AN HIV DRUG could stop one of the early changes in skin cancer cells that leads to them becoming resistant to treatment, according to a Cancer Research UK-funded study published in Cancer Cell* today (Monday).  

The researchers looked at melanoma skin cancers from 11 patients who had started standard treatment for the cancer**. They found that the cancer cells used a molecular switch to temporarily rewire themselves to become more able to withstand the drugs in the first two weeks of treatment, and then went on to develop permanent resistance through genetic changes.

The HIV drug, called nelfinavir, works by blocking the molecular switch which boosts cells’ ability to survive treatment. The research, carried out in mice, suggests that nelfinavir could be used in combination with standard skin cancer treatments to make them more potent and delay drug resistance, making available treatments effective for a longer period of time.

Professor Claudia Wellbrock, lead author from The University of Manchester, said: “In the first few weeks of standard treatment for skin cancer, the cancer cells become stronger and more robust against treatment.

“But if we can target skin cancer cells before they become fully resistant, we would have a much better chance of blocking their escape. And we think this research has brought us one step closer to making this a reality.”

Professor Nic Jones, Director of Cancer Research UK’s 91Ö±²¥ Institute, said: “Melanoma can be difficult to treat because the cancer becomes resistant to drugs quite quickly. But this exciting research means we might be able to fight back by blocking the first steps towards resistance, so that treatments are effective for longer.

“While drug resistance is a big challenge, we’re making great progress. Drug resistance in late stage skin cancer is still a big problem and something we need to tackle. We’ve seen big steps forward recently with the development of immunotherapies but this exciting approach could stop skin cancer developing resistance at an earlier point.”

NOTES FOR EDITORS

The image shows a group of cancer cells that have been treated with a drug targeting the MAPK pathway. The red cells (and yellow areas) are dying, the green cells are still alive.

For media enquiries please contact Fiona Dennehy on 020 3469 8300 or, out-of-hours, the duty press officer on 07050 264 059.

Or:

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 *Smith et al., Inhibiting drivers of non-mutational drug-tolerance is a salvage strategy for targeted melanoma therapy. Cancer Cell, 2016. DOI: 10.1016/j.ccell.2016.02.003.

**The researchers analysed melanomas from 11 patients undergoing treatment with vemurafenib or a dabrafenib and trametinib combination which are FDA approved. NICE recommends vemurafenib as a possible treatment for metastatic melanoma. Dabrafenib and trametenib combination treatment is under review by NICE and a result is expected in August 2016.

Working with medical colleagues across the world, Professor David Denning has entered the history books by publishing 15 scientific papers on the same day – providing 15 countries with evidence to combat the burden of fungal disease.

The surprising results demonstrate that whilst a high number of genetic changes have been recorded in the virus, it hasn’t changed at a functional level to become more or less virulent.

The findings, published in the journal Virology, demonstrate that the much higher death toll during the current outbreak, with the figure at nearly 10,500, isn’t due to mutations/evolution making the virus more deadly or more virulent.

Professor Simon Lovell from the Faculty of Life Sciences explains: “Using data from every outbreak since 1976 we were able to highlight what changes there had been in the RNA of the virus and then using specially developed tools predict the consequences of those changes. What we found was that whilst Ebola is mutating, it isn’t evolving to the point of adapting to become more or less virulent. The function of the virus has remained the same over the past four decades which really surprised us. Unfortunately this does mean the Ebola virus that has now emerged on several occasions since the 1970s will very probably do so again.”

Professor David Robertson says the findings can be seen as good news: “The fact that Ebola isn’t changing in a way that effects the virulence of the disease means that vaccines and treatments developed during this current outbreak have a very high chance of being effective against future outbreaks. It also means that methods to successfully tackle the virus should work again, so hopefully in the future an outbreak can be stopped from spreading at a much earlier stage.”

The team used a computational approach that PhD student, Abayomi Olabode, developed for analysing changes in HIV-1. This had highlighted adaptions within the virus in the context of protein structure. When they used it to study Ebola they expected to see similar things but didn’t.  

Professor Robertson points out the advantages of the computer-based approach: “We were able to do this research quickly and whilst the Ebola outbreak was still ongoing. The data generated by Gire et al. in 2014 was all freely available and our analysis technique is a safe way to study the virus without unnecessary exposure. This type of study could be used on future outbreaks to analyse what is happening in real time within the virus. This level of surveillance will only become more essential in the fight against contagious illness as we live in an increasingly globally connected society.”

The team also stress that, counter-intuitively, analysis is needed to identify when a virus becomes less potent. This is because infected individuals could potentially infect more people if they did not progress to severe illness. The deadly nature of Ebola means the symptoms can be identified at a relatively early stage and those who had been in contact with the patient during the infectious stage readily identified by contact tracing. If it becomes less deadly then it may take longer to spot those symptoms, if they can be spotted at all, or for the person to become ill increasing the chance of spreading the virus. An attenuated virus, although less deadly on an individual basis, could spread widely and thus ultimately cause many more deaths. 

Professor Tony Redmond from the University’s Humanitarian and Conflict Response Institute helped to coordinate the NHS response to Ebola in West Africa: “Like any medical response, the response to ebola must be supported by science. These are very important findings and emphasise that the spread of the virus in this outbreak owed as much to factors within the human community than within the virus itself.”

Professor Lovell concludes: “Our study demonstrates the vital role computational analysis can play during a virus outbreak. As scientists our role is to worry about the potential changes our research tool allows us to map what is happening within a virus and the consequences of any changes. Ebola will occur again, and it’s only through such close monitoring that we will contain it and ultimately eradicate it.”

Notes for editors

The paper “Ebola virus is evolving but not changing: no evidence for functional change in EBOV from 1976 to the 2014 outbreak” will be published in the journal Virology.

Data used from Gire, S. K. et al. (2014) Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak. Science 345, 1369-1372, doi:10.1126/science.1259657.

For image and interview requests please contact:

Morwenna Grills
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The University of Manchester

Tel: +44 (0)161 275 2111
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At the event in Seattle, USA, policy makers, doctors and researchers from around the world called for immediate action on fungal infections to save lives across the world. They were speaking at the world's first stakeholder meeting on fungal diseases, hosted by (Global Action Fund for Fungal Infections) and convened by The University of Manchester’s Professor David Denning, GAFFI’s president

Currently about 1,500,000 people die of AIDS and its complications each year. Probably 25-33% die of fungal infections, although exactly how many is not clear because of a lack of access to effective diagnostic tests. Over 400,000 are thought to die of aspergillosis complicating TB, yet diagnostics are not available in many countries.

GAFFI President and Professor of Infectious Diseases in Global Health at The University of Manchester, , convened the meeting in Seattle. He commented: “The toll due to fungal diseases is over 1 billion people, yet these diseases are poorly represented by most global health organisations and national public health bodies. Burdens vary by geography, country, co-infections, hospital hygiene and agricultural practices. Even though the global antifungal pharmaceutical market is about $8 billion and growing at 2-3% annually, there are a limited number of useful antifungals.”

Over 60 experts from major health agencies, including the World Health Organization, UNAIDS, Bill and Melinda Gates Foundation, Office for Global AIDS Coordination (PEPFAR), Centers for Disease Control –– and representatives from over 30 countries –– gathered to align efforts to improve management of fungal infections. 

Participants highlighted the lack of diagnostics and access to treatments, including the oldest antifungal drugs, that are major hurdles to improvements in many developing countries.

A new and preliminary economic model to analyse costs associated with treatment and care of fungal infections in Africa was introduced at the meeting.  The model indicated that early screening and treatment, before meningitis or pneumonia develop, is cost effective and could save patient lives.  If implemented, this regimen could potentially save $500 million and up to 140,000 lives annually, compared with later treatment.

TB is second only to HIV/AIDS as the greatest killer worldwide due to a single infectious agent. A common complication of TB is ‘chronic pulmonary aspergillosis,’ a lung fungal disease that mimics TB, and needs to be treated with antifungal drugs.

Diagnosis requires a simple antibody test, which is not available in many countries, especially in Africa. Incorrect diagnosis and treatment is therefore a common occurrence. An estimated 1,200,000 people suffer from this complication of TB, and most are never diagnosed or treated. GAFFI recently petitioned the WHO to make the key oral drug for this infection, itraconazole, an Essential Medicine.

Professor Denning continued: “Discussions covered many of the gritty problems facing patients unlucky enough to develop a serious fungal infection: from lack of knowledge amongst doctors, slow or non-existent diagnostics, to costly or unavailable generic antifungals. The time for action and alignment among AIDS and TB policy makers is now.”

Stakeholders jointly committed more action, collaboration and serious attention to the topic. “More should be done to reduce deaths,” Dr Swarup Sarkar from UNAIDS said during his presentation on the economic and AIDS deaths modelling. He continued: “Many people living with HIV are starting antiretroviral treatment too late and die prematurely as opportunistic infections take hold. This can be prevented if efforts are urgently scaled up to ensure the timely diagnosis of HIV as well as early screening and treatment of opportunistic infections.”

“There is much progress, but a lot is still to be done," he said after meeting with the President of Sierra Leone, and senior leaders of the international presence there including the UK Department for International Development, Ministry of Defence, World Health Organisation, United Nations, and Red Cross.

He was travelling with the  (IMC), a leading humanitarian health organisation, and one of the earliest responders to the crisis. Touring the IMC Ebola Treatment Centres deep in the countryside of Sierra Leone and Liberia, he said, “Panic, ignorance, and prejudice is what this virus survives on. To control it, we must be scientifically informed, and coolly calculating.”

He paid tribute to local communities and health workers who have borne the brunt. He applauded the doctors, nurses, and laboratory scientists from the UK National Health Service, and from hospitals in the United States and other countries working there, saying: “Their professionalism and meticulous daily work at the frontline of the epidemic is indeed helping to turn the tide.”

“Although we are now chasing Ebola instead of Ebola chasing us, there can be no faltering," says Professor Kapila.

“This epidemic is yet another wake-up call to do better to reduce poverty, improve heath and education and, above all else, bring decent governance in such countries.”

Professor Kapila was a UK Government adviser deeply engaged in Sierra Leone and Liberia more than 20 years ago during the civil wars there. Returning for the first time since then, he reflected: “What happened to all the international post-conflict aid that was poured in? Can we learn the right lessons now?

“What direction we take now – as Ebola recedes – is vitally important not just for West Africa but also for the rest of the world. As we have learnt from AIDS, SARS, Avian flu, and now Ebola, such conditions know no boundaries,” he said.

Professor Kapila is a leading humanitarian and health expert who has held leadership positions in the UN, World Health Organization, International Federation of Red Cross and Red Crescent Societies, and UK Department for International Development.

He teaches on the postgraduate course in  and undergraduate degree courses in . He is also part of the 91Ö±²¥ Academic Health Sciences Centre () Global Health Theme, a partnership between the University and six NHS Trusts in Greater 91Ö±²¥, where he advises on global health development and how health workers can support medics coping with natural and humanitarian disasters overseas.

Another University academic, Dr Amy Hughes, has been leading NHS volunteers in Sierra Leone. Read about her recent award from the Prime Minister .

The World Health Organization (WHO) has officially partnered with a research centre at The University of Manchester which promotes improvements in women’s health in low and middle income countries.

will work with WHO for four years, sharing expertise to help develop international guidelines for policy and practice, and training materials for midwives and skilled birth attendants working to improve labour and childbirth outcomes.  

The Director of the Centre, r said: “This accreditation is great news for us as it cements our relationship. Working with this major organisation can only assist in reducing childbirth associated mortalities and morbidities and improving care of mothers and babies.

“The work we do with our partners in Africa makes a huge difference to midwives and of course women, so, ultimately, the support of the WHO will allow us to do that more effectively.”

The designation builds on the Centre’s strong track record of working with the WHO, and allows the team in 91Ö±²¥ to maximise the impact of its growing portfolio of research, training and clinical practice activities aimed at reducing maternal mortality and morbidity.

Researchers from the Centre work very closely with midwives in East Africa, playing a leading role in the Lugina Africa Midwives Network () which offers mentoring and research training for health workers in six African countries. Midwives in the Network have identified research priorities, and have designed and carried out research on clinically important topics such as postnatal infection, neonatal emergencies, fistula care, prolonged labour and HIV.

Professor Lavender said: “We work with inspirational midwives who are working with limited resources and few developmental opportunities. The Centre for Global Women’s Health is helping to support them in their work.” 

The 91Ö±²¥ Centre joins more than 700 designated Collaborating Centres worldwide, working to support WHO’s international programmes. Professor Lavender said: “It is an honour to be associated with the WHO. Being a formal partner in this global network is a way of sharing good practice, finding solutions to childbirth problems and giving women the care that they deserve.”

Notes for editors

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Experts have found that clothes put on drying frames or draped over warm radiators raise moisture levels in our homes by up to 30 per cent, creating ideal breeding conditions for mould spores – and one in particular called aspergillus fumigatus, which can cause potentially fatal lung infections.                                                                 

Father of three, Craig Mather from Bolton knows first-hand the damage it can do. For years he dried washing in his bedroom and thought nothing of it. But when he contracted TB in 1997, the disease left his lungs weak, and aggravated the problems he had been left with after childhood asthma.

Craig, who is 43 and a fast food manager, explains: “I only started to recover when my consultant diagnosed chronic pulmonary aspergillosis and prescribed me special drugs to fight the fungal infection. However, I noticed coughing fits and night sweats – particularly when I had wet washing drying on the warm bedroom radiator.

“He told me that it could be making my problems worse, so for the last 12 months I haven’t dried my clothes indoors and I’ve noticed a huge improvement in my health. I can’t do strenuous physical activity, but I am off the drugs and only have to go back to the clinic for check-ups every four months – and I’m able to ride my bike again.”

and his team at the , in 91Ö±²¥, have issued the wet washing warning after treating a growing number of patients who have developed the condition from inhaling the Aspergillus fungal spores.

Dr Denning, who is Professor of Infectious Disease in Global Health at The University of Manchester explains: “It’s estimated that as many as 87 per cent of us dry our clothes indoors in the winter. One load of wet washing contains almost two litres of water, which is released into the room.

“Most of us are either immune to the fungus which grows in these humid conditions, or have a sufficiently healthy system to fight the infection. But, in asthma sufferers it can produce coughing and wheeziness, and in people with weak or damaged immune systems, such as cancer patients undergoing chemotherapy, Aids patients and people who, like Craig, have an auto-immune disease, the fungus can cause pulmonary aspergillosis – a condition which can cause irreparable, and sometime fatal, damage to the lungs and sinuses.

“My advice would be when in doubt, dry wet washing outside, in a tumble dryer or in a well ventilated indoor space away from bedrooms and living areas.

“Be safe rather than sorry,” he adds.

Notes for editors

For more information please contact Susan Osborne, Director of Communications at The Goodwork Organisation on 07836 229208.

The researchers from 91Ö±²¥ are joining colleagues from the Escola Paulista de Medicina-Federal University of São Paulo () to examine the prevalence and treatment of chronic pulmonary aspergillosis.

This infection is thought to affect over 17,850 people in Brazil, with 5,600 new cases every year. Follow up of patients with tuberculosis in Brazil in the 1980’s showed 21% to have evidence of Aspergillus infection, similar to the UK.

Yet chronic pulmonary aspergillosis is rarely diagnosed or treated in Brazil, because of a lack of awareness and diagnostic testing. As well as those with tuberculosis, patients with AIDS, asthma and chronic obstructive pulmonary disease are also susceptible to this infection, so actual numbers of sufferers may be twice what is currently recorded.

The University of Manchester’s is based at University Hospital of South 91Ö±²¥ NHS Foundation Trust (UHSM) and will lead the UK side of the new initiative.

He said: “While we treat nearly 400 UK patients with this condition, across the world, there are estimated to be about 3 million. Currently very few are diagnosed or treated, and after five years about 75% have died. This international program will have an impact throughout Brazil and Latin America.”

Funded by with matching funds from The University of Manchester, the programme encourages scientific exchange between universities in São Paulo and 91Ö±²¥, and will involve a study of patients from 17 hospitals in the Brazilian city.

Professor Arnaldo Lopes Colombo of (UNNIFESP) added: “This collaboration is of the utmost importance to Brazil in view of the huge number of undiagnosed fungal infections in the country. We aim to really understand who gets this long term, difficult to treat infection and improve our diagnostic techniques across the country.”

Notes for editors

For media enquiries, please contact Jamie Brown | Media Relations Officer | The University of Manchester | +44(0)161 275 8383 | Jamie.brown@manchester.ac.uk |

A commonly-used HIV drug has been shown to kill-off the human papilloma virus (HPV) that leads to cervical cancer in a world-first clinical trial led by The University of Manchester with Kenyatta National Hospital (KNH) in Nairobi.

Notes for editors

For further information, please contact Alison Barbuti, Media Relations Officer | Faculty of Medical and Human Sciences | The University of Manchester Tel: +44(0)161 275 8383 Email: alison.barbuti@manchester.ac.uk.

A University of Manchester professor and his wife have had their own DNA analysed for compatibility as part of the research for a new book out this week (August 29).

Professor Daniel Davis and his wife Katie’s experience is documented in The Compatibility Gene, published by Penguin, which discusses how our crucial compatibility genes may influence finding a life partner as well as our health and individuality.

Professor Davis said: “We each possess a similar set of around 25,000 human genes. Some of our genes vary from person to person, like those that give us a particular eye or hair colour. But my book is about the few genes – our compatibility genes – that vary the most between each of us. First and foremost these are immune system genes; they control how we combat disease. But recent research shows that they may be even more important than we once thought – there is evidence that they can influence how our brains are wired, how attractive we are, even how likely we are to reproduce.’’

“I’m used to writing academic papers looking at particular cells and genes but I had to write this book to highlight the wonder of this new research – take stock of the big picture - and make this fascinating new science accessible to everyone.”

The book explains how research has radically transformed knowledge of the way our bodies work - with profound consequences for medical research and ethics. The story begins with a small band of scientific pioneers who, during the Second World War, struggled to understand the mysteries of transplants and grafts. And continues to the Swiss zoologist who had people rank the sexiness of smells from worn T-shirts - and found the results related to our compatibility genes. Very recent experiments discussed in the book show that these same genes may also influence the likelihood of problems in pregnancy.

Professor Davis, Director of Research at the University of Manchester's Collaborative Centre for Inflammation Research, said finding out more about his and his wife’s genetic make-up had been a surprisingly nerve-wracking experience. The couple had their saliva sent to the Anthony Nolan Trust – a UK charity that helps match transplantation donors and recipients.

“The tubes were bar- coded and shuffled down a series of robotic instruments that first isolated the DNA and then made copies of our compatibility genes,” Professor Davis said. “Small beads, each having a different short piece of DNA attached, were added to a solution containing our genes. Beads with DNA just right to bind to one of our compatibility genes are picked out by a sensor, revealing which versions of these genes we have.”

Professor Davis discovered his compatibility genes were quite rare, while his wife’s were more common. One group of his genes were frequently found in Europe, particularly Eastern Europe, while the other set were common in India or Australia. His wife found she had a gene which would be helpful if she ever suffered an infection with HIV but which also increased her susceptibility to the auto-immune disease ankylosing spondylitis.

He said: “It’s not that any of my individual genes are unusual, but the combination of them is rare because they are usually found in different parts of the world. After being pleased that my genes were quite rare - which according to those smelly T-shirt experiments would mean lots of women would like my scent - I then realised this might not be so useful if I ever needed a transplant. In fact the advice they gave me was: Just don’t get ill!”

So does the book reveal the perfect set of genes? Professor Davis concludes: “Overall, nobody has a better or worse set of compatibility genes: there’s no hierarchy in the system. The fact that we differ is what’s important; the way our species has evolved to survive disease requires us to be different.”

To watch Professor Davis and his wife Katie on BBC Breakfast television, please click .

ENDS

Notes for editors

For further information or to request an interview with Professor Daniel Davis, please contact Alison Barbuti | Media Relations Officer | The University of Manchester

Tel. +44 (0)161 275 8383 | Mobile 07887 561 318 |Email: alison.barbuti@manchester.ac.uk

Professor Davis is available over the Bank holiday weekend.

Images available on request.

The Compatibility Gene By Daniel M. Davis is published in Allen Lane hardback, £20.00, on 29 August 2013. Ebook available.

Professor Davis is director of research at the University of Manchester's Collaborative Centre for Inflammation Research and a visiting professor at Imperial College, London. He has published over 100 academic papers, including papers in Nature and Science, and Scientific American, and lectures all over the world, including at the Royal Institution. He has previously won the Oxford University Press Science Writing Prize.

For further information about the book in the UK, please contact: Thi Dinh 020 7010 3156 / thi.dinh@uk.penguingroup.com

Globally and annually, over 300 million people suffer from serious fungal infections, resulting in 1,350,000 deaths – many of which are unavoidable.

Most serious fungal infections are hidden, occurring as a consequence of other health problems such as asthma, AIDS, cancer or organ transplants. Delays or missed diagnosis often lead to death, serious chronic illness or blindness.

Now, the newly formed multidisciplinary 91Ö±²¥ Fungal Infection Group (MFIG) hopes to make a difference with the recruitment of three leading experts from Edinburgh and London.

Professor Nick Read has moved from Edinburgh University and leads the group, while Dr Elaine Bignell from Imperial College, London, has been appointed as a Reader, and Dr Mike Bromley as a lecturer. 91Ö±²¥ senior lecturers, Dr Paul Bowyer and Peter Warn will also join the MFIG and will work alongside the already thriving research and teaching teams of Professors David Denning and Malcolm Richardson, and Dr Riina Richardson, to form this pioneering Group.

Professor Nick Read is an internationally-renowned fungal cell biologist with over 30 years of research experience and has pioneered the use of advanced live-cell imaging techniques with many fungi, including human pathogens.

Professor Read said: “The opportunity to develop cutting-edge, multidisciplinary science in the relatively neglected but extremely important topic of fungal infection will be internationally unique and I am very excited to be able to join and lead this team of talented scientists in 91Ö±²¥.”

The focus of the MFIG going forward is developing a profound understanding of the biology of the mechanistic basis of * fungal infection, identifying new antifungal drugs and human genetic risk profiling. The team will also work with the a partnership between The University of Manchester and six NHS Trusts which helps health care organisations reap the benefits of research and innovation to drive improvements in care.

Professor Ian Jacobs, University of Manchester Vice President and Dean of the Faculty of Medicine and Human Sciences added: “I am excited by the combination of strong clinical leadership, exemplified by the National Aspergillosis Centre, and internationally competitive science, which these new appointments bring. This fits perfectly with the strategy of our Faculty to develop outstanding science in to health benefit. MFIG can have an impact in the UK and internationally in a neglected area which is responsible for enormous suffering and over a million deaths every year.’’

ENDS

Notes for editors

For more information please contact Alison Barbuti | Media Relations Officer | Faculty of Medical and Human Sciences |The University of Manchester Tel. +44 (0)161 275 8383| Mobile 07887 561 318 |Email: alison.barbuti@manchester.ac.uk>

Certain types of papilloma virus might actually prevent cervical cancer, according to a new study by researchers from The University of Manchester.

There are over 100 different types of human papilloma virus (HPV). Cervical cancer is known to be caused by infection with approximately 14 so-called “high-risk” types of this virus. Researchers from 91Ö±²¥ looked at the different types of HPV found in cervical smears and invasive cervical cancers from HIV positive and HIV negative women in Kenya. They found high numbers of a specific type of HPV (type 53) in normal cervical smears from HIV positive women, but this was rarely found in HIV negative women. This sub-type was also never found in cervical cancers from either HIV positive or negative women.

Dr Ian Hampson, a Senior Lecturer in Viral Oncology from The University of Manchester who lead the study, said: “It is well known that HIV increases the number of different types of HPV found in any one patient which implies that HIV opens the door for infection with multiple types of HPV. If only high-risk types are present these will undoubtedly accelerate progression to cancer whereas if other types (eg type 53) are also present they may actually compete with the high-risk types to inhibit progression to cervical cancer.”
 

There are 270,000 deaths from cervical cancer globally each year with 85% of these occurring in countries with low resources. In Kenya it is the most common malignancy accounting for between 18 and 23 per cent of all diagnosed cases of cancer.

The study looked at women at samples taken from women in Kenya and results were analysed at The University of Manchester’s Viral Oncology Laboratories based at the Saint Mary’s Hospital. Completed by Dr Ian Hampson, Dr Lynne Hampson and Dr Innocent Orora Maranga the results have been published in The Open Virology Journal. The research is part of the 91Ö±²¥ Cancer Research Centre, a partnership between The Christie Hospital, The University of Manchester and Cancer Research.

Dr Hampson said the study suggested one possible explanation for why, in spite of a large increase in the numbers of HPV infections in HIV positive African women, there was not a corresponding increase in numbers of cases of cervical cancer. This could also explain why another African study had actually shown the risk of developing one specific type of cervical cancer actually dropped in HIV positive women, he said.

The researchers now plan to do more research in this area. “Our study was quite small and more research with larger sample numbers is now needed,” Dr Hampson said. “We also need to work out exactly how one type of HPV might suppress the cancer causing properties of another. If it can be proved that HPV type 53 can inhibit the cancer-causing properties of other high-risk types of HPV, this could potentially form the basis of a simple biological therapy to prevent this disease. This could be extremely useful in low resource countries who cannot afford expensive HPV vaccines.”

Notes for editors

The work was published in the Open Virology Journal and was funded by the Humane Research Trust, The Janice Cholerton Post Graduate Support Fund, The Caring Cancer Trust, The Cancer Prevention Research Trust and United in Cancer UK. Dr Maranga was part-funded by awards from the International Atomic Energy Association and Wellbeing of Women.
 

To view the article, please click .
 

For further information contact or to request an interview with Dr Hampson, please contact:
Alison Barbuti
Media Relations
Faculty of Medical and Human Sciences
The University of Manchester
Tel: 0161 275 8383
Email: alison.barbuti@manchester.ac.uk

Professor Terry Brown, working in partnership with Professor Charlotte Roberts from Durham University, used a next generation sequencing approach, including hybridization capture technology, to identify tuberculosis genes in a 19^th century female skeleton found in a crypt in Leeds.

Their study is part of wider research into the identification of strains of TB in skeletons dating from 100 AD to the late 19th century. It's hoped that understanding how the disease has evolved over time will help improve treatments and vaccines. TB rates have been increasing around the world, and it's estimated that one third of the world’s population has latent TB. After HIV it kills more people than any other infectious disease.

Certain strains of TB affect the sufferer's bones, especially in the spine. The marks made by the disease remain evident on the bones long after the person's death. It’s this evidence that Professor Roberts used to find suitable skeletons to screen for tuberculosis genes.

She sourced 500 skeletons from across Europe that showed evidence of TB dating from the Roman period to the 19^th century. Bone samples from these skeletons were screened for TB DNA, and of those 100 were chosen for this particular study.

Professor Roberts explains: "So many skeletons were needed as it's very hard to tell if any DNA will have survived in the bones. You don't really know if there will be any present until you start screening and in the past that has been a lengthy process."

Professor Terry Brown then took on the search for TB DNA in the skeletons. Each small section of bone was ground up and placed in a solution. That was then put in a special machine which captured every gene sequence in the DNA. Millions of sequences were captured and sent to a computer.

Professor Brown and his team then searched for the gene sequences for tuberculosis. Because it is a bacterial disease the bacteria's DNA can remain in the bones after death.

Talking about the process Professor Brown said: "Previously we could only scan the bone sample for specific genes. We wouldn’t see everything that was there which meant we could easily miss other genetic information that could be relevant. Using the hybridization screening meant we could search for different strains of TB, not just one."

About 280 bits of sequence in the DNA were found to match known tuberculosis genes. The data placed the historic strain of TB in a group that is uncommon today, but was known to have been present in North America in the 19^th century. In fact it was found to be very similar to a strain recorded in a tuberculosis patient in New York in 1905.

Discussing the results Professor Brown says: “The fact that this particular strain of TB was found in both North America and in the skeleton from 19^th century Yorkshire is not necessarily unusual. There were many migrants from Britain to America during the 19^th century so it makes sense that TB strains were spread.”

One of the downsides of hybridization capture identified by the researchers in this study was that it is possible to mistakenly identify DNA. Because it looks at all the sequences across the sample it may identify DNA that isn’t from the bone, but actually from the surrounding soil or environment where the skeleton was buried.

In this study the results were checked using the more traditional method of polymerase chain reactions and were found to be accurate. The researchers concluded that using hybridization capture and next generation gene sequencing is an accurate and effective way to obtain detailed genotypes of ancient varieties of tuberculosis. It could potentially be used to study other diseases. Their findings have been published in the journal The Proceedings of the National Academy of Sciences.

Professor Roberts says: “We’re really pleased with the results of this study and that the technology works. It will save a lot of time in the future. We now hope to publish more of the huge amounts of data we have acquired from the sequencing”

The scientists hope to compare their results with similar studies being done in America to assess what tuberculosis strains have been identified there. They’re interested in studying which strains were brought to the country by migrants and what impact those had on the native strains of the disease.

Notes for editors

Images for this story are available from the press office.

Professor Brown and Professor Roberts are available for interviews.

Please contact:

Morwenna Grills
Media Relations Officer
Faculty of Life Sciences
The University of Manchester

Tel: 0161 275 2111
Mob: 07920 087466
Email: Morwenna.Grills@manchester.ac.uk

“The news that Japanese researchers have successfully induced skin cells to behave like viable eggs, which have then been fertilised to create a new generation of mice, may well come to be seen as a scientific milestone.

“Though the research does not necessarily translate into humans, it appears to demonstrate that the genetic material found in every cell in the body can be put to use in the creation of offspring. In principle, this offers infertile women the opportunity to have children that are genetically related, even if they do not have viable eggs of their own: cells from another part of the body could be used and “reprogrammed” to behave as eggs would.

“At the same time, there is likely to be a number of concerns raised about the ethics and legal status of such a procedure. Putting the procedure to use in humans would be illegal under current UK law, since the synthesised eggs would not be what the Human Fertilisation and Embryology Act calls “permitted”.

“From an ethical point of view, there may be concerns raised about the safety of such procedures: for example, would any child created this way have any genetic “booby-traps” that might go off in later life?  It may not be easy to see such dangers when the experimental creature is as short-lived as a mouse. Concerns may also be raised about the idea that this represents creating children to order, and about human dignity.

“These concerns are probably over-done; it is certainly not obvious that they are definitively enough for us to be able to say that this research is in any way sinister.  In respect of the safety worry, for example, as long as the child were to have a life worth living, it is hard to see why it would ever be better for it not to have been created.

“What is more ethically problematic is the question of what it takes to be a mother in the first place.  If we think that someone cannot be a mother without a genetic link to the child she raises, then that would suggest that anyone who wants to be a mother but who cannot generate eggs of her own would have a reason to embrace technology such as this. But it is not at all clear that a genetic relationship is a necessary criterion of motherhood – for example, there are millions of women who adopt, or foster, who count themselves as mothers in a full and rich sense; the same applies to step-parents. Motherhood need not imply a genetic relationship.

“Moreover, it is worth pausing to consider the context of this research. Fertility research is expensive, as is its possible application.  Meanwhile, there are millions of people around the world who lack basic sanitation and who die from easily preventable disease; millions more currently have their lives threatened by malaria, HIV and so on. Hence while breakthroughs like this are, in their own terms, exciting and probably welcome, it is worth pausing to ask whether the money and effort expended might have been worth expending in other fields.”
 

Notes for editors

Dr Brassington is available for comment

For media enquiries

Mike Addelman
Press Officer
Faculty of Humanities
The University of Manchester
0161 275 0790
07717 881567
Michael.addelman@manchester.ac.uk
 

Lenox Green and his wife Heather have spent six evenings a week for the past eight years helping young people have fun in a safe environment, get good advice on a range of issues and achieve their potential.

Lenox has now been recognised at the University’s Social Responsibility and Volunteer of the Year Awards, an event which celebrates the amazing staff, students and alumni who go the extra mile for those less fortunate.

Lenox, a postgraduate office administrator in the School of Mathematics, is so well loved that when a local burglar broke into the centre, his mates made him take the loot back.

“They’re good kids,” he says. “And I get a lot out of it too – every month I get one of those magic moments. Only last week, at the end of the evening a four-year-old girl was waiting for her parents to pick her up and came into the table tennis room where the older kids normally play. I asked her if she wanted a go, she nodded her head, picked up the bat and for the first time in her life played table tennis; the look on her face was priceless. I see that all the time. It’s as simple as that really.”

Lenox started in his teens by helping with youth projects, summer camps and soup runs in China town then progressed to inviting homeless people round for meals. Then, 19 years ago, when he met and married Heather, they started running a drugs rehab centre from their home, as well as supporting recovering addicts in rehab centres and youth hostels.

They opened the Rainbow Christian Centre in 2003 to help addicts but, after speaking with locals, focused their attention on preventing addiction and the associated behaviour that led to it. Available 24 hours a day – Lenox has only taken one five-day holiday in 19 years – their projects include a gym for adults, youth groups, food handouts, Saturday social events, prison visiting, court appearances, family liaison and advice on housing, benefits, education, apprenticeships and debt. And in August of each year, he takes a week off work to run a play scheme.

The other award winners include student winner Jack Burke, who not only runs the Student Action soup kitchen, but has fought for its very survival.

BA History student Jack and his team prepare and deliver fresh food and drinks in a safe place where the homeless can share their concerns and problems. In addition, his detailed knowledge of the services available – obtained by various means, including meetings with members of the city council – makes a huge difference to those he helps.

And with the council constantly trying to move the soup kitchen out of the city centre, he has spent much of his own time looking at other possible venues, to ensure that it is in a safe place for both volunteers and homeless alike.

If that was not enough, Jack has successfully completed the BOGLE Stroll 55-mile walk twice to raise funds to enhance the soup kitchen.   

Alumni winner Estelle Goodwin, who studied for her MA in Ancient World Studies here, founded the charity KIN (Kibera in Need) which supports projects in the vast Kibera slum in Kenya.

Kibera, in Nairobi, is home to up to one million people who live in desperate conditions of poor housing and sanitation, high unemployment, HIV/Aids and low school attendance.

KIN started out helping the Kenyan NGO Riziki fund its small feeding programme, in which 50 Kibera residents got their main weekend meal every Saturday.

It has now developed an Education Support Scheme, a Child Guardianship Scheme, Microfinance and a series of seminars giving guidance on parenting, reproductive health and career choice; funds vocational training for around 220 children and young people; helps 800 plus small business clients; and is about to start a solar lighting project.

And the feeding programme has grown to 200 children and caregivers every week.

President and Vice-Chancellor of The University of Manchester, Professor Dame Nancy Rothwell, presented the awards. She told the award winners: “You give up the most valuable thing to all of us and that is time.”

View the film testimonials:

Notes for editors

Contact Jon Keighren, Media Relations Manager, The University of Manchester 0161 275 8384

Professor Kapila has extensive experience in the policy and practice of international development, humanitarian affairs, and diplomacy, including human rights, disaster and conflict management, and in global public health.

He is also Special Representative of the Aegis Trust for the prevention of crimes against humanity. Previously, he was Under Secretary General at the International Federation of Red Cross and Red Crescent Societies, the world’s largest humanitarian and development network.

Professor Kapila’s early career was in clinical medicine, primary health care, and public health in the NHS where he helped set up the UK’s first national HIV and AIDS programme at the Health Education Authority, becoming its deputy director. He later joined the UK Foreign and Commonwealth Office’s Overseas Development Administration (later Department for International Department), initially as senior health and population adviser and latterly as the first head of a new Conflict and Humanitarian Affairs Department.

Professor Kapila went on to become the Special Adviser to the United Nations High Commissioner for Human Rights in Geneva and then Special Adviser at the UN Mission in Afghanistan. Later, he led the UN’s largest country mission at the time as the United Nations Resident and Humanitarian Coordinator for the Sudan, and then became a Director at the World Health Organization. In 2003, he was awarded the CBE for his international service and received the Global Citizenship Award of the Institute for Global Leadership in 2007.

Professor Kapila, who will also work with the MAHSC (91Ö±²¥ Academic Health Science Centre) Global Health Theme and the University’s Humanitarian Conflict Response Institute, said: “What has attracted me to 91Ö±²¥ is its cosmopolitan outlook, its enterprising spirit, and its openness to work across disciplinary boundaries to find innovative solutions to some of the greatest problems that confront our shared humanity. I am honoured to be part of the team.”

Dean and Vice President of the Faculty of Medical and Human Sciences Professor Ian Jacobs said: “I am excited and delighted that Professor Kapila is joining 91Ö±²¥ Medical School and MAHSC. This reflects the development of our effort in global health and our determination to provide an outstanding educational experience for our medical students. Mukesh is internationally recognised for his contribution to and advocacy of human rights and humanitarian issues and it is a privilege to welcome him as a member of The University of Manchester and the 91Ö±²¥ Academic Health Science Centre.”

Ends

Notes for editors

For further information contact:

Aeron Haworth
Media Relations
Faculty of Medical and Human Sciences
The University of Manchester

Tel: 0161 275 8383
Mob: 07717 881563
Email: aeron.haworth@manchester.ac.uk

The study, carried out by researchers at The University of Manchester and the Medical Research Council’s National Institute for Medical Research and published in Nature, provides a blueprint for the design of new drugs to treat HIV infection, say the researchers.

Scientists in the United States and France recently discovered that a protein named SAMHD1 was able to prevent HIV replicating in a group of white blood cells called myeloid cells.

Now, crucially, the teams from 91Ö±²¥ and the MRC have shown how SAMHD1 prevents the virus from replicating itself within these cells, opening up the possibility of creating drugs that imitate this biological process to prevent HIV replicating in the sentinel cells of the immune system.

“HIV is one of the most common chronic infectious diseases on the planet, so understanding its biology is critical to the development of novel antiviral compounds,” said , who led the study in 91Ö±²¥’s School of Biomedicine.

“SAMHD1 has been shown to prevent the HIV virus replicating in certain cells but precisely how it does this wasn’t known. Our research has found that SAMHD1 is able to degrade deoxynucleotides, which are the building blocks required for replication of the virus.

“If we can stop the virus from replicating within these cells we can prevent it from spreading to other cells and halt the progress of the infection.”

Co-author Dr Ian Taylor, from the MRC’s National Institute for Medical Research, added: “We now wish to define more precisely, at a molecular level, how SAMHD1 functions. This will pave the way for new therapeutic approaches to HIV-1 and even vaccine development.”

The study was funded by the Medical Research Council, the European Union Seventh Framework Programme and the European Leukodystrophy Association.

Ends

Notes for editors

The paper, ‘HIV-1 restriction factor SAMHD1 is a deoxynucleoside triphosphate triphosphohydrolase,’ published in Nature, is available on request.

For further information contact:

Aeron Haworth
Media Relations
Faculty of Medical and Human Sciences
The University of Manchester

Tel: 0161 275 8383
Mob: 07717 881563
Email: aeron.haworth@manchester.ac.uk

Lawrence O Gostin, Professor of Global Health Law at the Georgetown University Law Center, will present a public lecture entitled ‘Meeting Basic Survival Needs of the World’s Least Healthy People: Toward a Framework Convention on Global Health.’

Professor Gostin is engaged in three major international initiatives on global health governance:

• A “Framework Convention on Human Services” for the World Bank—a multilateral treaty on the health care professional capacity in poor and middle income countries

• A “Framework Convention on Global Health”—a multilateral treaty ensuring “basic survival needs” for the world’s poor

• A Global Plan for Justice—a global compact to fund essential medicines, basic survival needs, and climate change.

Together with academic and civil society partners from around the world, Professor Gostin founded The Joint Action and Learning Initiative on National and Global Responsibilities for Health (JALI).

JALI is a global campaign for a Framework Convention on Global Health based on the human right to health. JALI was featured in the World Health Report 2010, and the JALI Steering Committee is convening three global stakeholders’ meetings in 2011: Johannesburg, South Africa; Delhi, India; and Bellagio, Italy.

In his lecture, Professor Gostin will discuss the JALI, addressing the following issues:

Despite enormous advances in science and medicine, much of the world’s population continues to suffer and die from preventable disease. Health has become one of the starkest illustrations of global inequality: there are millions of avoidable deaths every year impacting on development, education, and life expectancy. To challenge this inequality and develop strategies to promote and fulfill the unrealized but not unrealizable human right to health, a global coalition of civil society and academia is collaborating on JALI.
  
The JALI’s ultimate goal is to secure, through collaborative research and advocacy, a Framework Convention on Global Health – a global health treaty that would, for the first time, express a shared vision for realizing the human right to the highest attainable standard of health and enabling all people to have their essential health needs met. It envisions a treaty that sets clear priorities, coordinates presently fragmented activities, ensures scalable and sustainable economic and human resources, clarifies national and international responsibilities, and creates accountability at all levels, including through monitoring, performance evaluation, and enforcement.
 
It believes that a campaign to establish a global health agreement with a strong foundation in the international right to health grows out of the last few decades of health activism, particularly the successes of the AIDS advocacy movement. An international global health agreement is the logical next step to follow the Millennium Development Goals (MDGs), and should be adopted by 2015.  It would remain rooted in the UN Millennium Declaration that countries have an individual and “collective responsibility to uphold the principles of human dignity, equality and equity at the global level”.

Members of the public can register their intention to attend this free event by emailing isei@manchester.ac.uk. The lecture, in University Place, Theatre A, Oxford Road, The University of Manchester, takes place at 6pm and will last approximately 90 minutes.

Ends

Notes for editors

‘Meeting Basic Survival Needs of the World’s Least Healthy People: Toward a Framework Convention on Global Health,’ a public lecture by Professor Lawrence O Gostin, takes place on Wednesday, 1^st June, from 6pm to 7pm in Lecture Theatre A, University Place, Oxford Road, The University of Manchester M13 9PL.

Professor Gostin is available for media interviews on the morning of Wednesday, June 1. Journalists wishing to attend the lecture can do so through the press office.

Lawrence O Gostin is Professor of Global Health Law at the Georgetown University Law Center, Professor of Public Health at the Johns Hopkins University, Director of the O’Neill Institute for National and Global Health law, Director of the Center for Law and the Public’s Health at Johns Hopkins and Georgetown Universities, and Director of the World Health Organization Collaborating Center on Public Health Law and Human Rights. A biography is available here:

For further information contact:

Aeron Haworth
Media Relations
Faculty of Medical and Human Sciences
The University of Manchester

Tel: 0161 275 8383
Email: aeron.haworth@manchester.ac.uk

University of Manchester researchers, working with colleagues in Newark, USA, have developed a new test that can not only better diagnose Aspergillus infection, but can also spot signs of antifungal resistance to azoles – the class of drugs used to treat patients with aspergillosis.

Using the new test, which uses direct molecular detection rather than culturing the fungus in a Petri dish, the team found that 55% of aspergillosis patients had telltale signs known as ‘markers’ that indicated they had developed resistance to azoles. The findings compare to resistance rates of 28% carried out by the team just two years ago using traditional culturing methods.

Furthermore, the study – published in the prestigious US journal Clinical Infectious Diseases – discovered azole-resistance markers in three-quarters of the small number of aspergillosis patients (eight) whom had never been treated with an azole, suggesting widespread dissemination of resistance.

“Aspergillus significantly worsens asthma symptoms and causes life-threatening infections in those with long-term lung infections or damaged immune systems, such as chemotherapy and transplant patients or people with HIV,” said David Denning, Professor of Medicine and Medical Mycology at The University of Manchester and Director of the National Aspergillosis Centre at the University Hospital of South 91Ö±²¥ NHS Foundation Trust.

“Using an ultrasensitive, real-time test for Aspergillus, similar to the method used to diagnose HIV, MRSA and influenza, we have directly detected azole resistance in people with aspergillosis, without first culturing the fungus in a dish. The presence of Aspergillus was detected in many more samples than using traditional culture methods, and 55% were found to contain azole-resistance markers.

“This is an extraordinarily high rate of resistance, possibly related to fungicide use in agriculture – more than a third of ‘pesticides’ used by UK farmers are azoles – and long treatment courses in patients, so the findings have major implications for the sustainability of azoles for human antifungal therapy.”

The azoles itraconazole (Johnson & Johnson), voriconazole (Pfizer) and posaconazole (Merck) have annual sales of more than $1bn annually. Conventional diagnosis of aspergillosis is limited by poor culture yield, and so the true frequency of azole resistance has been unclear.

In this latest study, the researchers analyzed phlegm from patients with allergic and chronic lung disease caused by Aspergillus and found that almost twice the proportion of individuals tested had resistance markers in their sample compared to a Petri dish (or culture) study carried out by the team in 2008/9.

Professor Denning added: “Not only is molecular testing much more sensitive than conventional culture for diagnosis, but it enables testing for resistance, which until now has been impossible if cultures are negative. Given the rising frequency of resistance in Aspergillus in northern Europe, China and the United States, this study provides key data for doctors to shift antifungal therapy in the face of resistance."

Ends

Notes for editors

A copy of the paper, Denning DW, Park S, Lass-Florl C, Fraczek MG, Kirwan M, Gore R, Smith J, Bueid A, Bowyer P, Perlin DS. High frequency triazole resistance found in non-culturable Aspergillus fumigatus from lungs of patients with chronic fungal disease. Clin Infect Dis 2011;52:1123-9, is available on request.

A copy of the 2009 study, Bueid A, Howard SJ, Moore CB, Richardson MD, Harrison E, Bowyer P, Denning DW. Azole antifungal resistance in Aspergillus fumigatus - 2008 and 2009. J Antimicrob Chemother 2010;65:2116-8, is also available.

The primary molecular detection test is Myconostica’s MycAssay Aspergillus, commercialized through Myconostica, a University of Manchester spin-out company, founded by Professor David Denning.

Further information concerning Aspergillus and aspergillosis can be found on

For further information contact:

Aeron Haworth
Media Relations
Faculty of Medical and Human Sciences
The University of Manchester

Tel: 0161 275 8383
Mob: 07717 881563
Email: aeron.haworth@manchester.ac.uk

A widely used drug could be used to prevent cervical cancer caused by infection with the human papilloma virus (HPV), say scientists.

University of Manchester researchers, working with colleagues in Canada, have discovered how the antiviral drug lopinavir attacks HPV by switching on a natural viral defence system in infected cells.

The study, published in the journal , builds on the team’s previous work in 2006 that first identified lopinavir as a potential therapeutic for HPV-related cervical cancer following laboratory tests on cell cultures.

“Since publishing our earlier work, we have now found that lopinavir selectively kills HPV-infected, non-cancerous cells, while leaving healthy cells relatively unaffected,” said , from 91Ö±²¥’s School of Cancer and Enabling Sciences.

“This is a very significant finding as these cells are not cancer cells but are the closest thing to being like the cells found in a pre-cancerous HPV infection of the cervix. In addition we were also able to show that lopinavir kills these HPV-infected cells by re-activating a well-known antiviral system that is suppressed by HPV.”

In many developing countries, HPV-related cervical cancer is still one of the most common women’s cancers accounting for approximately 290,000 deaths per year worldwide. The same virus also causes a significant proportion of cancers of the mouth and throat in both men and women and this disease is showing an alarming increase in developed countries, such as the UK, where it is now more than twice as common as cervical cancer.

Although in the developed world vaccination programmes against HPV are well underway, these are not effective in women already infected with HPV. Furthermore, the current vaccines do not protect against all types of HPV and they are expensive, which will limit their use in countries with limited resources. A cheap and preferably self-administered treatment that could eliminate early-stage HPV infections before these have developed into cancers would therefore have distinct health advantages.

Dr Hampson said: “Our results suggest that for this drug to work against HPV it would be necessary to treat virus-infected cells of the cervix with roughly 10-15 times the concentration that is normally found in HIV-infected patients taking lopinavir as tablets. This implies that, for this treatment to work, it would need to be locally applied as a cream or pessary.”

Co-author on the paper, , added: “These results are very exciting since they show that the drug not only preferentially kills HPV-infected non-cancerous cells by re-activating known antiviral defence systems, it is also much less toxic to normal non-HPV infected cells.

“Lopinavir is obviously safe for people to take as tablets or liquid but our latest findings provide very strong evidence to support a clinical trial using topical application of this drug to treat HPV infections of the cervix.”

The research in 91Ö±²¥ was carried out by the Hampsons’ PhD student, Gavin Batman, who was funded by the Humane Research Trust charity, with additional funding supplied by the Caring Cancer Trust and the Cancer Prevention Research Trust.

Ends

Notes for editors

A copy of the paper, ‘,’ is available on request.

For further information contact:

Aeron Haworth
Media Relations
Faculty of Medical and Human Sciences
The University of Manchester

Tel: 0161 275 8383
Mob: 07717 881563
Email: aeron.haworth@manchester.ac.uk

Salim Mohammed has followed in the footstep of his friend Sammy Gitau by making the remarkable journey from Mathare slum, then to Kibera slum to graduate at the University’s renowned Institute for Development Policy and Management.

Following his degree success, he will start in a senior post in an international NGO and will be based in East Africa.

Salim’s graduation follows Sammy’s story, which made the headlines across the world on December 13 2007 – exactly three years ago today.

Salim was abandoned by his mother and spent the first four years of his life on the streets of Nairobi with his grandmother, a vegetable hawker.

When he turned five, he was sent to an orphanage in Mathare where he later became inspired to help other children like himself.

At 16, Salim led a sports programme involving over 2,000 young people and after graduating at high school, became an HIV/AIDS educator in Mathare where today, 20 percent of all residents are HIV positive.

In 2001, he helped found Carolina for Kibera (CFK), an international, NGO which fights abject poverty and helps prevent violence through community-based development.

Kibera is thought to be one of the largest slums in Africa. Families of up to 5 often sleep in tiny shacks with mud walls, corrugated roof, and a dirt or concrete floor.

There is little electricity or running water – and political and communal violence is widespread.

CFK was named a Time Magazine and Gates Foundation “Hero of Global Health” in 2005.

Salim said:” Sammy had a lot of influence on my thoughts in terms of coming to 91Ö±²¥ - though it’s something I really felt would help me in my work.

”I’m sure the experience will also help me channel my energy more effectively.

“It’s so difficult sometimes to separate academic theory and practice- but I think it’s important to understand how one can complement the other.”

He added: “My year in 91Ö±²¥ has been fantastic and I hope it will enable me to go from strength to strength and make some impact in Africa.

“I would also like to thank my Programme Director and tutor, Dr Paul Barry, Nikki Banks, a PhD student who has been very supportive to me, and my friends and course colleagues at IDPM.”

Dr Barry said: “It’s been a privilege and a delight to be able to support Salim in this part of his life journey.

“His substantial life experience in managing development projects, including Carolina for Kibera, qualified him uniquely to follow the MSc in Management and Implementation of Development Projects (MSc MIDP).

“He’s a remarkable person, tremendously engaged, who cares hugely about his fellow students and fellow man.

“Congratulations to him for his well deserved distinction.

“But this is by no means the end of his journey – and I am certain he will go on to do great things wherever he works.”

Notes for editors

Images are available

For media enquires contact:

Mike Addelman
Media Relations
Faculty of Humanities
University of Manchester
0161 275 0790
07717 881567

The Euro 1.2 million funded consortium of institutions, including the University’s  Institute for Development Policy and Management, will devise and deliver a community based system for HIV Treatment.

The cash has been provided by the EU’s ACP Science and Technology Programme (2010-2013).

The 91Ö±²¥ team of Sarah Bracking, Philip Woodhouse, David Lawson, Tanja Mueller and Christine Walmsler will look at international monitoring and quality control of community based systems.

It will also examine their effectiveness from the perspective of the communities themselves.

Project leader Dr Sarah Bracking, said: “As access to HIV treatment becomes more widely available in sub-Saharan Africa, the need for enhanced access to voluntary HIV counselling and testing  becomes even greater.

“Our specialist experience in the  factors and areas which influence the efficacy of interventions for the support of HIV/AIDS affected persons will equip us well for this task..

“Poverty and limited health services in Africa present barriers to adherence to antiretroviral therapy

“We need innovative options other than facility based methods for delivery and monitoring such therapy.

“Our project will  tackle these challenges.”

The project team will become part of a larger community of researchers, policy makers, academics and civil society in the project countries of Malawi, Tanzania, Zimbabwe, Mozambique, Botswana and Namibia.

Notes for editors

For media enquiries contact:

Mike Addelman
Media Relations
Faculty of Humanities
The University of Manchester
0161 275 0790
07717 881567
michael.addelman@manchester.ac.uk

HIV-1 is responsible for the AIDS pandemic that currently affects 33 million people worldwide. HIV-1 originated as the result of cross-species transmissions of Simian Immunodeficiency Virus (SIV) found in chimpanzees, which is presumed to be a result of people coming into contact with infected bush meat. HIV/AIDS was first recognised by the scientific community in the 1980, while the first introduction into the human population is estimated to have been near the beginning of the twentieth century in the region of the Democratic Republic of Congo.  

Now a French team, in collaboration with David Robertson and Jonathan Dickerson at The University of Manchester, have found the first definitive transfer of HIV-1 from a non-chimpanzee source, a gorilla. The unusual HIV-1 infection was found in a Cameroonian woman who had moved to Paris. It probably represents a new human lineage (tentatively named group P) that is distinct from those previously identified: group M (responsible for the pandemic), group O and group N (both mainly restricted to Cameroon).  

The 62-year-old woman presented with symptoms shortly after she had moved to Paris in 2004. Due to discrepancies in her viral load testing her French doctors investigated and found she was infected with a new strain more closely related to SIV from gorillas than HIV from humans.  

The woman is the only human known to be infected with the new HIV-1 strain (RBF168) so far. However, before moving to Paris, she had lived in a semi-urban area of Cameroon and had no contact with gorillas or bush meat. In addition, lab studies of the virus have showed that it can replicate in human cells. As a result the team expect to see this strain elsewhere.  

Dr Robertson, from 91Ö±²¥’s Faculty of Life Sciences, said: “The discovery of this novel HIV-1 lineage highlights the continuing need to monitor closely for the emergence of new HIV variants. This demonstrates that HIV evolution is an ongoing process. The virus can jump from species to species, from primate to primate, and that includes us; pathogens have been with us for millions of years and routinely switch host species.”  

He added: “It also highlights how human mobility can rapidly transfer a virus from one geographical location to another as has been dramatically evident with the recent emergence of swine flu.”  

The 91Ö±²¥ team contributed the computer/evolutionary analysis to the study, ‘A new human immunodeficiency virus derived from gorillas’, published in the latest Nature Medicine (2 August 2009). The French team are part of a network of laboratories that has been monitoring HIV genetic diversity.

Notes for editors

For more information, a copy of the paper or an interview with Dr David Robertson, contact University of Manchester Media Relations Officer Mikaela Sitford on 0161 275 2111, 07768 980942 or Mikaela.Sitford@manchester.ac.uk.  

A copy of the paper ‘A new human immunodeficiency virus derived from gorillas’is available from the Nature press site or from press@nature.com.  

The University of Manchester’s Faculty of Life Sciences, with 1,700 undergraduate students, more than 1,000 people involved in research, £135 million in active research grants and £170 million investment in state-of-the-art facilities, is one of the largest and most successful unified research and teaching organisations of its kind in Europe. See .