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There's always something new to read about the Faculty, whether it's a new discovery by one of our academics, an award won by one of our students, or an upcoming event.

Most press releases will specify media contacts, but if in doubt, please get in touch with our Media Relations Officer, Michael Addelman, at or on +44 (0)161 275 2111.

Latest news

New home-based self-help psychological therapy reduces anxiety and depression in people with heart disease
(6 February 2023)

A study led by Greater Manchester Mental Health NHS Foundation Trust (GMMH) and the University of Manchester (UoM), and funded by the National Institute for Health and Care Research (NIHR) has found that a psychological therapy called Metacognitive Therapy (MCT) can reduce symptoms of depression, anxiety and post- traumatic stress in heart disease patients when delivered in a self-help format.

Continued ear wax services crucial, say Manchester researchers
(27 January 2023)

A new study by University of Manchester audiologists has highlighted the difficulties people face with impacted ear wax.

Study shows impact of high GP turnover on service and health
(24 January 2023)

A new study by University of Manchester researchers has revealed the stark impact that high turnover of GPs has on patients’ health outcomes and the service they receive in England.

Major funding for Manchester will help find new cancer treatments
(23 January 2023)

The search for new cancer treatments in Manchester is to receive a major funding investment of up to £3m, providing future hope for people diagnosed with the disease.

Does COVID really damage your immune system and make you more vulnerable to infections? The evidence is lacking
(20 January 2023)

Over the past month or two, many northern hemisphere countries including the US and the UK have seen a large wave of respiratory viral infections. These include RSV (respiratory syncytial virus), flu and COVID in all ages, as well as bacterial infections such as strep A in children.

Sometimes these infections can be very serious. The UK has seen a huge surge in hospital admissions during winter, putting the health service under further stress.

This had led some to question whether COVID damages our immune systems, leaving those who have been infected more vulnerable to other infectious diseases like the flu.

Another idea put forward to explain the surge in respiratory viruses is that children “missed out” on common childhood infections during the height of the pandemic, and that this has left them more vulnerable to these infections now owing to an “immunity debt”. But how credible are these explanations?

COVID and our immune systems

The human immune system has evolved to deal with a host of different infections. It has a variety of weapons it can deploy which work together not only to eradicate infectious agents, but also to remember them for a more rapid and tailored response upon any subsequent encounter.

Likewise, many infectious agents have developed tricks to try to evade our immune system. For example, a parasite called Schistosoma mansoni disguises itself to avoid the immune system detecting it.

SARS-CoV-2, the virus that causes COVID-19, similarly has tricks up its sleeve. Like many other viruses, it’s been shown to evade host immunity, particularly newer variants. Recent studies showed it can interfere with immune cells’ ability to detect it within cells. This is concerning, but it’s not clear that such changes impact immunity to other infections.

Short-lived changes in a person’s immune defences are normal when they’ve been exposed to an infection. Several studies have now shown that, in response to SARS-CoV-2, specialised white blood cells called lymphocytes grow in number. These lymphocytes also display changes in their features typical of cell activation, such as changes in surface proteins.

Such changes may sound dramatic to the non-expert if taken out of context (called “ascertainment bias”). But they’re normal and merely indicate that the immune system is working as it should. Research has confirmed that, for most people, the immune system regains balance following recovery.

Some exceptions

SARS-CoV-2, like many viruses, doesn’t affect everyone equally. We’ve known for some time that certain groups, including older people and those with underlying health complications such as diabetes or obesity, can be more susceptible to severe disease when they contract COVID.

This vulnerability is associated with an irregular immune response to SARS-CoV-2 that results in inflammation. Here we see, for instance, reduced numbers of lymphocytes and changes to immune cells known as phagocytes.

Still, for most of these vulnerable people, the immune system returns to normal over the next two to four months. However, a small subset of patients, particularly those who had severe COVID or have underlying medical issues, retain some changes beyond six months after infection.

The significance of these findings isn’t clear, and longer-term studies considering the impact of underlying health conditions on immune function will be needed. But for most people, there’s no evidence to suggest immune damage following a COVID infection.

For some people with underlying health conditions, immune changes appear to last longer. pikselstock/Shutterstock

What about long COVID?

Emerging evidence suggests the most marked and persistent differences in immune cells after a COVID infection occur in people who have developed long COVID.

So far, no data points to immune deficiency in long COVID patients. But an overactive immune response can actually cause harm, and the immune cell changes seen in long COVID patients seem consistent with a vigorous immune response. This may explain the variety of post-infection consequences and symptoms that people with long COVID face.

Immunity debt

The “immunity debt” hypothesis suggests the immune system is like a muscle requiring near-constant exposure to infectious agents to keep it functioning. So, the argument goes, a lack of exposure due to lockdowns damaged immune development, especially in children, by making our immune systems “forget” earlier knowledge. This supposedly left them more vulnerable to infections when social mixing returned to normal.

Though this idea has gained traction, there’s no immunological evidence to support it. It’s not true to say we require a constant background of infection for our immune system to work. Our immune systems are immensely robust and powerful. For example, immune memory to the 1918 influenza pandemic was still evident after 90 years.

It’s also not strictly true to say children weren’t exposed to viruses during the early pandemic. Lockdowns didn’t commence until after waves of the usual winter respiratory infections in 2019/2020, and schools in the UK reopened in autumn 2020 with variable preventive measures, so children were still exposed to infections, including COVID-19.

The cold-causing viruses didn’t completely vanish by any means. For example, there was a significant RSV outbreak in the UK in 2021.

Nonetheless, lockdowns and other protective measures probably did reduce exposure to viruses, and for some children this shifted when and at what age they were first exposed to viruses such as RSV. This, taken alongside a high background of COVID, and relatively poor COVID and flu vaccine uptake, could all be making this season particularly bad. However, a change in the timing of when people are exposed leading to a surge of infections doesn’t necessarily mean that individual immunity has been damaged.

Our knowledge of the immune response to COVID is rapidly expanding. The most consistent findings show how well vaccines are protecting us from the very worst effects of SARS-CoV-2 and that, post-vaccination, our immune system is working exactly as it should.

However, findings of altered immune signatures in some recovered patients and those with long COVID require further investigation.The Conversation

Sheena Cruickshank, Professor in Biomedical Sciences, University of Manchester

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Group course can be standard treatment for anxiety and depression, trial finds
(12 January 2023)

The first ever trial of a revolutionary group approach to anxiety and depression has shown it is no less effective than the one on one sessions thousands of people receive on the NHS every day.

Researchers reveal worrying rise in antipsychotic prescriptions for children and young people
(10 January 2023)

The proportion of children and adolescents prescribed antipsychotics in English general practice doubled from 0.06% to 0.11% between 2000 and 2019, find researchers at The University of Manchester’s Centre for Women’s Mental Health.

Targeting variant of common protein may dramatically boost effectiveness of breast cancer treatment
(5 January 2023)

A rare variant of a protein present in nearly all human cells may hold the key to improving the effectiveness of breast cancer treatment, according to University of Manchester research funded by Breast Cancer Now.  

Study reveals huge extent of fungal disease in India
(3 January 2023)

Over fifty million Indians are affected by serious fungal disease, 10% of which are from potentially dangerous mould infections researchers from India and Manchester have shown.

Supporting a child with long COVID – tips from parents of children living with the condition
(3 January 2023)

Long COVID is the patient-preferred term used to describe symptoms lasting more than four weeks after a COVID-19 infection. Children and young people can also suffer from long COVID following even a mild infection with the virus. The latest figures from the UK’s Office for National Statistics show an estimated 69,000 children are living with long COVID, 41,000 of whom have had symptoms for at least a year.

The most common symptoms of long COVID in children are fatigue and headaches, but young people can also have a range of other symptoms including chest pain, persistent cough, dizziness, nausea, abdominal pain, anxiety and low mood.

We don’t know whether all children with long COVID will recover or how long this will take. Parents’ narratives suggest that symptoms may fluctuate over time, and that it’s not uncommon to have a period of apparent recovery and then relapse some months later. The course of the illness is not linear.

While every child will have specific problems and individual needs, there are some suggestions we can make to help parents or guardians support their child or young person with long COVID. Two of us (Binita and Tracy) have children with long COVID, and the following tips are based on our own experiences.

1. Believe your child

Long COVID is an “invisible” illness, so children can look well. At the start of the illness we both sent our children to school when they said they weren’t feeling well enough, putting it down to them not wanting to go to school, or some sort of anxiety.

Looking back, this was the wrong thing to do. They got worse by “pushing through”. Our advice is to listen to your child, don’t push them and seek medical advice to ensure there’s no other underlying cause for their symptoms.

If your child is not being believed by a healthcare professional, there’s no harm in asking for a second opinion, or sharing available information with the professional. Long COVID is a well recognised condition in children but sadly, there’s still poor awareness among some medical professionals.

2. Resting and pacing

Energy can be likened to money in the bank. If you keep spending without topping up, you soon get into debt. In long COVID, using up energy without planning rest can result in a “crash” or relapse. It can then take several days to accumulate enough energy to get going again.

Many don’t realise that even activities like watching TV and being on social media can drain energy for those with long COVID. Work with your children to consider how much energy different activities require (you might categorise activities into low, medium and high energy) and ensure that each activity is followed by rest, particularly those that expend more energy.

Activities may also need to be adjusted. For example, our children can no longer participate in sports but do more drawing and craft, when energy levels allow.

3. Seek support at school

Some children with long COVID may have cognitive impairment (also called “brain fog”), sensitivity to lights or sounds, and fatigue – all of which present barriers to learning at school.

Adaptations to learning may be needed. Breaking information down into smaller chunks, reduced lesson times, and a quiet environment can help. Our advice is to speak to the school about having a care plan for your child and ensuring lessons are adapted appropriately.

Children with long COVID are likely to lack energy. Prostock-studio/Shutterstock

Separately, COVID reinfection carries a risk of symptom relapse or deterioration for children with long COVID, which can cause anxiety for families when sending children to school.

We would advise that children with long COVID have a risk assessment at school to reduce the chance of reinfection. This can include looking at limiting the child’s exposure to larger groups (for example, in assembly or the canteen), ensuring classrooms are well ventilated, and allowing the use of a FFP2 mask if the child wishes to wear one.

4. Mental health

Long COVID can be debilitating and isolating. Focusing on what children and young people have lost can drive despair, hopelessness and a feeling of being trapped.

We’ve tried to practise “acceptance” with our children. This involves accepting the situation we’re in and avoiding focusing on negative thoughts and feelings. We spend a lot of time emphasising what our children can still do, setting realistic goals, celebrating wins, and trying not to grieve too much over what has been lost.

It’s also important that parents and family members are kind to themselves and each other. Caring for a sick child is difficult for the whole family. If you need mental health support yourself, speak to a healthcare professional.

5. Non-medical treatments

Medical therapies for treating long COVID are limited pending research trials, and access to specialist long COVID clinics for children and young people is difficult to come by, with only 15 hubs across England.

There are, however, some things you can do at home that may help manage your child’s symptoms. Many people have an overactive “fight or flight” response after viral infections, including COVID-19, due to effects on their autonomic nervous system. This can impact heart rate and blood pressure, as well as gut and bladder function. Reducing screen time and caffeine (particularly in the evenings) and breathing exercises can help reduce fight or flight hormones.

6. Information and support

Primary care has a key role in supporting young people with long COVID and their families, including liaising with schools where necessary. So seek the support of your GP.

Caring for a child with long COVID can incur increased costs and may mean you cannot work as much as previously, or at all. Depending on how long your child has been unwell and the severity, they may be eligible for a disability living allowance or other benefits.

There’s a lot of misinformation out there about long COVID, so it’s important to access trusted sources of information. The Long COVID Kids charity offers a useful support pack for children and families as well as the opportunity to connect with other kids and families affected by long COVID. Our children have found this support invaluable.The Conversation

Carolyn Chew-Graham, Professor of General Practice Research, Director of Clinical Academic Training, Keele University; Binita Kane, Honorary Senior Lecturer, School of Biological Sciences, University of Manchester, and Tracy Briggs, Clinical Senior Lecturer, Division of Evolution, Infection and Genomics, University of Manchester

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Photo by Kelly Sikkema on Unsplash 

University members recognised in New Year Honours
(31 December 2022)

A new Knight and a Dame are among the University of Manchester people recognised in the New Year Honours, the first to be granted by King Charles III.

Scientists turn to astrophysics to measure body clock in hospital patients
(20 December 2022)

An interdisciplinary team led by University of Manchester scientists has adapted a technique originally developed to analyse data from stars to devise a way of accurately measuring the human body clock in hospital patients.

Biology medicine and health: a review of our top stories
(20 December 2022)

2022 was another bumper year for news from the Faculty of Biology, Medicine and health. Here are some of our highlights:

In January we showed how early data for multivariant COVID-19 vaccine booster shows promise. The first results of an early trial of a multivariant COVID-19 vaccine booster, launched in Manchester in September 2021, showed it is driving a comprehensive immune response.

Coronavirus (Public domain  Centers for Disease Control and Prevention's Public Health Image Library)

In March, our scientists show how plastic exposure in pregnancy could explain low weight in newborn boys. A team led by scientists at The University of Manchester discovered how exposure in pregnant mothers to a chemical found in many plastics alters the expression of a protein linked to fetal growth restriction (FGR) in boys.

Newborn Baby

In  April we revealed the worrying news that  around 33%  of GPs are likely to quit direct patient care within five years, according to the elevenths GP Worklife Survey by University of Manchester researchers.


In May we found out we had retained our  ‘Leadership status  in Openness’ award on Animal Research

Mice 2 July 2016

In June,  a trial of new new talking therapy for men in prison who struggle with suicidal thoughts and feelings  to prevent prisoner suicide was  launched. The team of clinicians, academics, researchers, service users and carers will study the effects of Cognitive Behavioural Suicide Prevention therapy within prisons.

Talking therapy mental health

In August we showed how  a viral role in Alzheimer's Disease had been discovered. Researchers from Oxford’s Institute of Population Ageing, Tufts University and The University of Manchester discovered that common viruses appear to play a role in some cases of Alzheimer’s disease (AD).


In September we brought to you the news that a  biologic therapy for very young children with a moderate to severe form of a common skin condition had been shown to be safe and effective in an international trial which involved University of Manchester clinical scientists working within the Clinical Trials Facility at Royal Manchester Children’s Hospital. The study of the drug, dupilumab, in inadequately  controlled eczema was the first large-scale randomised double-blind trial of a monoclonal antibody (a lab-made protein that binds to certain targets in the body) for any skin disease, in patients aged six months to six years. 

Baby skin

Also in September we showed how £6.95 million Global Health Research Unit on Neurodevelopment and Autism for children in South Asia is to launch with the help of University of Manchester expertise. The NIHR Global Health Research Unit on Neurodevelopment and Autism in South Asia Treatment and Evidence  -known as NAMASTE - has been awarded by the National Institute of Health and Care Research (NIHR) using UK aid from the UK Government which supports global health research.

India autism training

In November a study sheds new light on benefits to children of water fluoridation. Fluoridation of the water supply may confer a modest benefit to the dental health of children, a seven-year-study led by University of Manchester researchers  has concluded.



And last but not least, this month we've been celebrating  our prestigious openness award for our pioneering work on communicating animal research to the public.

Opennes award Dec 2022



New figures provide latest data on veterans suicide
(16 December 2022)

A new study from The University of Manchester has found that veterans are at no greater risk of suicide than the general population.

Racism is ‘fundamental cause’ of COVID-19 vaccine hesitancy among ethnic minorities
(15 December 2022)

Racism is the ‘fundamental cause’ of COVID-19 vaccination hesitancy among ethnic minority groups, according to a newly published briefing from the Runnymede Trust and The University of Manchester’s Centre on the Dynamics of Ethnicity.

World-first genetic test for babies' hearing wins major award
(14 December 2022)

A team who led the research for a world-first genetic test that could save the hearing of hundreds of babies each year, has won the New Statesman Positive Impact in Healthcare Award 2022.

Pioneering Manchester bags prestigious openness award
(7 December 2022)

The University of Manchester has bagged a prestigious openness award for its pioneering work on communicating animal research to the public.

Hearing loss: headphones and concerts could put young people at risk – here’s how to protect yourself
(28 November 2022)

A recent study published in BMJ Global Health has estimated that over one billion people worldwide aged 12-34 years could be at risk of noise-induced hearing loss. The systematic review and meta-analysis found that 24% of young people engage in unsafe listening practices when using a personal listening device (such as headphones), while an estimated 48% do so at least once a month by attending noisy events (such as concerts or clubs).

In this study, “unsafe listening” relates to not only how loud the noise is, but for how long a person is exposed. A person’s maximum recommended noise exposure dose is no more than 85 dB (decibels) for eight hours a day. This is roughly as loud as city traffic or a busy restaurant.

For every three decibel increase in noise, this equates to a doubling in sound energy – meaning that the exposure time should be halved (known as the “three dB rule”). So if the sound in a typical concert is around 105 dB, a person would exceed their daily noise dose within approximately five minutes of being there. Headphones and earphones can reach similar levels when put up to maximum volume.

Frequently engaging in unsafe listening practices can lead to permanent hearing loss. Fortunately, there are many easy things you can do to lower this risk.

Knowing your risk

It’s important to note this study only estimates the number of young people who could be at risk of hearing loss – it does not report on how many people have already developed hearing loss due to unsafe listening practices. The authors acknowledge that more well-designed studies are needed to better understand the effects of recreational noise exposure across the lifespan.

However, we do know from studies on other types of noise just how harmful it can be to hearing. For example, studies investigating the effects of occupational noise exposure (such as from loud construction machinery) have shown that it’s linked with high levels of hearing loss and tinnitus (a ringing or buzzing sensation in the ears). In such jobs, average daily noise exposures can exceed 100 dB. Similar problems have also been found in the music industry, with approximately 64% of pop-rock musicians reporting to have hearing loss.

In theory, the delicate parts of the inner ear are equally as susceptible to damage from loud music as they are from noisy machinery and power tools. Regular exposure to high levels of noise can destroy the sensory hair cells in the ear that are responsible for amplifying everyday sounds. Damage to them is irreversible, meaning that noise-induced hearing loss is permanent.

Early symptoms of hearing damage can include muffled hearing (like having wool in your ears) and tinnitus – both of which can be common after exposure to loud noise. But even though these symptoms may disappear within a couple of hours or days, it has been suggested that these symptoms could still be initial warning signs of more insidious damage to parts of the inner ear.

While these early signs of hearing loss might be nothing more than a minor annoyance when you’re young, as hearing loss worsens it can have a major impact on quality of life. Some studies have even shown it’s associated with depression and cognitive decline later in life. This is why it’s vital to look after your hearing even when you’re young.

Protecting your hearing

The first and most effective way to reduce the risk of hearing loss is to eliminate the noise at its source. In other words, turn the volume down. This is easy to do with personal listening devices, since many smartphones are already wired to alert you when you’ve been listening for too long at a high volume.

But turning the volume down can be harder to do when attending loud events. To protect yourself, limit your exposure – either by moving away from the sound source (avoid standing in front of loudspeakers) or taking a break in a quiet space every 15 minutes or so. It’s also recommended you give your ears at least 16 hours rest if you spend around two hours in a 100 dB environment, such as a club or concert.

You could also use hearing protection devices (such as earplugs) at noisy events. These are usually considered as a last line of defence, but may be the best option if you are unable to limit your exposure – or don’t want to.

Disposable foam earplugs will help to prevent noise-induced hearing loss if worn correctly. But they aren’t really designed for listening to music and can make music sound muffled, which puts many people off using them. Musicians’ earplugs are a better solution, as these are designed to evenly balance noise reduction across all frequencies, which preserves the quality of the music.

Even if you follow these measures to protect your hearing, it’s still advisable to get your hearing checked by an audiologist. While there’s no rule on how regularly you should get your hearing checked when you’re young, some audiologists recommend having at least one test done in your 20s to serve as a baseline, and then to get retested approximately every five years to monitor any changes.

But if you’re regularly exposed to noise or already have some hearing loss, it’s advised you get your hearing checked more frequently. You should also contact your GP immediately if you notice any sudden changes in your hearing.The Conversation

Samuel Couth, Research Associate, Hearing Science, University of Manchester

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Precision medicine trial opens for rare adult and paedatric cancers
(23 November 2022)

Cancer Research UK, The University of Manchester and Roche Products Ltd (‘Roche’), today (Wednesday 23rd), announce that they have opened a multi-drug, precision medicine trial for people with rare cancers who need more treatment options.

Earbuds: can they be used as hearing aids?
(16 November 2022)

Hearing loss is a major global issue. Around 5% of the world population, 430 million, have disabling hearing loss. With ageing populations, this burden will only increase.

The primary remedy is the simple hearing aid. It is an essential helpmate to ensure continued social contact and quality of life. Simple, but not necessarily cheap. They cost around US$1,000 (£850) per ear for a reasonable quality device – not an insubstantial amount, especially in times of austerity. Although, in the UK they are free on the NHS.

The basic function of a hearing aid is to amplify sound in a pattern to match the profile of the loss of hearing sensitivity in the wearer. Legally, a hearing aid can only be dispensed by a registered clinician. But a new class of devices, called personal sound amplification products (PSAPs), bypass this legal restriction.

A PSAP is not a difficult device to build. Most of us already carry the core components around in our pockets in the form of a smartphone. A microphone, some computer processing and either a loudspeaker or earpiece are “all” that you need.

The processing, in the form of apps, has been available for many years. In its simplest form, even the ability to separately control the treble and bass of your smartphone performs like a PSAP.

Taking this further, a new paper from researchers in Taiwan reports on the possible use of earbuds as PSAPs, specifically Apple AirPods, incorporating the Apple “Live Listen” function. Live Listen allows the microphone on an iPhone to amplify audio and transmit it wirelessly to AirPods.

Using technical measures, a few of these models meet some of the required performance standards for PSAPs. In the paper, volunteers with hearing impairment were assessed on their ability to repeat back speech presented in either quiet or in noise. The researchers reported similar improvements in performance to those available from either a premium or a basic hearing aid when compared with unaided hearing.

Does this mean that the extensive development work put into hearing aids over the past 100 years has been usurped? Not really.

Hearing aids aren’t cheap. krolya25/Shutterstock

The most common form of hearing loss that can’t be fixed with surgery is the loss in the cellular mechanisms of the cochlea – the tiny snail-shaped organ that sits at the end of the ear canal. This loss is not like blocking your ears. A person loses the sensitivity to soft sounds, but loud sounds often appear just as loud as to a person with unimpaired hearing.

The solution is an automatic volume control: turning up quiet sounds and turning down too-loud sounds. This automatic control can be performed in a smartphone app so that the user always has a comfortable listening experience. Since hearing loss also varies with audio frequency, the behaviour of the automatic volume controls has to change with frequency.

A modern hearing aid performs multiple channels of automatic volume control but has a host of other features operating at the same time. For example, reducing interfering noises, preventing squealing and operating “directional microphones” to focus on the desired sound source. All of these features contribute to the long-term wearability of any hearing aid. This latest study is light on detail as to what processing was performed in the AirPods other than the use of volume control.

Not a long-term fix

So why are hearing aids more expensive than PSAPs? When an audiologist measures hearing loss, they also look to identify the causes of the loss – which can be many more than just the changes expected with old age. Some of these causes can be very serious and require treatment. This necessary human expertise has to be paid for.

There are also serious consequences of untreated or under-treated hearing loss. Uncorrected losses of our senses are associated with longer-term declines in mental abilities, with an increased risk of dementia. These declines are identifiable only over many years, or even decades, and are associated with massive costs – costs that will need to be covered by families and healthcare systems.

The researchers in the new study say that PSAPs “could potentially bridge the gap between persons with hearing difficulties and their first step to seeking hearing assistance”. But it would be unwise to see them as a long-term fix.The Conversation

Michael A Stone, Senior Research Fellow, Division of Human Communication, Development and Hearing, University of Manchester

This article is republished from The Conversation under a Creative Commons license. Read the original article.

My work investigating the links between viruses and Alzheimer’s disease was dismissed for years – but now the evidence is building
(16 November 2022)

This article is part of the Insights Uncharted Brain series. There are many competing theories about what causes Alzheimer’s disease. Here, Ruth Itzhaki reflects on a career dedicated to one of the more controversial lines of research.

When I was about seven or eight, I asserted that I wanted to be a scientist, or so my parents told me years later, even though I would have had little idea of what that word meant. In my mind, I was perhaps associating it with making momentous discoveries that were immediately recognised and applauded by the whole world. Soon after, I avidly read Madame Curie, the book by Eve Curie about her mother Marie and how she overcame poverty and the many challenges faced by women in the late 19th and early 20th century to become a Nobel prize-winning scientist. Marie Curie became my lodestar for the future and thanks to my parents’ support and self-sacrifice, I did eventually become a scientist.

Marie Curie won two Nobel Prizes in 1903 for Physics and in 1911 for Chemistry. Shutterstock/Everett Collection

Many years later, I found myself confronting what seemed like insuperable odds just as Curie did, though in very different circumstances. I have been an independent researcher since the age of 26 when I completed my PhD. My subsequent research in a Cambridge University department on chromatin (a complex of DNA and proteins) went well. Then, after eight years, my husband and I moved to Manchester where the head of the institute where I worked for 12 years decided to end my contract, leaving me jobless and lab-less.

In the decades that followed, my research into viruses as a possible cause of Alzheimer’s disease was greeted with much hostility, and almost all my funding applications were refused: a hostility that has continued for 25 years and which has only recently abated, thanks to mounting evidence.


I, along with my tiny research group, survived only through the award of a few small grants from more open-minded charities and companies interested in new approaches. Once I even managed to swap a business class ticket to the US (that was provided for me to speak at a conference) for economy class, so I could use the several thousand-dollar surplus for my lab instead.

But, after years of struggle, there is finally hope for this line of research. An anti-viral trial for Alzheimer’s – the first ever – is now taking place at Columbia University. This study is building on the years of work done by my team. Meanwhile, our latest research is looking into the way infectious illnesses increase the risk of Alzheimer’s.

Dementia brought home

Career and academic challenges can always be balanced with the help of a support network: a family. I was always lucky with mine. During many of these years, my husband, Shaul Itzhaki, a retired academic who had worked on nucleic acid biochemistry, supported my struggles and never once suggested that I change to a safer, more conventional and non-contentious topic. He was always touchingly happy with any successes I had, and I will always remember our celebratory days when I was awarded a Beit Memorial Fellowship for Medical Research, and later a Newnham College Fellowship, during our years in Cambridge.

Sadly, he died in April 2022, after suffering for about ten years from vascular dementia (a dementia distinct from Alzheimer’s disease but with many similar symptoms) and latterly, from a fractured femur that disabled him. The last four or so years were particularly hard to endure as he became increasingly aware of his failing memory. The term “brain fog” is often used in this context, but to me, it seemed more like a mist through which he could very dimly see or perceive what he was struggling to recall; the frustration – desperation, perhaps – that he felt at his inability to grasp, hold, then voice these elusive thoughts was pitiful.

The author in her laboratory. Author provided

I often took him to talks on topics such as the climate, migration, history and ageing, hoping to keep his mind occupied. He seemed to understand many of them, but afterwards, he was quite unable to discuss them, as his memory and ability to speak were declining inexorably. Communication of any type between us was slowly becoming impossible, although he was the person with whom I had once shared my thoughts and hopes, just as he had done with me, and it became particularly sad and unsettling, as we had had so many interests in common. Eventually came the realisation that I had “lost” him. It was a bereavement – the loss of him as a person, loss of a mind, not the death of a body; he was existing but not really living.

Another common feature of dementia – sudden changes of mood – affected him during these years. He had been a generally gentle, courteous person. But when, at times, the illness overcame his natural traits, he became violently angry, often for no obvious reason. Part of the problem was that his sense of location had faltered and often during the evenings he became convinced that we were about to leave and go “home” to Manchester, a place we had left in 2013. He would ask repeatedly and anxiously when we had to leave to catch the train to get there. Television programmes, even those on historical events, which would have been of particular interest to him, had to be vetted as he lost himself within them. So that after watching one that dealt with, say, the horrors of war, he thought that he was actually living in that frightening world.

Of course, there are so many families going through what my family went through. And there will be many more. That fact has provided one of the main motives for my pursuing my research, despite all the difficulties that have come with it.

Early challenges

During the last five years, studies supporting the idea of a viral role in Alzheimer’s disease have greatly increased. Despite this, there is still much opposition to the concept, while many in the field still ignore it.

I am often asked why there has been such hostility. A charitable explanation is that the possible role of a virus in dementia is difficult for others to assess because it straddles two very different topics: virology and Alzheimer’s disease. Also, many cannot grasp the concept that people can be infected but not affected (asymptomatic, when the virus resides in the brain without causing symptoms) so they dismiss the data. Either way, I have always stressed that many possible factors lead to Alzheimer’s disease – a viral role is just one of them.

My interest in this particular area began, rather unpromisingly, in 1978 when the aforementioned head of institute ended my work contract. The reason he cited was that my research on chromatin, and on the effects of carcinogens on chromatin, was “rather individualistic”. I thought this was an extraordinarily inept criticism, as I had generally been acknowledged as being an innovative researcher, and innovation is surely the key to good research. The funding body offered me a post in Glasgow, but that would have meant leaving my husband and children in Manchester.

Luckily, I was immediately given a home in the lab of a medical virologist friend, Richard Sutton. Sutton was an eccentric and pioneering man. He was dogged and wiley, in an endearing way. It was Sutton who first suggested to me the possibility of viral involvement in Alzheimer’s disease.

The argument for the role of the cold sore virus, herpes simplex type 1 (HSV1), in Alzheimer’s disease was first suggested by American neuropathologist Melvyn Ball in 1984. But he did not pursue the idea in any practical way. Sutton and I carried out what was probably the first convincing experiment seeking the DNA of HSV1 in the human brain. We had predicted that it might be detectable in the brain of immunosuppressed patients because in the absence of an adequate immune system to keep it under control, the virus would be able to multiply. We did indeed find it, and published our results in 1986.

The central concept

HSV1 is mainly transmitted by oral-to-oral contact, causing oral herpes (cold sores). Globally, an estimated 3.7 billion people under age 50 (67%) have HSV1 infection. Most infections are asymptomatic.

Over the years, the supportive data we gathered for the key role of HSV1 in Alzheimer’s led me to propose a central concept: that HSV1 is a major cause of Alzheimer’s disease; that in many people, the virus travels to the brain, probably in middle age, and remains present there in latent (dormant) form, but is frequently activated by episodes of stress, head injury, immuno- suppression and infections. These “reactivations” lead to productive HSV1 infection and inflammation (and consequent damage to the brain) over the years. The accumulated damage leads eventually to the development of the disease.

The possible role of HSV1, specifically, was proposed for three main reasons. The locations of the damage the virus causes in the brain during the rare but extremely serious acute disease herpes simplex encephalitis (HSE) – caused by HSV1 – are precisely the main sites of damage found in the brains of patients with Alzheimer’s disease.

The other reasons for implicating HSV1 were that it is very common, affecting at least 80% of the population (in earlier decades more probably 90%), and its ability to remain dormant in the body for years.

These features meet two main characteristics of Alzheimer’s disease: that it is all too common, and that it almost always waits until old age to strike its victims. Certain other infectious agents are probably involved too, perhaps individually or in combination, but so far these have been less well studied than HSV1.

The laboratory work

I was offered a more long-term prospect for my research in a department of the University of Manchester’s Institute of Science and Technology. The head of the department, John Cronley Dillon, was a larger-than-life character, a bon viveur and art lover, full of novel ideas and wild enthusiasm. He encouraged me to build up a research group (minuscule though it was) and eventually we started the research on HSV1 and Alzheimer’s.

It was known that when a person is infected with HSV1, the virus resides lifelong in the peripheral nervous system (PNS) – the part of the nervous system that doesn’t include the brain and the spinal cord — in a latent state. It is dormant until it is activated by events such as stress. In 1989 we decided to look for HSV1 in the brain, using the technique of polymerase chain reaction, or PCR. We used PCR to examine DNA extracted from autopsy specimens of Alzheimer’s disease patients.

This was the first time PCR, then a new technique, had been used for this purpose. The principle of PCR is to detect a specific sequence in the target DNA by chemically amplifying it, thereby making it vastly more sensitive than the methods used in the previous few studies seeking HSV1 DNA in the brain. However, this method was prone to contamination and could produce spurious data. This meant that my poor PhD student, Gordon Jamieson, spent many frustrating months trying to get it to work satisfactorily. So we were overjoyed when we detected, unambiguously, the DNA of the virus in the brain in 1991.

This was the first microbe to be detected in the human brain (in controls, in the absence of a disease). We were puzzled, though, as to why the virus was present in a high proportion of brains – both control brain specimens (people who had not been diagnosed with Alzheimer’s) as well as the brains of patients who had died with the disease. This near equality of prevalence does not undermine the role of HSV1 in Alzheimer’s, as some in the field have asserted. Many of the control brains were, in fact, infected with HSV1 but were asymptomatic.

So people can be infected but be asymptomatic, indicating that infection alone is not sufficient to cause disease. A very relevant example is that of cold sores which afflict only a proportion (ranging from 20-40%) of those infected with HSV1. The other 60-80% are asymptomatic. Clearly, another factor determines the degree of damage caused by the virus.

Other supporting factors

That was something we identified in 1997 when we discovered that the virus confers a high risk of Alzheimer’s disease when in the brains of people who carry a specific genetic factor. We were extremely excited by this finding, but also apprehensive about adverse reactions of some in the field, as had occurred before when we discovered HSV1 DNA in elderly brains.

So we were even more excited when, after I’d suggested examining cold sore sufferers (via a small blood sample), to find what variant of the specific genetic factor they carried, we discovered that it was the same variant as for Alzheimer’s. In other words, the same variant of the genetic factor conferred a risk of damage in the peripheral nervous system, as well as the central nervous system.

Of course, the question arose as to what it is doing, if anything, in the brain. Is it residing there merely as a passenger, doing little or nothing, or does it cause damage?

We investigated this by examining cerebrospinal fluid (the liquid that bathes the brain) looking for antibodies to the virus. We detected these antibodies in most samples of cerebrospinal fluid, again, consistently, in both Alzheimer’s patients and those in the age-matched control groups. This showed that indeed the virus was not just a passive fellow traveller.

We then decided to find if there were direct links between the effects of HSV1 infection and Alzheimer’s. Very hesitantly, like explorers in a new continent, we infected human brain cells with HSV1, then stained the cells with antibodies to the specific abnormal proteins seen in Alzheimer’s brains – amyloid and tau.

To our surprise and delight we saw accumulations of both types of protein. Also, we found amyloid deposition in the brains of infected mice. However, getting the results published was a Sisyphean task and journal reviewers’ comments were often incredulous.

We subsequently used a very complex technique (in-situ PCR) which revealed that in tissue sections of brain, most of the viral DNA was located very specifically within amyloid plaques. This suggested that amyloid might act to cage the virus, thereby inactivating it. All this work provided strong support for a major role of HSV1 in Alzheimer’s, and much has since been extended by other labs.

We also discovered that anti-herpes treatment was protective because it substantially reduced the damage level in the cell cultures we were testing. This further supported a role for the virus in the disease – and pointed to a potential treatment.

A heretic shunned

But a viral role in the development of Alzheimer’s was still seen as heretical by many researchers, so our papers continued to be rejected by one journal after another.

For academics, having research published in top journals is often central to keeping your job and career progression because of the perceived value to universities (related to university league table rankings, supposed research quality and performance management).

Similarly, almost all of our grant applications over that 25 years were refused, too, which was even more serious as without funding, the people in my lab couldn’t be paid nor materials bought. I was very fortunate in having three successive post-doctoral researchers, Woan-Ru Lin, Curtis Dobson, and especially Matthew Wozniak, who were so dedicated that they were willing to continue to work even when on repeated short-term contracts (sometimes for less than 12 months).

So most of my time was taken up in writing research proposals and filling in application forms, interspersed with writing and submitting articles to journals, and when rejected, trying another. I had to face derision and hostile rants unaccompanied by any meaningful, scientific criticism from reviewers. A typical example was: “This grant essentially centres on a question of belief; are viruses important in Alzheimer’s disease, in my view they are not.”

Each rejection seemed like the end of the world. It was a heart-stopping moment when opening the envelope or email from the funding body and scanning the lines in the hope of finding the words, “I’m pleased to tell you …” – though all too often, I found the words, “I regret to tell you”. I hid, weeping tears of despair, while a part of my brain questioned whether the work really was nonsensical and whether the ideas were just wild fantasies.

At conferences, I was often shunned by prominent people in the field. My poster presentations were too (posters were the poor man’s alternative to giving a talk, a privilege I was rarely given). Although, hearteningly, I found that younger people were interested and excited by the research.

Later, I benefited from the generosity of a colleague, Janusz Kulikowski. Kulikowski was another eccentric who lived an upside-down life, working at night and either sleeping during the day or else amusing himself by lobbing provocative remarks at colleagues. He was really interested in our research, despite working in the totally different field of vision research.

I do realise of course that many others have suffered refusals of grant applications, and I understand how especially heartbreaking it is for those at the start of their career, as it usually means the end of all their hopes and dreams of becoming a scientist. I realise too that I had been exceptionally lucky in being able to do such utterly engrossing work – a continuous, totally fascinating puzzle and challenge – and in having a loving family.

But after each rejection my fear that the work would end was overwhelming. When I did get a grant – any grant – I was elated: the world sparkled. I was so happy and exuberant, not just with the funding but with the fact that some people in the field were supportive of, or at least willing to consider, a possible role for HSV1. I felt so encouraged, vindicated and ready to face any challenge in my work or from fellow scientists, and brimming over with ideas for new approaches.

Quite often in the later years, some strongly supported our central concept. But there was a huge divide between them and its opponents. And the hostility continues to this day. In 2019, an application by a colleague to a US funding body for a clinical trial of an antiviral for Alzheimer’s was refused. I was involved as an adviser because it was based on my lab’s research, though I was not an applicant.

One reviewer said: “This application is peripherally related to the idea that Human Herpes Virus (HHV) infection could play a role in Alzheimer’s disease pathogenesis … the evidence is weak, the supporting data are weak.” The second reviewer proclaimed: “The novelty of this approach appears to be quite lacking. The suggestion of latent microbe-based activation by (unknown) factors coincident with a ‘deteriorating immune system’ as the cause for Alzheimer’s seems like hand waving”: poetic perhaps, but hardly a brilliant display of scientific disputation. In fact, no adverse comments had ever been supported by any scientific argument, despite a public assertion once by a senior government official that the HSV1/Alzheimer’s work had been refuted (though when challenged, he was unable to cite any such article).

Most researchers acknowledge that new, surprising and challenging ideas should be viewed with caution. But ideas should not be dismissed without any deliberation. Perhaps another major reason for the hostility is that many people in the field have been working for several decades on amyloid as a cause, and so are understandably distressed on learning that it might not be a direct cause, except in rare familial cases. This occurs despite our repeatedly stressing that numerous factors contribute to Alzheimer’s and amyloid is clearly an important feature.

Exciting developments

But, as the Columbia University study shows, attitudes to the topic of Alzheimer’s and HSV1 are slowly, but steadily, improving. Of course, I am very happy about this, for the sake of patients and their carers. And I have to admit that recognition of the work on HSV1 is personally gratifying as, like most people, I am heartened to know that my work has achieved something.

I am pleased that the research that I and others are carrying out is now moving forwards in even more exciting directions, including the use of a 3D bioengineered human brain model which, when infected with HSV1, displays many Alzheimer’s-like characteristics.

We are now investigating the effects of infectious diseases and a possible role for vaccinations. This follows an explanation I published with my then-senior post-doctoral associate, Curtis Dobson, to account for the finding that certain vaccines decreased the risk of Alzheimer’s disease. We suggested that infections might reactivate latent HSV1 in the brain and that vaccines might decrease the consequent risk of Alzheimer’s disease by reducing the occurrence of such infectious diseases.

For example, in the case of shingles – which is caused by another type of herpes virus, varicella zoster virus (VZV) – a recent study I carried out with Manchester University epidemiologists showed that vaccination against the disease may protect against the development of Alzheimer’s. Two subsequent studies showed the same result. However, much further work needs to be done to elucidate the findings that certain types of vaccine appear to reduce the risk of Alzheimer’s.

Scraping of a skin lesion showing characteristic giant cells in a patient with chicken pox (Varicella Zoster Virus), a type of herpes. Shutterstock/David A Litman

I, along with researchers at Tufts University, then decided to find out if VZV (which also causes chickenpox) plays a role similar to HSV1 in causing brain damage leading to the development of Alzheimer’s.

Our results showed that VZV infection of the cells does not lead to the formation of the main characteristic Alzheimer’s features in the brain. However, VZV infection does result in certain other Alzheimer’s-like features, including increased inflammation. And – importantly – VZV was seen to reactivate the latent HSV1 infection in the brain model, with the consequent occurrence of Alzheimer’s-like characteristics. This is consistent with our suggestion that infections reactivate latent HSV1 in the brain.

The recent evidence that another herpes virus, Epstein Barr, is a cause of another brain disease (multiple sclerosis) strengthens the likelihood of viral involvement in certain other such diseases.

We now plan to find out if other infections cause HSV1 reactivation from latency. If they do, the obvious corollary would be to try to limit infections by vaccination, and by improving standards of hygiene and living conditions – a particular need in developing countries – to reduce microbial transmission.

In addition, we now have some exciting preliminary findings suggesting that percussive brain injury (for example, concussion) can cause HSV1 reactivation. This is a very different type of injury from infection and the results suggest that the virus might be pivotal in the brain’s response to diverse types of damage.

This is an exciting field of study and I hope bright young scientists will enter it. Nobody said being a scientist was easy, but with the right encouragement from family, friends and open-minded peers, it is amazing what challenges can be overcome.

Ruth Itzhaki, Professor Emeritus of Molecular Neurobiology at the University of Manchester and a Visiting Professorial Fellow, University of Oxford

This article is republished from The Conversation under a Creative Commons license. Read the original article. For you: more from our Insights series:

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COVID: inhalable and nasal vaccines could offer more durable protection than regular shots
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Sheena Cruickshank, University of Manchester

As the pandemic continues, many countries are rolling out COVID booster vaccines. In the UK, the autumn booster campaign is offering a fourth dose to those at higher risk from a COVID infection, including people with certain underlying medical conditions, and those aged over 50.

The autumn booster shots are bivalent vaccines, meaning they target the original strain of SARS-CoV-2 (the virus that causes COVID-19) alongside the omicron variant.

These vaccines are effective at topping up and broadening our immunity. But we expect that, as we’ve seen with the original COVID shots, the protection they provide, particularly against becoming infected, drops off in the months afterwards.

So we need to consider a vaccine strategy that will provide longer-term immunity. A new kid on the block – mucosal vaccines – could offer promise on this front.

Mucosal vaccines are delivered in your nose or throat, as sniffable or inhalable formulations. They may sound new but actually we’ve been using them for years to vaccinate against diseases such as flu.

While conventional needle-in-your-arm vaccines induce a more systemic immune response, mucosal vaccines do something different. Viruses such as SARS-CoV-2 enter our systems via our nose and mouth when we breathe in small virus-containing droplets. This means immunity in our nose, mouth and throat really matters to stop infections.

Mucosal vaccines are designed to target this “mucosal immune system”. The mucosal immune system has the potential to stop the virus in its tracks when it enters the body, so scientists predict that mucosal vaccines could prevent infection.

Mucosal immunity may also be better at getting our immune system to remember SARS-CoV-2. Memory cells are specialised long-lived immune cells that remember the virus and carry instructions for our immune cells to be quickly deployed if it attacks again. Systemic vaccines are not so good at activating the memory cells in our nose and throat, but mucosal vaccines are.

Meanwhile, the fact that mucosal vaccines work locally could mean a smaller dose is needed. This, coupled with less stringent storage requirements compared with some conventional vaccines, may mean mucosal vaccines could be deployed more efficiently in resource-poor countries and be an important tool for vaccine equity.

Mucosal vaccines would probably also be a lot more appealing to those with needle phobias. Roughly 26% of the UK population admit to being afraid of needles, with the highest rates of phobia seen in youth, black and Asian groups – groups we know have lower vaccine uptake and more vaccine hesitancy.

Mucosal vaccines could make a big difference for people with needle phobias. Gatot Adri/Shutterstock

The advantages are clear – but what does the evidence say?

Several mucosal vaccine candidates are being explored in pre-clinical and clinical trials. Results just published on a nasal booster vaccine in mice showed that robust mucosal immune responses were induced in the nasal and upper respiratory tracts.

Similarly encouraging results have been reported in macaque monkeys and hamsters. Several trials are underway to see if these results can be replicated in humans.

Iran, Russia, India and China have already introduced mucosal vaccines despite published data on their candidate vaccines remaining sparse. But some data has been publicly released.

Results from phase II human trials of an inhalable vaccine, now being rolled out in China, were released as a preprint (a study yet to be peer-reviewed). While the study didn’t assess mucosal responses, it did show that systemic antibody levels were higher and remained higher over the six months assessed compared with a conventional booster.

But the picture is mixed. A phase I trial of a nasal formulation of the Oxford AstraZeneca vaccine showed little to no induction of mucosal immunity and weaker systemic antibody responses compared with a conventional vaccine.

The reasons for these disparities are not clear, but they could include the method of delivery. The administration of mucosal vaccines requires precise engineering and aerosol science to ensure the small droplets containing the vaccine are easily inhaled.

Several strategies have been used to deliver mucosal vaccines including nebulisers (a machine that turns liquids into a fine mist that can be inhaled), nasal sprays and inhalable devices like the inhalers asthmatics commonly use.

The particle size, formulation (the ingredients and how they’re combined), as well as the vaccine’s ability to stick to and enter our cells will all affect how effectively the vaccine particles are taken up in the body. This is called the vaccine’s “bioavailablity”. We still have a lot to learn about which delivery strategy is optimal for which vaccine.


So where does this leave us?

This pandemic is still very much ongoing. And we’re learning more all the time about the long-term implications of COVID infections on our health, including heart complications and long COVID.

This, coupled with the emergence of ever-more persistent variants, mean it’s important to keep protecting ourselves and our loved ones from the worst effects of the disease. Vaccines are some of the best weapons we have.

It will be important to watch and learn from the mucosal vaccine rollout in other countries and scrutinise their data when it’s released.

Meanwhile, given the urgent need for long-term vaccines, it would seem prudent to invest in strategies, not just for the development but also the manufacture of such vaccines. They could be an invaluable tool in this pandemic, but also against many other infections, including those we have yet to encounter.The Conversation

Sheena Cruickshank, Professor in Biomedical Sciences, University of Manchester

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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Funding awarded to researchers exploring the role of community assets in improving health outcomes.
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The Arts and Humanities Research Council (AHRC) has awarded researchers at The University of Manchester funding to partner with local communities to tackle health inequalities across the UK.

The award comes as part of a new wave of research projects announced to investigate the role of community assets such as parks and galleries in improving health outcomes. The projects are funded as part of the second phase of the £26 million, UK Research and Innovation (UKRI) Mobilising Community Assets to Tackle Health Inequalities investment. This multi-year research programme is funded primarily by the Arts and Humanities Research Council (AHRC) and aims to use existing local resources to create a fairer and healthier society.

Building on previous success; 
The first phase of the programme was announced earlier this year and funded projects which looked at how to scale up small, local approaches to tackle health inequalities. This second phase is a consortia-building phase, which will fund 16 projects up to £250,000 each to facilitate cross-partner collaboration, incorporating relevant non-academic partners, including community groups and health system organisations. 

These consortia will conduct new research and develop community asset hubs with the aim of coordinating large-scale projects for their communities as part of the final phase of the programme to be launched in 2023.

Organisations of Hope, led by Principal Investigator, Dr Simon Parry, explores how creativity, culture and heritage address inequities in Greater Manchester, with an initial focus on mental health and dementia.  It will build a creative health coalition in Greater Manchester from a diverse group of organisations and individuals that represent communities, cultural organisations, charities, health and care providers and local government. The partners will work together to understand how existing creative health assets can improve health and wellbeing and increase equity by tackling the social determinants of health. 

The initial group includes researchers from The University of Manchester and King’s College London; key staff from the Greater Manchester Integrated Care Partnership, its flagship organisation Dementia United and the Greater Manchester Combined Authority; as well as charities who work with communities like Cartwheel Arts, Action Together and 42nd Street.

For more information, please contact:

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Gene mutations should be tested routinely for ovarian cancer, say scientists
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