Pollen Food Syndrome (PFS) – also known as oral allergy syndrome or pollen food allergy syndrome – causes affected individuals to experience an allergic reaction when consuming raw plant foods, and triggers can vary depending on an individual’s pollen sensitisation, which in turn is affected by geographical location. A guideline, published in Clinical & Experimental Allergy, has been developed for the diagnosis and management of PFS.
The guideline was drafted by the British Society of Allergy & Clinical Immunology Standards of Care Committee. The correct diagnosis of PFS ensures the avoidance of a misdiagnosis of a primary peanut or tree nut allergy or confusion with another plant food allergy to non-specific lipid transfer proteins. The characteristic foods involved, and rapid-onset oropharyngeal symptoms, mean PFS can often be diagnosed from the clinical history alone. Management focuses on avoiding known trigger foods, which may appear to be simple, but can be difficult if coupled with a pre-existing food allergy, or for individuals following a vegetarian/vegan diet.
“More studies on the effect of PFS on health-related quality of life are needed to dispel the myth that because it usually manifests with mild symptoms, PFS is easily managed, and does not adversely affect the individual,” the authors wrote. “The number of foods and concern about new food triggers means dietary restrictions are often overly strict, so more research on novel treatments of PFS, including food immunotherapy, needs to be undertaken.”
In the Journal of Applied Physics, researchers developed a method to identify aortic valve stenosis using complex network analysis that is accurate, simple to use, and low-cost.
Aortic valve stenosis occurs when the aortic valve narrows, constricting blood flow from the heart through the artery and to the entire body. In severe cases, it can lead to heart failure. Identifying the condition can be difficult in remote areas because it requires sophisticated technology, and diagnoses at early stages are challenging to obtain.
“Many rural health centres don’t have the necessary technology for analysing diseases like this,” said author M.S. Swapna, of the University of Nova Gorica and the University of Kerala. “For our technique, we just need a stethoscope and a computer.”
The diagnostic tool works based on the sounds produced by the heart. The organ creates a “lub” noise as it closes the mitral and tricuspid valves, pauses as ventricular relaxation occurs and the blood fills in, then makes a second noise, “dub,” as the aortic and pulmonary valves close.
Swapna and her team used heart sound data, collected over 10 minutes, to form a graph. This was then split into sections, with each part representing with a node on the graph. If the sound in that portion of the data was similar to another section, a line was drawn between the two nodes.
In a healthy heart, the graph showed two distinct clusters of points, with many nodes unconnected. In contrast, a heart with aortic stenosis contained many more correlations and edges.
“In the case of aortic stenosis, there is no separation between the ‘lub’ and ‘dub’ sound signals,” explained Swapna.
The researchers used machine learning to examine the graphs and identify those with and without disease, achieving a classification accuracy of 100%. Their method takes the correlation of each point under consideration, making it more accurate than others that only consider the strength of the signal, and it does so in less than 10 minutes. As such, it could be useful for early-stage diagnoses.
So far, the method has only been tested with data, not in a clinical setting. The authors are developing a mobile application that could be accessed worldwide. Their technique could also be used to diagnose other conditions.
“The proposed method can be extended to any type of heart sound signals, lung sound signals, or cough sound signals,” said Swapna.
Researchers have proposed a new therapy for preeclampsia that corrects the defects identified in placental cells, and restores placental and foetal weight, which they report in the journal Redox Biology. The treatment, tested in two rodent models, successfully lowers blood pressure in the mother and resolves the characteristic preeclampsia symptoms of proteinuria and cardiovascular abnormalities.
Preeclampsia is a placental dysfunction that affects approximately 2 to 8% of pregnant women worldwide. It can have potentially complications for mother and child, and longer-term consequences for the mother. Preeclampsia symptoms are primarily arterial hypertension, proteinuria, abnormal coagulation in the placenta, cardiovascular abnormalities in the mother and foetal growth restriction. Treatments for preeclampsia are limited and mostly involve aspirin as a preventative measure, reducing the procoagulant state in the placenta and partly relieving pressure on the vascular network.
Preeclampsia is characterised by a defective placenta caused by trophoblast dysfunction. Trophoblasts are placental cells that help organise and manage the vascular network which provides the essential resources for foetal growth. At the molecular level, preeclampsia is characterised by an uncontrolled increase in oxidative stress, with excessive production of various reactive species including reactive oxygen and nitrogen species. There is a genetic component: the first gene to be identified as being implicated in the genetic forms of preeclampsia was the STOX1 transcription factor, which controls the expression of thousands of genes, especially those involved in the production of nitric oxide (NO).
In a transgenic mouse model, high accumulation of STOX1 in the placenta induced a preeclampsia-like syndrome. In preeclampsia, NO, a powerful vasodilator that promotes blood flow to the placenta, is mobilised to produce potentially toxic molecules (nitrosative stress) and its levels become insufficient in the placental vascular network, affecting trophoblast function and the vascular network and destabilising other reactive species. This creates a vicious circle and causes uncontrollable oxidative/nitrosative stress with multiple complications, also affecting maternal blood vessel cells, with potentially fatal consequences.
NO is produced by a family of enzymes known as nitric oxide synthases (NOSs). Finding a way of restoring NO production in the placenta via NOSs could represent an effective new therapy to treat preeclampsia. A years-long collaboration gave rise to a potential solution. The scientists’ research was based on trophoblasts overexpressing STOX1 and on two rodent models of preeclampsia, one mimicking early-onset forms via placental overexpression of STOX1 and the other mimicking late-onset forms by partial occlusion of the lower abdominal aorta.
The research revealed a cascade of events that ultimately led the scientists to propose a new therapy. Treating trophoblasts with BH4 (tetrahydrobiopterin, a cofactor that stabilises the NOS enzyme producing NO) corrected the defects identified in these cells, restoring production of NO rather than potentially toxic molecules. More importantly, administering BH4 to the two preclinical rodent models restored placental and foetal weight. Finally, in the early-onset STOX1 preclinical model with significant arterial hypertension and proteinuria, the BH4 treatment corrected blood pressure, excess protein in urine, and cardiovascular abnormalities in the mother. The results even suggest that the treatment may be effective in addressing the long-term effects of preeclampsia on mothers (vascular abnormalities in the brain, kidneys, heart and liver).
This research is the first step towards the development of a therapy for preeclampsia. Genetic analyses of placentas treated with BH4 showed that it corrects the expression of several genes disrupted by excess STOX1 differently than the deregulation induced by aspirin in the placenta. The scientists therefore propose that a treatment combining BH4 and aspirin could be the ultimate therapeutic solution for many cases of preeclampsia. This hypothesis needs to be validated in clinical trials.
A new epidemiological study published in The Lancet shows that patients with autoimmune disease have a substantially higher risk (between 1.4 and 3.6 times depending on which autoimmune condition) of developing cardiovascular disease (CVD) than people without an autoimmune disorder. This excess risk is comparable to that of type 2 diabetes, a well-known risk factor for cardiovascular disease.
Although earlier research has suggested associations between various different autoimmune disorders and a higher risk of cardiovascular disease, these studies were often too small and limited to selected autoimmune or selected cardiovascular conditions to draw conclusive evidence on the necessity of CVD prevention among patients with autoimmune disease.
At the annual congress of the European Society of Cardiology, researchers presented the outcome of a thorough epidemiological investigation into possible links between 19 of the most common autoimmune disorders and CVD. The research shows for the first time that cardiovascular risks affect autoimmune disease as a group of disorders, rather than selected disorders individually.
The whole cardiovascular disease spectrum
In the study, the authors show that the group of 19 autoimmune disorders they have studied accounts for about 6% of cardiovascular events. Importantly, excess cardiovascular risk was visible across the whole cardiovascular disease spectrum, beyond classical coronary heart disease, including infection-related heart disorders, heart inflammation, as well as thromboembolic and degenerative heart disorders, suggesting the implications of autoimmunity on cardiovascular health are likely to be much broader than originally thought. Furthermore, the excess risk was not explained by traditional cardiovascular risk factors such as age, sex or smoking. Another noteworthy finding: the excess risk is particularly high among patients with autoimmune disorders under 55 years and suggests that autoimmune disease is particularly important in causing premature cardiovascular disease, with the potential to result in a disproportionate loss of life years and disability.
The study was based on UK electronic health with data from about one-fifth of the current UK population. The researchers assembled a cohort of patients newly diagnosed with any of the nineteen autoimmune disorders. They then looked at the incidence of twelve cardiovascular outcomes – an unprecedented granularity that was made possible by the very large size of the dataset – in the following years, and they compared it to a matched control group. The risk of developing CVD for patients with one or more autoimmune disorders was on average 1.56 times higher than in those without autoimmune disease. The excess risk also rose with the number of different autoimmune disorders in individual patients. Among the disorders with the highest excess risk were systemic sclerosis, Addison’s disease, lupus and type I diabetes.
Need for targeted prevention measures
The results show that action is needed, said Nathalie Conrad, lead author of the study. “We see that the excess risk is comparable to that of type 2 diabetes. But although we have specific measures targeted at diabetes patients to lower their risk of developing cardiovascular disease (in terms of prevention and follow-up), we don’t have any similar measures for patients with autoimmune disorders.” Conrad also noted that the European Society of Cardiology guidelines on the prevention of cardiovascular diseases, do not yet mention autoimmunity as a cardiovascular risk factor, only mentioning specific disorders such as lupus, nor do they list any specific prevention measures for patients with autoimmune disease.
Conrad hopes the study will raise awareness among patients with autoimmune disease and clinicians involved in the care of these patients, which will include many different specialties such as cardiologists, rheumatologists, or general practitioners. ‘We need to develop targeted prevention measures for these patients. And we need to do further research that helps us understand why patients with an autoimmune disorder develop more cardiovascular diseases than others, and how we can prevent this from happening.’
The underlying mechanisms are still poorly understood. Conrad said: “The general hypothesis is that chronic and systemic inflammation, which is a common denominator in autoimmune disorders, can trigger all sorts of cardiovascular disease. Effects of autoimmune disease on connective tissues, small vessels, and cardiomyocytes, and possibly some of the treatments commonly used to treat autoimmunity are also likely to contribute to patients’ cardiovascular risk. This really needs to be investigated thoroughly.”
Developing Type 2 diabetes or hypertension earlier in life is linked to the earlier development of the most common form of glaucoma, according to a study published in Clinical Ophthalmology. These findings could lead to better screening protocols for primary open-angle glaucoma (POAG), the leading cause of irreversible blindness worldwide, which makes up nearly 90% of all cases of glaucoma.
“Currently, we lack the tools to cure glaucoma, but with enough advanced notice, we can preserve patients’ vision. Early detection of glaucoma is the key to better control of intraocular pressure and preventing blindness,” said study leader Karanjit Kooner, MD, PhD, MBA, Associate Professor of Ophthalmology at UTSW.
Tens of millions of people have POAG around the globe. Because this disease has few symptoms in its earliest stages, Dr. Kooner explained, patients are frequently diagnosed in its later stages when vision has already been permanently damaged. Although researchers have identified several risk factors for POAG – including Type 2 diabetes, hypertension, migraines, and obstructive sleep apnoea — how they might influence the onset of POAG is not well understood.
To answer this question, Dr Kooner and his colleagues collected data from the medical records of 389 of his patients with POAG. The researchers found no link between migraines and/or obstructive sleep apnoea and the age of POAG onset. However, the researchers found that the age of Type 2 diabetes and/or hypertension diagnosis was significantly linked with the onset of POAG – the earlier patients presented with either or both of these conditions, the earlier they tended to develop POAG.
Dr Kooner noted that both Type 2 diabetes and hypertension are diseases that affect blood vessels of both the optic nerve and retina, thus potentially causing changes that predispose patients to POAG, another condition with a vascular root. If these connections hold up in future research, he said, Type 2 diabetes and hypertension could be added to the list of factors that can trigger POAG screening — including a family history of POAG, elevated intraocular pressure, and Black race — and lead to earlier diagnosis of POAG, preserving patients’ vision and quality of life.
An outbreak of a pandrug-resistant nosocomial pathogen was interrupted by not using hospital sinks during COVID, according to Basma Mnif, Professor of Microbiology at Habib Bourguiba University Hospital of Sfax, Tunisia. In her presentation at the 14th SAFHE Southern African Healthcare Conference, she said that infection control methods to eradicate the pathogen failed and that other research indicated it was necessary to replace the sinks entirely.
Multidrug-resistant organisms (MDRO) are a growing threat in hospitals, especially to critically ill patients.
Over 2017 to 2021, 90 critically ICU patients in a Tunisian hospital were infected with pandrug-resistant Proteus mirabilis strains. This is the first known long-term outbreak by pandrug-resistant P. mirabilis strains.
P. mirabilis is an uncommon nosocomial pathogen causing opportunistic infections. P. mirabilis survives well in the natural environment and is increasingly implicated in nosocomial outbreaks worldwide.
The all-cause mortality rate in the infected was 47%, with patients ranging in age from 16 to 78 years. The average length of stay before infection was 23.56 days.
An outbreak was recognised in April 2017, and IDC measures were taken to contain it. The outbreak was suppressed but reoccurred in July and December. Analysis revealed overlapping ICU stays of infected patients, suggesting horizontal, intra-ICU transmission. Lab analysis of phenotypes revealed two clones, A and B, both with drug resistance genes, to which a third clone was added in 2018. This Clone C proved to have resistance to all known antibiotics.
During the COVID pandemic in 2020, hospital sinks were not used and enhanced infection prevention interventions were deployed. This period coincided with a complete absence of P. mirabilis infections. The outbreak resumed in 2021, with the same three clones causing infections in patients.
“The outbreak intermission during COVID could be related to the enhanced protection measures implemented during this period,” Prof Mnif noted, “but we think that the sinks are in fact the reservoirs of these MDRO, and must in fact be removed and replaced, and the chemical disinfection that we had performed was not sufficient to control the outbreak.”
The outbreak highlighted the need for proper infection control protocols. Hospital wastewater is a major source of outbreaks, Prof Mnif pointed out. A study found that “over the past 20 years, there have been 32 reports of carbapenem-resistant organisms in the hospital water environment.”
She said when it came to replacing the sinks, hospitals should “respect FGI guidelines, especially in having sufficient depths of the sink, deep enough to prevent splashing.” Having sufficient pressure and splash reduction measures such as splash guards are also important, Prof Mnif added.
Although there are CDC guidelines to help prevent colonisation, there is no clear strategy for eradication for when a sink is colonised. There is likely genetic interchange between organisms in biofilms, something which needs to be investigated further, as well as means of eradication.
About 50% of all mothers of children with autism spectrum disorder (ASD) had raised levels of depressive symptoms over 18 months, while rates were much lower (6% to 13.6%) for mothers with neurotypical children in the same period, according to a new study in Family Process.
Additionally, thought past studies suggest that having a parent with depression increases the child’s risk of mental health and behaviour problems, this study found something different.
“We found mothers’ higher symptoms of depression did NOT predict increases in children’s behaviour problems over time, including among families with a child with autism who experience a lot of stress,” said first author and UCSF Assistant Professor Danielle Roubinov. “That was surprising and good news.”
“Being the parent of a child with special needs is inherently challenging every day,” noted senior author UCSF Professor Elissa Epel. “It is a prototypical example of chronic stress, which is why we have been focusing on caregiving moms in our studies that examine effects of stress on health.”
“We already know from this sample that mothers with more depression tend to have signs of faster biological aging, such as lower levels of the anti-aging hormone klotho and older immune cells, on average,” added Prof Epel. “Here, we wanted to understand the impact of their depression on their child, and vice versa.”
A One-Way Street
Child behaviour problems predicted higher levels of maternal depression down the road, regardless of ASD status. The inverse effect was not seen, ie prior maternal depression didn’t predict later child behaviour problems.
Asst Prof Roubinov said that mothers of children with ASD need not feel guilty over their depressions impact on their children’s behaviours. “We hope these findings will reassure mothers that it’s both common to struggle with some depression in this high-stress situation of chronic caregiving, and that their depression likely isn’t making their child’s behavioural issues worse.”
Self-blame and guilt among parents of ASD children is common and predicts worsening depression and lower life satisfaction over time, the team’s past research shows.
In the current study, the researchers repeatedly measured maternal depression and children’s behaviour problems in 86 mother-child dyads across 18 months. Half of the mothers had children with ASD and half had neurotypical children. The children were aged 2–17 years old, with 75% being primary school age or younger.
Maternal depression was measured using the Inventory of Depressive Symptoms, a self-report scale completed by mothers. Child behaviour was measured through maternal report on the Child’s Challenging Behavior Scale, which focuses on externalising behaviours such as tantrums, aggression and defiance.
Few studies on maternal depression, child behaviour in ASD context
Bidirectional associations between maternal depression and child behaviour problems have been reported in prior research but few studies have examined these relationships in families with autism.
Families with autism tend to experience more marital conflict, lower relationship satisfaction, and many other challenges, said Ass Prof Roubinov, noting that a “stressful family environment may spill over onto family members” and changing their interactions. “We wanted to see whether the link between maternal and child mental health was different in the context of a high-stress family system, such as when a child has autism.”
Although the study acknowledged that families with a child with ASD experience high levels of stress, the authors were cautious to note that stress is not their only defining characteristic.
“Many mothers of children with autism also report high levels of emotional closeness and positive interactions with their children,” Asst Prof Roubinov said. “These are important experiences that supportive programs can build upon.”
The researchers offered mindfulness classes after the study to the participants to help manage parenting stress, and this improved their mental health.
It is important to experience and notice positive emotions and joy, despite having a more challenging life situation, said Prof Epel.
“Given the effects of chronic stress on health and mood, caregiving parents need extraordinary emotional support in addition to the special services for their child,” she said. “It’s as vital to provide support for parents’ mental health as it is for children’s mental health.”
Physicians should be on the lookout for parental distress and ready to offer resources for parents, especially for parents of special needs children, she said. The researchers said future studies should also look at associations between maternal depression and children’s internalising symptoms (eg, withdrawal, anxiety, emotional reactivity).
Johannesburg, 30 August 22: Kagan Keklik has taken the reigns as General Manager South Africa & Country Lead of multinational pharmaceutical and healthcare company, Sanofi, in South Africa, at a time when revolutionary technology and medical interventions are set to change lives across Africa.
With all the business acumen needed, a passion for science and expertise across several therapeutic areas and products, Keklik is already inspiring excellence in the 500 plus workforce that he leads in South Africa.
Keklik has over 20 years of experience in the pharmaceutical sector where the positions he has held have spanned from managing products to leading teams in the Middle East, Eurasia, and South Asia. He has been with Sanofi for nearly 13 years, making him well-poised to take the company to new heights.
“Sanofi is dedicated to finding answers for patients by developing breakthrough medicines and vaccines. Our purpose is to chase the miracles of science to improve the lives of patients, partners, communities and our own people. We provide potentially life-changing treatments and life-saving vaccines to millions of people as well as affordable access to our medicines in some of the world’s poorest countries,” says Keklik.
Keklik is excited about the potential of the South African market. “South Africa is considered the gateway to the African continent and is an important market for the Sanofi Group. The people are driven and dynamic and there are great opportunities for growth. We are passionate about knowledge and technology transfer to ensure the local manufacturing of medicines. We sincerely look forward to helping to make a difference and I look forward to working with my team to drive change in the region,” says Keklik.
Keklik is a great proponent for forging important alliances, such as the strategic partnership with South African manufacturer, Biovac, for the local manufacture of vaccines through the transfer of manufacturing excellence, skills, and knowledge.
Keklik’s vision takes this even further: “As a world leader in the development and delivery of vaccines, we fully support continued investment in localised manufacturing and the sustainability of local vaccine supply. Through long-term partnerships such as the one we have with Biovac, we can ensure that South Africa can be a manufacturing hub that will improve the distribution of vaccines into neighboring countries.”
Supported by a strong team, Keklik is enthusiastic about unlocking not only the potential of the region but also of Sanofi itself. He sees himself as a transformative leader and believes in inspiring and empowering individuals and teams to achieve the company’s goals. At the same time, he is prepared to push limits to make a difference in both the prescription and over-the-counter medication markets.
“We are focused on growth and believe this can be achieved if we lead with innovation and accelerate efficiencies. I’ll be focusing on these levers over the next few years to ensure Sanofi maintains its position as a leading healthcare company, not only in South Africa, but throughout the region,” says Keklik.
A new study has found that teenagers have a hard time discerning between fake and true health messages. Only 48% of the participants trusted accurate health messages (without editorial elements) more than fake ones. Meanwhile, 41% considered fake and true neutral messages equally trustworthy and 11% considered true neutral health messages less trustworthy than fake health messages. The results highlight a need for better training of teenagers to navigate a world where fake health news is so widespread.
Health mis- and disinformation are a serious public health concern, with an increased spread of fake health news on social media platforms in the last few years. Previous research has shown that online health messages are mostly incomplete and inaccurate and have potentially harmful health information. Fake health news can lead to poor health choices, risk-taking behaviour, and loss of trust in health authorities.
“There has been an explosion of misinformation in the area of health during the COVID pandemic,” said principal investigator Dr Radomír Masaryk, of Comenius University.
While most research on message credibility has focused on adults, Dr Masaryk and his colleagues investigated whether teenagers are similarly equipped.
“As adolescents are frequent users of the internet, we usually expect that they already know how to approach and appraise online information, but the opposite seems to be true” Dr Masaryk said.
The researchers found that 41% of teenagers couldn’t tell the difference between true and fake online medical content. Additionally, poor editing of health messages was not perceived as a sign of low trustworthiness. These latest findings were published in Frontiers in Psychology.
Teenagers and the media
As so-called ‘digital natives’, modern teenagers are the world’s most well-connected group, with 71% of the world’s youth using the internet.
Studies have shown that teens increase their risky behaviour in response to positive portrayals of risky behaviour in the media, such as smoking and drinking. On the other hand, online health information that supports information provided by professionals can lead to healthy lifestyle changes, self-care, and treatment compliance.
Teenagers look at the structural features of a website, such as language and appearance, to evaluate online information. For example, authoritative organisations, trusted brands, or websites with business-like language tend to be more trusted.
Previous research on message trustworthiness with adolescents identified five editorial elements that deduced perceived message credibility: superlatives, clickbait, grammar mistakes, authority appeal, and bold typeface. Based on this prior study, the researchers developed a method to evaluate the effects of manipulation with content and format of health online messages on their trustworthiness in an adolescent sample.
They presented 300 secondary school students (aged between 16 and 19 years old) with seven short messages about the health promoting effects of different fruits and vegetables. The messages had different levels: fake message, true neutral message, and true message with editorial elements (superlatives, clickbait, grammar mistakes, authority appeal, and bold typeface). Participants were then asked to rate the message’s trustworthiness.
The participants were able to discern between overtly fake health messages and health messages whether true or slightly changed with editing elements; 48% of participants trusted the true neutral health messages more than the fake ones. However, 41% of participants considered fake and true neutral messages equally trustworthy and 11% considered true neutral health messages less trustworthy than fake health messages.
Clickbait less likely to work
“Putting trust in messages requires identification of fake versus true content,” said Dr Masaryk.
In the case of health messages that seem plausible and reasonable, teenagers could not tell the difference between true neutral health messages and health messages with editorial elements. Teenagers did not seem to decide on the trustworthiness of a message based on editing cues.
“The only version of a health message that was significantly less trusted compared to a true health message was a message with a clickbait headline,” continued Dr Masaryk.
The results highlight a need for better instruction of teenagers to spot editing cues that give away the quality of a piece of information. The authors suggest focusing on health literacy and media literacy training, and skills such as analytical thinking and scientific reasoning.
“Analytical thinking and scientific reasoning are skills that help distinguish false from true health messages,” Dr Masaryk concluded.
A new universal flu vaccine protects against diverse variants of both influenza A and B viruses in mice, according to a new study published in the journal PLOS Pathogens.
The researchers designed a single, universal influenza vaccine candidate with key cross-protective, less variable parts of the influenza A and B viruses: multi-neuraminidase protein subtypes known to be major antiviral drug targets and the universally conserved M2 ectodomain protein.
The researchers, from the Institute for Biomedical Sciences at Georgia State University, report that mice vaccinated with an immune stimulating virus-like particle displaying multiple neuraminidase subtypes and conserved M2 portions of antigens were protected against influenza A seasonal variants and pandemic potential viruses (H1N1, H5N1, H3N2, H9N2 and H7N9) and influenza B (Yamagata and Victoria lineage) viruses containing substantial antigenic variations.
Viral variants emerge when flu pathogens change their major surface haemagglutinin protein that binds to host receptor molecules. Continuous mutational changes in the flu haemagglutinin proteins result in immune escape and sever disease.
Current influenza vaccines are based on strain-specific immunity to haemagglutinin, a highly variable target of immune protection. The effectiveness of the seasonal vaccine is unpredictable and could be below 20% because of continuous changes in haemagglutinin proteins. Influenza therefore remains a significant risk to human health worldwide.
“We developed a single, universal vaccine entity that induced immunity to conserved M2 ectodomain and multi subtype neuraminidase proteins and was found to be effective in conferring broad cross protection against antigenically diverse influenza A and B viruses in young and aged mice,” said Professor Sang-Moo Kang, senior author of the study. “This study provides impactful insight into developing a universal influenza vaccine inducing broad immunity against both flu A and B variants in young and aged populations.”
This study supports a novel strategy for creating a universal vaccine against influenza A and B viruses. A single construct displaying multiple cross protective proteins has the capacity to induce immunity to M2 and multi-subtype neuraminidase proteins of influenza A and B viruses, as well as offer broad cross protection against sickness and mortality under lethal flu virus challenges in mice, according to the study.
Vaccinating mice with this universal vaccine candidate induced broad neuraminidase inhibition, M2 ectodomain specific antibodies and T cell immune responses. Comparable cross protection was induced in aged mice.
The study warrants further testing of this unique, universal va ccine candidate in ferrets, which have similar respiratory tracts to humans.