Tag: covid

Categories : COVIDTags :

Time is Running out to Develop a Paxlovid Alternative

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Photo by CDC on Unsplash

Researchers from Rutgers University in the U.S. believe that they are ahead in a race to find an oral COVID-19 treatment to supplement or replace the antiviral Paxlovid. Their report, published in Science, shows that an alternative medication, a viral papain-like protease inhibitor, inhibits disease progression in animals while also possessing an important advantage over Paxlovid – fewer prescription drug contraindications.

“COVID-19 remains the nation’s third leading cause of death, so there’s already a massive need for additional treatment options,” said Jun Wang, senior author of the study and associate professor at Rutgers. “That need will grow more urgent when, inevitably, COVID-19 mutates in ways that prevent Paxlovid from working.”

The Rutgers team hoped to make a drug that interfered with viral papain-like protease (PLpro), a protein that performs important functions in all known strains of COVID-19.

Creating such a drug required detailed information about PLpro’s structure, which Wang’s team got from the Arnold Lab at Rutgers’ Center for Advanced Biotechnology and Medicine (CABM).

Precise knowledge of PLpro’s structure enabled Wang’s team to design and synthesise 85 drug candidates that would bond to – and interfere with – this vital protein.

“The PLpro crystal structures showed an unexpected arrangement of how the drug candidate molecules bind to its protein target, leading to innovative design ideas implemented by professor Wang’s medicinal chemistry team,” said Eddy Arnold, who is a professor at CABM.

Laboratory testing established that the most effective of those drug candidates, a compound dubbed Jun12682, inhibited several strains of the SARS-CoV-2 virus, including strains that resist treatment with Paxlovid.

Oral treatment with Jun12682 on SARS-CoV-2-infected mice was shown to reduce viral lung loads and lesions while improving survival rates.

“Our treatment was about as effective in mice as Paxlovid was in its initial animal tests,” said Wang, who added the experimental drug appears to have at least one major advantage over the older drug.

“Paxlovid interferes with many prescription medications, and most people who face the highest risk of severe COVID-19 take other prescription medicines, so it’s a real problem,” Wang said.

“We tested our candidate Jun12682 against major drug-metabolising enzymes and saw no evidence that it would interfere with other medications.”

Source: Rutgers University

Categories : COVID Ethics and LawTags :

Pretoria High Court Judgement On COVID-19 Vaccinations

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Photo by Bill Oxford on Unsplash

On 05 January 2023, the COVID Care Alliance NPC and other applicants brought an urgent court application against the South African Health Products Regulatory Authority (SAHPRA), including the President of the Republic of South Africa and others to prevent people from being vaccinated.

The applicants wanted the court to order that all COVID-19 vaccines programs must be stopped and that all COVID-19 vaccination sections in healthcare facilities in South Africa must be closed, and the effective withdrawal from circulation of the vaccines. The applicants also sought an order interdicting the approval of vaccines for emergency authorisation or registration.

On 27 February 2024, the Pretoria High Court dismissed with costs an application filed by the applicants on the grounds that the applicants do not have the right to prevent others, who do not share in their beliefs or opinions, from being vaccinated.

SAHPRA submitted evidence to the Court to show that the applicants’ attempt to prevent government from using vaccines to address the COVID-19 pandemic was misguided, and the applicants heavily relied on hearsay and speculation, as well as supported their arguments with the opinion of persons who were not experts.

Source: SAHPRA

Categories : COVID Respiratory DiseasesTags :

New T Cell ‘Rescue’ Therapy Promising for ARDS

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Credit: Scientific Animations CC4.0

Promising trial results indicate that a new type of cell therapy could improve the prognosis of those who are critically ill with acute respiratory distress syndrome (ARDS) resulting from severe COVID.

Published in the journal Nature Communications, Professor Justin Stebbing of Anglia Ruskin University (ARU) is the joint senior author of the new study investigating the use of agenT-797, MiNK Therapeutic’s allogeneic, unmodified invariant natural killer T (iNKT) cell therapy.

The iNKT cell therapy has the effect of rescuing exhausted T cells and prompting an anti-inflammatory cytokine response, potentially activating anti-viral immunity to help these patients fight infection as well as to reduce severe, pathogenic inflammation of the lung.

The new research was carried out at three medical centres and found that agenT-797, which is also under investigation in cancer trials, could be manufactured rapidly, had a tolerable safety profile, and appeared to have a positive effect on mortality among critically unwell Covid-19 ARDS patients receiving intensive care.

The exploratory trial included 20 mechanically ventilated patients with severe ARDS secondary to Covid-19. Of the 20 patients in the trial, 14 survived (70%) at 30 days (compared to a control group of 10%), and there was an 80% lower occurrence of bacterial pneumonia amongst those who received the highest dosage of agenT-797, compared to those who received fewer cells.

Twenty-one patients were treated overall (the main trial, plus one under compassionate use), which included five who were also receiving veno-venous extracorporeal membrane oxygenation (VV-ECMO), known as ‘the most aggressive salvage therapy’ for critically ill patients with ARDS.

In VV-ECMO, deoxygenated blood is pumped through a membrane lung and returned to the body via a cannula. This trial is believed to be the first immune cell therapy of any type to be used in critically unwell patients undergoing VV-ECMO.

Survival of the VV-ECMO cohort was 80% after 30 and 90 days, and 60% after 120 days. This compares favourably to overall survival of 51% for patients with Covid-19 who were treated with just VV-ECMO at the same institution, during the same timeframe.

Joint senior author Justin Stebbing, Professor of Biomedical Sciences at Anglia Ruskin University (ARU) in Cambridge, England, said: “During this small, exploratory study we observed that MiNK’s iNKT cell treatment, which is also being advanced for people with cancer, triggered an anti-inflammatory response in ARDS patients.

“Despite a poor prognosis, critically ill patients treated with this therapy showed favourable mortality rates and those treated at the highest dose also had reduced rates of pneumonia, underscoring the potential application of iNKT cells, and agenT-797 in particular, in treating viral diseases and infections more broadly.

Source: Anglia Ruskin University

Categories : Gastrointestinal Respiratory DiseasesTags :

Gut Microbiome Composition Affects Sensitivity to Respiratory Viruses

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Gut Microbiome. Credit Darryl Leja National Human Genome Research Institute National Institutes Of Health

The composition of microbiota found in the gut influences how susceptible mice are to respiratory virus infections and the severity of these infections, according to Georgia State University researchers. The findings, published in the journal Cell Host & Microbe, report that segmented filamentous bacteria, a bacterial species found in the intestines, protected mice against influenza virus infection when these bacteria were either naturally acquired or administered.

This protection against infection also applied to respiratory syncytial virus (RSV) and severe acute SARS-CoV-2. To maintain this protection, the study noted that segmented filamentous bacteria required immune cells in the lungs called basally resident alveolar macrophages.

In this study, the researchers investigated how differences in specific microbial species can impact outcomes of respiratory virus infections and how they might do so, which hasn’t been well defined previously.

They studied mice with discrete microbiome differences and mice differing in only the presence or absence of segmented filamentous bacteria.

Viral titers in the lung were measured several days after infection and varied significantly depending on the nature of the microbiome of the different animal groups.

“These findings uncover complex interactions that mechanistically link the intestinal microbiota with the functionality of basally resident alveolar macrophages and severity of respiratory virus infection,” said Dr. Andrew Gewirtz, co-senior author of the study and Regents’ Professor in the Institute for Biomedical Sciences at Georgia State.

The study found that in segmented filamentous bacteria-negative mice, basally resident alveolar macrophages were quickly depleted as respiratory virus infection progressed.

However, in segmented filamentous bacteria-colonised mice, basally resident alveolar macrophages were altered to resist influenza virus infection depletion and inflammatory signaling.

The basally resident alveolar macrophages disabled influenza virus, in large part by activating a component of the immune system referred to as the complement system.

“We find it remarkable that the presence of a single common commensal bacterial species, amidst the thousands of different microbial species that inhabit the mouse gut, had such strong impacts in respiratory virus infection models and that such impacts were largely attributable to reprogramming of basally resident alveolar macrophages,” said D. Richard Plemper, co-senior author of the study, Regents’ Professor and director of the Center for Translational Antiviral Research at Georgia State.

“If applicable to human infections, these findings will have major implications for the future risk assessment of a patient to advance to severe disease.”

“We find it highly unlikely that segmented filamentous bacteria is the only gut microbe capable of impacting the phenotype of alveolar macrophages, and consequently, proneness to respiratory virus infection,” Gewirtz said.

“Rather, we hypothesize that gut microbiota composition broadly influences proneness to respiratory virus infection. Microbiota mediated programming of basally resident alveolar macrophages may not only influence the severity of acute respiratory virus infection, but may also be a long-term post-respiratory virus infection health determinant.”

Source: Georgia State University

Categories : Ageing GenderTags :

COVID, Opioid Pandemic Widen Gender Gap in Life Expectancy in the US

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Photo by Tim Kilby on Unsplash

Women have long been known to outlive men. But new research published in JAMA Internal Medicine shows that, at least in the United States, the gap has been widening for more than a decade. Among the factors driving the trend are the COVID pandemic and the opioid overdose epidemic.

The study, led by UC San Francisco and Harvard T.H. Chan School of Public Health, found the difference between how long American men and women live increased to 5.8 years in 2021, the largest since 1996. This is an increase from 4.8 years in 2010, when the gap was at its smallest in recent history.

The pandemic, which took a disproportionate toll on men, was the biggest contributor to the widening gap from 2019–2021, followed by unintentional injuries and poisonings (mostly drug overdoses), accidents and suicide.

“There’s been a lot of research into the decline in life expectancy in recent years, but no one has systematically analysed why the gap between men and women has been widening since 2010,” said the paper’s first author, Brandon Yan, MD, MPH, a UCSF internal medicine resident physician and research collaborator at Harvard Chan School.

Life expectancy in the US dropped in 2021 to 76.1 years, falling from 78.8 years in 2019 and 77 years in 2020.

The shortening lifespan of Americans has been attributed in part to so-called “deaths of despair.” The term refers to the increase in deaths from such causes as suicide, drug use disorders and alcoholic liver disease, which are often connected with economic hardship, depression and stress.

“While rates of death from drug overdose and homicide have climbed for both men and women, it is clear that men constitute an increasingly disproportionate share of these deaths,” Yan said.

Interventions to reverse a deadly trend

Using data from the National Center for Health Statistics, Yan and fellow researchers from around the country identified the causes of death that were lowering life expectancy the most. Then they estimated the effects on men and women to see how much different causes were contributing to the gap.

Prior to the COVID pandemic, the largest contributors were unintentional injuries, diabetes, suicide, homicide and heart disease.

But during the pandemic, men were more likely to die of the virus. That was likely due to a number of reasons, including differences in health behaviours, as well as social factors, such as the risk of exposure at work, reluctance to seek medical care, incarceration and housing instability. Chronic metabolic disorders, mental illness and gun violence also contributed.

Yan said the results raise questions about whether more specialised care for men, such as in mental health, should be developed to address the growing disparity in life expectancy.

“We have brought insights to a worrisome trend,” Yan said. “Future research ought to help focus public health interventions towards helping reverse this decline in life expectancy.”

Yan and co-authors, including senior author Howard Koh, MD, MPH, professor of the practice of public health leadership at Harvard Chan School, also noted that further analysis is needed to see if these trends change after 2021.

“We need to track these trends closely as the pandemic recedes,” Koh said. “And we must make significant investments in prevention and care to ensure that this widening disparity, among many others, do not become entrenched.”

Source: University of California – San Francisco

Categories : COVID Mental HealthTags :

Having Pets did not Result in Better Well-being During COVID

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Photo by Pauline Loroy on Unsplash

Although pets are generally perceived as having a positive impact on well-being, a new study has found that there was no association between well-being and owning a pet during the COVID pandemic. This finding, published in the Personality and Social Psychology Bulletin, was in spite of pets owners reporting that pet ownership improved their lives.

There is a general understanding that pets have a positive impact on one’s well-being. A new study by Michigan State University found that although pet owners reported pets improving their lives, there was not a reliable association between pet ownership and well-being during the COVID-19 pandemic.

The study assessed 767 people over three periods in May 2020. The researchers took a mixed-method approach that allowed them to look at several indicators of well-being while also asking people in an open-ended question to reflect on the role of pets from their point of view. Pet owners reported that pets made them happy. They claimed pets helped them feel more positive emotions and provided affection and companionship. They also reported negative aspects of pet ownership like being worried about their pet’s well-being and having their pets interfere with working remotely.

However, when their happiness was compared to nonpet owners, the data showed no difference in the well-being of pet owners and nonpet owners over time. The researchers found that it did not matter what type of pet was owned, how many pets were owned or how close they were with their pet. The personalities of the owners were not a factor.

“People say that pets make them happy, but when we actually measure happiness, that doesn’t appear to be the case,” said William Chopik, an associate professor in MSU’s Department of Psychology and co-author of the study. “People see friends as lonely or wanting companionship, and they recommend getting a pet. But it’s unlikely that it’ll be as transformative as people think.”

The researchers explored several reasons why there is not a difference between the well-being of pet owners and nonpet owners. One of them being that nonpet owners may have filled their lives with a variety of other things that make them happy.

Source: Michigan State University

Categories : COVIDTags :

New SARS-CoV-2 Variant BA.2.86 not as Resistant to Antibodies as First Feared

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Image by Fusion Medical on Unsplash

Researchers studying the new SARS-CoV-2 variant BA.2.86 have found that the new variant was not significantly more resistant to antibodies than several other circulating variants. Their study, published in The Lancet Infectious Diseases, also showed that antibody levels to BA.2.86 were significantly higher after a wave of XBB infections compared to before, suggesting that the vaccines based on XBB should provide some cross-protection to BA.2.86.

The recently emerged BA.2.86 is very different from any other currently circulating variants. It includes many mutations in the spike gene, reminiscent of the emergence of Omicron.  The virus uses the viral spike to infect cells and is the main target for our antibodies.  When the spike mutates, it comes with the risk that our antibodies are less effective against this new ‘variant’, and therefore that our protection from infection is reduced and that vaccines may need to be updated.

“We engineered a spike gene that matches that of the BA.2.86 variant and tested the blood of Stockholm blood donors (specifically those donations made very recently) to see how effective their antibodies are against this new variant. We found that although BA.2.86 was quite resistant to neutralising antibodies, it wasn’t significantly more resistant than a number of other variants that are also circulating”, says Daniel Sheward, lead author of the study and Postdoctoral researcher in Benjamin Murrell’s team at Karolinska Institutet.

An important question is whether upcoming updated vaccines that are based on the XBB variant will boost protection against BA.2.86.  To determine whether antibodies triggered by infection with XBB may be effective against this new variant, Ben Murrell’s team also compared samples taken before and after XBB spread in Sweden.

“We also found that antibody levels to BA.2.86 were significantly higher after a wave of XBB infections compared to before, suggesting that the vaccines based on XBB should provide some cross-protection to BA.2.86. However, BA.2.86 was resistant to all available monoclonal antibody therapeutics that we tested,” says Daniel Sheward.

Public health agencies need to know what the current level of immunity to this new variant is, and whether the vaccines are sufficient must be updated.  Monoclonal antibodies also represent an important option for some patient groups, such as the immunocompromised – for the clinicians, it’s important to know which if any, monoclonal antibody therapeutics will be effective against the variants that are circulating.  

“I think the main message is that there is currently no reason to be alarmed over this new variant and that it’s probably a good idea to get a booster vaccine when they are offered.  However, another ‘omicron-like’ event is also a reminder that we shouldn’t get complacent”, says Benjamin Murrell, Principal researcher at the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet.

Source: Karolinska Institutet

Categories : Cardiovascular Disease COVIDTags :

Study Explains a Link between COVID and Increased Cardiovascular Risk

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Source: Wikimedia CC0

A study published in the journal Nature Cardiovascular Research shows that SARS-CoV-2 can directly infect the arteries of the heart and cause the fatty plaque inside arteries to become highly inflamed, increasing the risk of heart attack and stroke. The findings may help explain why certain people who get COVID have a greater chance of developing cardiovascular disease, or if they already have it, develop more heart-related complications.

In the National Institutes of Health (NIH)-funded study, researchers focused on older people with atherosclerotic plaque, who died from COVID. However, because the researchers found the virus infects and replicates in the arteries no matter the levels of plaque, the findings could have broader implications for anybody who gets COVID.

“Since the early days of the pandemic, we have known that people who had COVID have an increased risk for cardiovascular disease or stroke up to one year after infection,” said Michelle Olive, PhD, acting associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute (NHLBI), part of NIH. “We believe we have uncovered one of the reasons why.”

Though previous studies have shown that SARS-CoV-2 can directly infect tissues such as the brain and lungs, less was known about its effect on the coronary arteries. Researchers knew that after the virus reaches the cells, the body’s immune system sends in macrophages to help clear the virus. In the arteries, macrophages also help remove cholesterol, and when they become overloaded with cholesterol, they morph into a specialised type of cell called foam cells.

The researchers thought that if SARS-CoV-2 could directly infect arterial cells, the macrophages that normally are turned loose might increase inflammation in the existing plaque, explained Chiara Giannarelli, MD, PhD, associate professor in the departments of medicine and pathology at New York University’s Grossman School of Medicine and senior author on the study. To test their theory, Giannarelli and her team took tissue from the coronary arteries and plaque of people who had died from COVID and confirmed the virus was in those tissues. Then they took arterial and plaque cells – including macrophages and foam cells – from healthy patients and infected them with SARS-CoV-2 in a lab dish. They found that the virus had also infected those cells and tissues.

Additionally, the researchers found that when they compared the infection rates of SARS-CoV-2, they showed that the virus infects macrophages at a higher rate than other arterial cells. Cholesterol-laden foam cells were the most susceptible to infection and unable to readily clear the virus. This suggested that foam cells might act as a reservoir of SARS-CoV-2 in the atherosclerotic plaque. Having more build-up of plaque, and thus a greater number of foam cells, could increase the severity or persistence of COVID.

The researchers then looked at the predicted inflammation in the plaque after infecting it with the virus. They observed the release of inflammatory cytokines, also known to promote the formation of even more plaque. The cytokines were released by infected macrophages and foam cells. The researchers said this may help explain why people who have underlying plaque buildup and then get COVID may have cardiovascular complications long after getting the infection.  

“This study is incredibly important as it adds to the larger body of work to better understand COVID,” said Olive. “This is just one more study that demonstrates how the virus both infects and causes inflammation in many cells and tissues throughout the body. Ultimately, this is information that will inform future research on both acute and Long COVID.”

Though the findings conclusively show that SARS-CoV-2 can infect and replicate in the macrophages of plaques and arterial cells, they are only relevant to the original strains of SARS-CoV-2 that circulated in New York City between May 2020 and May 2021. The study was conducted in a small cohort of older individuals, all of whom had atherosclerosis and other medical conditions; therefore, the results cannot be generalised to younger, healthy individuals.

Source: National Institutes of Health

Categories : COVID Medical IndustryTags :

From Molecule to the Shelf

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Bada Pharasi, CEO of The Innovative Pharmaceutical Association of South Africa (IPASA)

Lessons from the COVID-19 pandemic have underlined the importance of continued investment into pharmaceutical innovation and R&D to not only bring life-saving medications to those in need, but to improve public health outcomes, writes Bada Pharasi, CEO of The Innovative Pharmaceutical Association of South Africa (IPASA).

From treatments for cancer, cardiovascular diseases and more recently, the COVID-19 vaccine, the pharmaceutical industry has made significant progress in the development of over 470 medications in the last 10 years alone.1

While the innovative pharmaceutical process typically takes between 10 and 15 years from discovery to regulatory approval2 – owing to factors including immense R&D costs, regulatory compliance, and the protection of patents3 – the fast-tracked development and approval of COVID-19 vaccines laid bare the need for pharmaceutical companies to be prepared to mitigate the risk of future outbreaks – and this means continued investment in innovation and R&D.

The pandemic underlined the need for countries to be prepared for outbreaks on the horizon. To ensure we can meet the next challenge, pharmaceutical innovations must match the pace at which diseases mutate. This kind of innovation is non-negotiable and requires continued investment as a safeguard against losing lives and endangering South Africa’s fragile healthcare system.

As we are in the midst of a cholera epidemic, as well as the recent measles outbreak,4 it’s important to continue driving innovation to treat diseases, with medicines developed by innovative pharmaceutical companies benefiting millions across the country every day.

This is evidenced by mortality rates for HIV/AIDS and TB in the country falling by 59.2% and 55.7% between 2007 and 2017, with at least 60 new medicines currently in the R&D pipeline to treat TB.5

While patents in pharmaceutical innovation protect the originators’ intellectual property, it is important that innovative medications be developed to ensure a continuous pipeline of access to generics once the patent has lost its exclusivity. This will drive consumer accessibility and affordability of life-saving treatments and medications that may otherwise be unattainable for many.

As we continue racing against the proverbial clock in protecting against current and future diseases, pharmaceutical companies should continue to invest in innovation and R&D to outsmart existing dreaded diseases, and provide agility and preparedness should the next unknown pandemic threaten. Our health, and lives, depend on it.

References:
1. #AlwaysInnovating: The pharmaceutical innovation journey [Internet]. IFPMA. 2023 [cited 2023 Jun 28]. Available from: https://www.ifpma.org/initiatives/alwaysinnovating/
2. Derep M. What’s the average time to bring a drug to market in 2022? [Internet]. N-SIDE; 2022 [cited 2023 Jun 28]. Available from: https://lifesciences.n-side.com/blog/what-is-the-average-time-to-bring-a-drug-to-market-in-2022
3. Ancliff S. 10 challenges facing the pharmaceutical industry in 2024 [Internet]. [cited 2023 Jun 29]. Available from: https://blog.i-nexus.com/10-challenges-facing-the-pharmaceutical-industry
4. Yoganathan V. Prepare for more pandemics in the future, experts warn [Internet]. Juta MedicalBrief. Medical Brief; 2023 [cited 2023 Jun 30]. Available from: https://www.medicalbrief.co.za/prepare-for-more-pandemic-in-the-future-experts-warn/
5. South Africa – the innovative hub for pharmaceutical development [Internet]. B2B Central. New Media; 2021 [cited 2023 Jun 29]. Available from: https://www.b2bcentral.co.za/why-south-africa-is-an-innovation-hub-for-pharmaceuticals/

Categories : Immune System VaccinesTags :

Can People Accurately Assess the Strength of Their Immune Systems?

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Photo by Brittany Colette on Unsplash

People often say whether they feel like their immune system is ‘down’ – but could there be some truth to this? A recent study showed that when freshly vaccinated people self-assessed the strength of their immune response, their estimates correlated well to their measured antibody levels. They were even more accurate when their immune response was weak. The results were published in the journal Biological Psychology.

At the University of Konstanz, Stephanie psychologist Dimitroff researches the connection between our brain and our immune system. “Listen to your body,” she concludes from her study. “The field of medicine is moving towards greater patient orientation. Our findings support the idea that patients’ self-perceptions provide valuable clues about their state of health. Physicians should listen to them more.”

Communication between the immune and nervous systems

One part of our brain, the insula, receives information from the body and gives us a basic impression of its condition, which until now was assumed to be quite general in nature. Stephanie Dimitroff’s study now suggests that our brain can perceive the body’s condition more specifically than previously thought. Is it possible that our brain can assess the state of our immune system?

“Of course, our brain does not count antibodies. But our immune system is intrinsically connected to the central nervous system,” Dimitroff explains. “The immune system is regulated via this connection. And our brain also receives information from the immune system.”

This communication between the immune system and the central nervous system is key for our sense of well-being or illness. “It is important to know here: When we feel ill, for example, we have a cold, this feeling is caused quite significantly by the immune system’s communication with the central nervous system,” says Dimitroff. “The brain receives signals that something is wrong with the body and causes the feeling of illness as a result.”

The same flow of information between the immune and nervous systems can generally also take place when the body is not ill. This means it could be possible that this communication process gives us an impression of our immune system even when we are healthy. Stephanie Dimitroff’s study investigates whether this is actually the case.

Results of the study

The study looked at people who had received the COVID-19 vaccine. This group of participants was chosen because a particularly large number of people received the vaccine in the summer of 2021, when the study was conducted. 166 people between the ages of 18 and 59 participated in the study.

After vaccination, the participants in the study were able to assess surprisingly well how strongly their immune system was positioned to fight the respective illness. This was especially true for people who had developed only a few antibodies. In fact, 71% of participants who did not feel well protected after vaccination also had a below-average immune response. “Our most notable finding is that those who felt they had not produced high levels of antibodies after vaccination were often correct in their assessment.”

By contrast, participants who assessed their immune response as good were not always right. However, all of those who had a particularly strong immune response also reported feeling well protected.

Alternative interpretations

For Stephanie Dimitroff, however, it is still too early to draw any final conclusions. The psychologist is considering other possible causes, including the placebo effect. This is because communication between the brain and the immune system runs in both directions. The signals from our brain can therefore also influence our immune system. People who firmly believe in vaccination or are basically optimistic could thus actually develop a better immune defence (placebo effect) and also feel better protected. It is therefore possible that belief in the effectiveness of a vaccine is what improves its efficacy, and this could also explain the high accuracy of the self-assessments.

“Our results suggest that it is quite likely that people have a real ability to assess their own health. However, I cannot rule out that there is a combination of effects at play, including the placebo effect and/or feelings of optimism,” Dimitroff says. In her view, it would make sense to repeat the study in order to confirm the results and rule out alternative causes.

Source: University of Konstanz