12% reported feeling more confident asking other people out
    • 12% said they had more dates

    With reports that around 12% of the US population have used weight-loss drugs such as Wegovy and Ozempic, researchers were keen to examine the social and psychological effects these medications may be having.

    One of the study’s authors, Dr Amanda Gesselman, said: “GLP-1 use is rising among single adults and it’s starting to influence more than just how people look and feel about themselves.

    “These shifts have the potential to reshape how people build intimacy in today’s dating landscape. For example, as users report reduced appetites and lower interest in alcohol, the classic dinner-and-drinks date may give way to new methods of connecting.”

    The research highlighted how just over half of those using weight-loss drugs reported an impact on their sex lives, both positively and negatively, including:

    • 18% said their sexual desire increased; 16% said it decreased
    • 16% reported feeling more comfortable with how they look naked; 14% said they feel less comfortable
    • 16% said their sexual function improved; 12% said it got worse

    Dr Justin Lehmiller, another of the study’s authors, said: “I think there’s a very nuanced story to tell here. How these drugs impact your sex life will depend on a variety of factors, including drug dosage and drug type, speed of weight loss, starting and ending weight, and how much you changed your health and fitness habits at the same time.”

    The survey revealed significant differences between men and women, with men reporting both more positive and more negative side effects of the drugs.

    Men were twice as likely as women to report an increase in libido, were happier with their bodies and said they had improved sexual function, but men were also twice as likely to experience low libido since taking the medication, along with feeling worse about their bodies and reporting a drop in sexual function.

    The research also found that weight-loss medication is boosting men’s dating lives more than women’s. Men were more likely to feel more confident in how they look, and more likely to report more online matches and dates.

    However, more than half of men felt they would be judged for taking the weight-loss drugs compared to just 35% of women.


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  • Africa: Long-Covid, Viruses and ‘Zombie’ Cells – New Research Looks for Links to Chronic Fatigue and Brain Fog

    Africa: Long-Covid, Viruses and ‘Zombie’ Cells – New Research Looks for Links to Chronic Fatigue and Brain Fog

    Millions of people who recover from infections like COVID-19, influenza and glandular fever are affected by long-lasting symptoms. These include chronic fatigue, brain fog, exercise intolerance, dizziness, muscle or joint pain and gut problems. And many of these symptoms worsen after exercise, a phenomenon known as post-exertional malaise.

    Medically the symptoms are known as myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS). The World Health Organization classifies this as a post viral fatigue syndrome, and it is recognised by both the WHO and the United States Centers for Disease Control and Prevention as a brain disorder.

    Experiencing illness long after contracting an infection is not new, as patients have reported these symptoms for decades. But COVID-19 has amplified the problem worldwide. Nearly half of people with ongoing post-COVID symptoms – a condition known as long-COVID – now meet the criteria for ME/CFS. Since the start of the pandemic in 2020, it is estimated that more than 400 million people have developed long-COVID.

    To date, no widely accepted and testable mechanism has fully explained the biological processes underlying long-COVID and ME/CFS. Our work offers a new perspective that may help close this gap.

    Our research group studies blood and the cardiovascular system in inflammatory diseases, as well as post-viral conditions. We focus on coagulation, inflammation and endothelial cells. Endothelial cells make up the inner layer of blood vessels and serve many important functions, like regulating blood clotting, blood vessel dilation and constriction, and inflammation.

    Our latest review aims to explain how ME/CFS and long-COVID start and progress, and how symptoms show up in the body and its systems. By pinpointing and explaining the underlying disease mechanisms, we can pave the way for better clinical tools to diagnose and treat people living with ME/CFS and long-COVID.

    What is endothelial senescence?

    In our review, our international team proposes that certain viruses drive endothelial cells into a half-alive, “zombie-like” state called cellular senescence. Senescent endothelial cells stop dividing, but continue to release molecules that awaken and confuse the immune system. This prompts the blood to form clots and, at the same time, prevent clot breakdown, which could lead to the constriction of blood vessels and limited blood flow.

    By placing “zombie” blood-vessel cells at the centre of these post-viral diseases, our hypothesis weaves together microclots, oxygen debt (the extra oxygen your body needs after strenuous exercise to restore balance), brain-fog, dizziness, gut leakiness (a digestive condition where the intestinal lining allows toxins into the bloodstream) and immune dysfunction into a single, testable narrative.

    From acute viral infection to ‘zombie’ vessels

    Viruses like SARS-CoV-2, Epstein-Barr virus, HHV-6, influenza A, and enteroviruses (a group of viruses that cause a number of infectious illnesses which are usually mild) can all infect endothelial cells. They enable a direct attack on the cells that line the inside of blood vessels. Some of these viruses have been shown to trigger endothelial senescence.

    Multiple studies show that SARS-CoV-2 (the virus which causes COVID-19 disease) has the ability to induce senescence in a variety of cell types, including endothelial cells. Viral proteins from SARS-CoV-2, for example, sabotage DNA-repair pathways and push the host cell towards a senescent state, while senescent cells in turn become even more susceptible to viral entry. This reciprocity helps explain why different pathogens can result in the same chronic illness. Influenza A, too, has shown the ability to drive endothelial cells into a senescent, zombie-like state.

    What we think is happening

    We propose that when blood-vessel cells turn into “zombies”, they pump out substances that make blood thicker and prone to forming tiny clots. These clots slow down circulation, so less oxygen reaches muscles and organs. This is one reason people feel drained.

    During exercise, the problem worsens. Instead of the vessels relaxing to allow adequate bloodflow, they tighten further. This means that muscles are starved of oxygen and patients experience a crash the day after exercise. In the brain, the same faulty cells let blood flow drop and leak, bringing on brain fog and dizziness.

    In the gut, they weaken the lining, allowing bits of bacteria to slip into the bloodstream and trigger more inflammation. Because blood vessels reach every corner of the body, even scattered patches of these “zombie” cells found in the blood vessels can create the mix of symptoms seen in long-COVID and ME/CFS.

    Immune exhaustion locks in the damage

    Some parts of the immune system kill senescent cells. They are natural-killer cells, macrophages and complement proteins, which are immune molecules capable of tagging and killing pathogens. But long-COVID and ME/CFS frequently have impaired natural-killer cell function, sluggish macrophages and complement dysfunction.

    Senescent endothelial cells may also send out a chemical signal to repel immune attack. So the “zombie cells” actively evade the immune system. This creates a self-sustaining loop of vascular and immune dysfunction, where senescent endothelial cells persist.

    In a healthy person with an optimally functioning immune system, these senescent endothelial cells will normally be cleared. But there is significant immune dysfunction in ME/CFS and long-COVID, and this may enable the “zombie cells” to survive and the disease to progress.