̽��ֱ�� of Cambridge - Mark Wills

Professor Duncan Richards appointed as Head of Department of Medicine

Anonymous — Fri, 06 Dec 2024 16:59:07 +0000

Professor Richards joins Cambridge from the ̽��ֱ�� of Oxford, where he has been since 2019. His particular research interest is the demonstration of clinical proof of concept of novel therapeutics through the application of experimental medicine techniques, especially human challenge studies.

As Climax Professor of Clinical Therapeutics, director of the Oxford Clinical Trial Research Unit (OCTRU), and the NIHR Oxford Clinical Research Facility, he led a broad portfolio focused on new medicines for multiple conditions. His focus has been the acceleration of promising new drug treatments through better decision-making in early phase clinical trials.

Professor Richards also brings with him a wealth of experience in a number of Pharmaceutical R&D clinical development roles. In 2003 he joined GSK and held a number of roles of increasing responsibility, latterly as Head of Clinical Pharmacology and Experimental Medicine, including directorship of GSK’s phase 1 and experimental medicine unit in Cambridge (CUC).

Commenting on his appointment, Professor Richards said: “As a clinical pharmacologist, I have been fortunate to work across a broad range of therapeutic areas over the years. I am excited by the breadth and depth of expertise within the Department of Medicine and look forward to working with the first-class scientific team. My goal is to work with the Department team, the Clinical School, and hospitals to maximise the impact of the important work taking place in Cambridge.”

Members of the department’s leadership team are looking forward to the continued development of the department under Professor Richards, building on its legacy of collaboration and groundbreaking translational research to drive our future success.

Professor Mark Wills, Interim Head of Department of Medicine, said: “Duncan brings to his new role a fantastic breadth of experience, which encompasses his clinical speciality in pharmacology, extensive experience of working within the pharmaceutical industry R&D at senior levels and most recently establishing academic clinical trials units and human challenge research facilities.

“I am very excited to welcome Duncan to the Department and looking forward to working with him, as he takes on the role of delivering of the Department of Medicine’s vision to increase the efficacy of translation of its world class fundamental research, and its impact upon clinical practice and patient wellbeing.”

Menna Clatworthy, Professor of Translational Immunology and Director of the Cambridge Institute for Therapeutic Immunology and Infectious Disease (CITIID), said: "Duncan has a wealth of leadership experience in biomedicine, in both academia and pharma. That skillset will be invaluable in ensuring the Department of Medicine continues to deliver world-leading research to transform patient outcomes."

Charlotte Summers, Professor of Intensive Care Medicine and Director of the Victor Phillip Dahdaleh Heart & Lung Research Institute, said: “Duncan’s exemplary track record of translating fundamental scientific discoveries into therapies that benefit patients will help us further increase the impact of our research as we continue our mission to improve human health.”

̽��ֱ��appointment underpins the recently announced five-year collaboration between GSK and the ̽��ֱ�� of Cambridge, the Cambridge-GSK Translational Immunology Collaboration (CG-TIC). ̽��ֱ��£50 million investment will accelerate research and development in kidney and respiratory diseases to improve patient outcomes.

Professor Richards will assume the role in February 2025, replacing Interim Head of Department Dr Mark Wills who was appointed after the departure of Professor Ken Smith in January 2024. Dr Wills will continue as Director of Research and Deputy Head of the Department of Medicine as well as leading his research group.

Professor Richards trained in medicine at Oxford ̽��ֱ�� and after junior doctor roles in London, he returned to Oxford as Clinical Lecturer in Clinical Pharmacology. His DM thesis research was on a translational model using platelet ion flux to interrogate angiotensin biology and he is author of the Oxford Handbook of Practical Drug Therapy and the 3rd edition of Drug Discovery and Development.

Professor Richards has been a core member of the UK COVID-19 Therapeutics Advisory Panel. He is a member of the Oxford Bioescalator Management Board, UK Prix Galien Prize Committee, and the therapeutic advisory committee of several national platform clinical trials.

Professor Duncan Richards has today been announced as the new Head of the Department of Medicine at the ̽��ֱ�� of Cambridge.

I am excited by the breadth and depth of expertise within the Department of Medicine and look forward to working with the first-class scientific team

Duncan Richards

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

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Biological ‘fingerprints’ of long COVID in blood could lead to diagnostic test, say Cambridge scientists

cjb250 — Mon, 19 Jul 2021 07:39:19 +0000

̽��ֱ��team has received funding from the National Institute for Health Research to develop a test that could complement existing antibody tests. They also aim to use similar biological signatures to develop a test and monitor for long COVID.

While most people recover from COVID-19 in a matter of days or weeks, around one in ten people go on to develop symptoms that can last for several months. This can be the case irrespective of the severity of their COVID-19 – even individuals who were asymptomatic can experience so-called ‘long COVID’.

Diagnosing long COVID can be a challenge, however. A patient with asymptomatic or mild disease may not have taken a PCR test at the time of infection – the gold standard for diagnosing COVID-19 – and so has never had a confirmed diagnosis. Even antibody tests – which look for immune cells produced in response to infection – are estimated to miss around 30% of cases, particularly among those who have had only mild disease and or beyond six months post-initial illness.

A team at the ̽��ֱ�� of Cambridge and Cambridge ̽��ֱ�� Hospitals NHS Foundation Trust has received £370,000 from the National Institute for Health Research to develop a COVID-19 diagnostic test that would complement existing antibody tests and a test that could objectively diagnose and monitor long COVID.

̽��ֱ��research builds on a pilot project supported by the Addenbrooke’s Charitable Trust. ̽��ֱ��team has been recruiting patients from the Long COVID Clinic established in May 2020 at Addenbrooke’s Hospital, part of Cambridge ̽��ֱ�� Hospitals NHS Foundation Trust.

During the pilot, the team recruited 85 patients to the Cambridge NIHR COVID BioResource, which collects blood samples from patients when they are first diagnosed and then at follow-up intervals over several months. They now hope to expand their cohort to 500 patients, recruited from Cambridgeshire and Peterborough.

In their initial findings, the team identified a biomarker – a biological fingerprint – in the blood of patients who had previously had COVID-19. This biomarker is a molecule known as a cytokine produced by T cells in response to infection. As with antibodies, this biomarker persists in the blood for a long time after infection. ̽��ֱ��team plans to publish their results shortly.

Dr Mark Wills from the Department of Medicine at the ̽��ֱ�� of Cambridge, who co-leads the team, said: “We need a reliable and objective way of saying whether someone has had COVID-19. Antibodies are one sign we look for, but not everyone makes a very strong response and this can wane over time and become undetectable.

“We’ve identified a cytokine that is also produced in response to infection by T cells and is likely to be detectable for several months – and potentially years – following infection. We believe this will help us develop a much more reliable diagnostic for those individuals who did not get a diagnosis at the time of infection.”

By following patients for up to 18 months post-infection, the team hopes to address several questions, including whether immunity wanes over time. This will be an important part of helping understand whether people who have been vaccinated will need to receive boosters to keep them protected.

As part of their pilot study, the team also identified a particular biomarker found in patients with long COVID. Their work suggests these patients produce a second type of cytokine, which persists in patients with long COVID compared to those that recover quickly and might be one of the drivers behind the many symptoms that patients experience. This might therefore prove to be useful for diagnosing long COVID.

Dr Nyarie Sithole, also from the Department of Medicine at the ̽��ֱ�� of Cambridge, who co-leads the team and helps to manage long COVID patients, said: “Because we currently have no reliable way of diagnosing long COVID, the uncertainty can cause added stress to people who are experiencing potential symptoms. If we can say to them ‘yes, you have a biomarker and so you have long COVID’, we believe this will help allay some of their fears and anxieties.

“There is anecdotal evidence that patients see an improvement in symptoms of long COVID once they have been vaccinated – something that we have seen in a small number of patients in our clinic. Our study will allow us to see how this biomarker changes over a longer period of time in response to vaccination.”

At the moment, the team is using the tests for research purposes, but by increasing the size of their study cohort and carrying out further work, they hope to adapt and optimise the tests that can be scaled up and speeded up, able to be used by clinical diagnostic labs.

As well as developing a reliable test, the researchers hope their work will help provide an in-depth understanding of how the immune system responds to coronavirus infection – and why it triggers long COVID in some people.

Dr Sithole added: “One of the theories of what’s driving long COVID is that it’s a hyperactive immune response – in other words, the immune system switches on at the initial infection and for some reason never switches off or never goes back to the baseline. As we’ll be following our patients for many months post-infection, we hope to better understand whether this is indeed the case.”

In addition, having a reliable biomarker could help in the development of new treatments against COVID. Clinical trials require an objective measure of whether a drug is effective. Changes in – or the disappearance of – long-COVID-related cytokine biomarkers with corresponding symptom improvement in response to drug treatment would suggest that a treatment intervention is working.

Markers in our blood – ‘fingerprints’ of infection – could help identify individuals who have been infected by SARS-CoV-2, the coronavirus that causes COVID-19, several months after infection even if the individual had only mild symptoms or showed no symptoms at all, say Cambridge researchers.

Because we currently have no reliable way of diagnosing long COVID, the uncertainty can cause added stress to people who are experiencing potential symptoms. If we can say to them ‘yes, you have a biomarker and so you have long COVID’, we believe this will help allay some of their fears and anxieties

Nyarie Sithole

Annie Spratt

Tired looking woman

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

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Scientists launch a pre-emptive strike on deadly post-transplant infection

ta385 — Tue, 23 Feb 2021 12:45:00 +0000

Around 80% of the UK population is currently infected with human cytomegalovirus (HCMV) and in developing countries this can be as high as 95%. ̽��ֱ��virus can remain dormant in our white blood cells for decades and, if it reactivates in a healthy individual, does not usually cause symptoms. But, for people who are immunocompromised, HCMV reactivation can be devastating.

HCMV reactivation has been identified in COVID-19 patients, though scientists do not yet understand the relationship between the two viruses. Reactivation or re-infection in transplant recipients can lead to severe illness, including organ rejection and, in some cases, death.

More than 200,000 kidney, lung and stem cell transplants take place globally every year and HCMV reactivation occurs in more than half of these cases. For reasons scientists don’t yet fully understand, immunosuppressants appear to encourage the virus to reactivate as well as compromising the patient’s ability to fight it. There remains no effective vaccine against HCMV and anti-viral therapies often prove ineffective or detrimental.

Now, a team from the ̽��ֱ�� of Cambridge’s School of Clinical Medicine has identified a drug type and treatment strategy that could dramatically reduce these devastating reactivation events. ̽��ֱ��study, published in the journal PNAS, describes how scientists exposed HCMV-infected blood samples to a wide-range of ‘epigenetic inhibitors’ – drugs widely used in cancer treatment – hoping to prompt the latent virus to produce proteins or targetable antigen that are visible to our immune system.

They discovered that a particular group of these drugs, ‘bromodomain inhibitors’, successfully reactivated the virus by forcing it to convert its hidden genetic instructions into protein. This then enabled T-cells in the blood samples to target and kill these previously undetectable infected cells.

̽��ֱ��study is the first to identify the involvement of human host bromodomain (BRD) proteins in the regulation of HCMV latency and reactivation but also proposes a novel ‘shock and kill’ treatment strategy to protect transplant patients.

Lead author Dr Ian Groves said: “We’re looking to purge the patient’s viral reservoir before they go into the operating theatre and before they start taking immunosuppressants, when they would become extremely vulnerable to the virus reactivating. In other words, we’re proposing a pre-emptive strike.

“Prior to transplantation, many patients will have a relatively healthy immune system, so when the virus puts its head above the parapet, its cover is blown, and the immune system will see it and kill the cells it’s been hiding in. Ideally, donors would also be treated to avoid re-infecting recipients.”

There are similar drugs in Phase 1–3 clinical trials around the world for other intended uses, mainly in the treatment of cancers but also Type 2 diabetes-related cardiovascular disease.

Dr Groves said: “This would be the first type of treatment to reduce HCMV infection levels pre-transplant in order to lower the chances of virus reactivation during immune suppression after transplantation. Our findings could lead to thousands of lives being saved every year.”

“In addition to the terrible human suffering this virus causes, treating its effects adds enormously to the high costs already incurred by transplantation. It’s a really serious issue for health services in wealthy nations and a desperate one in developing countries. Our findings offer an opportunity to transform this horrible situation.”

̽��ֱ��study builds on over 25 years of extensive research into the molecular biology of HCMV and its immune evasion tactics (funded by the Medical Research Council). ̽��ֱ��researchers hope their study could eventually help doctors fight HCMV on other fronts, including in maternity and neo-natal care. HCMV affects at least 1% of all live births in developed countries, and many more in developing countries. These children can be left with brain damage and hearing loss, but congenital infection during pregnancy can also lead to miscarriage.

Reference

I. J. Groves et al., ‘Bromodomain proteins regulate human cytomegalovirus latency and reactivation allowing epigenetic therapeutic intervention’. PNAS (2021). DOI: 10.1073/pnas.2023025118

A potential new treatment to protect immunosuppressed patients from human cytomegalovirus (HCMV) has been discovered by scientists at the ̽��ֱ�� of Cambridge. Their study shows that certain epigenetic inhibitors expose and help to destroy dormant HCMV infections, which often reactivate to cause serious illness and death in these vulnerable groups. Subject to clinical trials, their proposed ‘shock and kill’ treatment strategy offers hope to transplant patients across the world.

Our findings could lead to thousands of lives being saved every year

Ian Groves

Sasin Tipchai via Pixabay

Surgeons at work in an operating theatre

Funding

This research was supported by GlaxoSmithKline and the Medical Research Council.

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Silent killer

lw355 — Fri, 13 Sep 2013 13:14:24 +0000

To catch the herpes virus human cytomegalovirus (HCMV) you must be exposed to someone who has it. This isn’t difficult: it is carried by around 65% of the population. Once in the body, HCMV persists for life owing to its clever ability to avoid our immune system and to go into hiding inside our cells in a latent state. Now, research is identifying changes in these cells that could lead to a new route to eradicating the virus.

“HCMV can be acquired very early in childhood, and the number of people infected gradually rises throughout life,” said Professor John Sinclair, a molecular virologist in the Department of Medicine. “ ̽��ֱ��active virus can not only be passed from an infected mother to her child in breast milk but can easily be transferred from child to child in saliva – one child puts a toy in their mouth, then it’s passed to another child who does the same, and the virus is passed on. It’s also a sexually transmitted disease, so there’s another increase in infections when people become sexually mature.”

Once acquired, the virus goes into a latent state in the body. If it reactivates in healthy people, their immune responses prevent it from causing disease. But when the immune system is suppressed, active HCMV becomes dangerous. It is a major cause of illness and death in organ and bone marrow transplant patients, who are given drugs to deliberately suppress their immune system and prevent their body rejecting the transplant. With an increasing demand for transplants in the UK, HCMV is set to become a growing problem.

“If it’s not treated well, or it develops resistance to antiviral drugs, HCMV can lead to pneumonitis – inflammation of the lung tissue – and, in the most extreme case, it replicates all over the body and the patient ends up with multiple organ failure,” said Dr Mark Wills, a viral immunologist working alongside Sinclair in the Department of Medicine.

“Tissue from donors carrying the virus often has to be used for transplants because there are so few donors and so many people carrying the virus,” said Sinclair. “By transplanting bone marrow, or an organ from someone with the infection, you’re giving the patient the virus and you’re immune-suppressing them. That’s the worst of both worlds.”

And HCMV is not a worry just for transplant patients. “HCMV is now the leading cause of infectious congenital disease – that is, disease present at birth,” said Sinclair. Women in early pregnancy who are newly infected with HCMV or whose HCMV reactivates are at real risk, and this can lead to disease in their unborn baby. HCMV also targets HIV-AIDS patients, where a progressive failure of the immune system allows this opportunistic infection to thrive.

There is no vaccine to prevent HCMV infection, and the antiviral drugs available to treat it have significant toxicity and only limited effectiveness. In addition to the problem of viral resistance, drugs can only target HCMV in its active state, which means the virus can never be fully eradicated. “You can suppress the virus down to a very low level, but you can never get rid of the latent reservoir with the currently available antiviral drugs,” said Wills.

Sinclair and Wills, who have just received their fifth consecutive five-year grant from the Medical Research Council (MRC), have focused on understanding how the virus maintains this latent infection in specialised cells of the immune system and how the immune system is prevented from eliminating the virus from the body.

“ ̽��ֱ��belief has always been that, in its latent state, HCMV was just sitting there doing nothing, waiting to reactivate,” said Sinclair. “But we’ve started to identify major changes in latently infected cells, and we think these are targetable with novel drugs and immunotherapies.

“One change is in a transporter protein normally used by the cell to pump out things it needs to get rid of,” he added. “If you put the chemotherapy drug vincristine on a healthy cell, the cell will pump it out and survive. Working with Paul Lehner at the Cambridge Institute for Medical Research we found that, during latent infection, this transporter protein is less effective, making the cell more prone to killing by vincristine.” Their results were published in Science in April 2013.

“In addition to treatment with drugs, we’re looking into immunotherapies – treatments based on using the patient’s immune system,” said Wills. “Clearly, the difficulty is that all healthy people have very good immune responses to the virus, yet we all still carry it and can never get rid of it. There must be a problem here – the virus is deliberately trying to evade the immune system by manipulating it.”

Sinclair and Wills are trying to understand how the virus does this while in its latent state. Their findings show that HCMV disrupts the proper activation of the immune system by manipulating small signalling molecules called cytokines and chemokines, which normally help to kick-start the process of removing a foreign invader. “Now we know this, we can start to think about intervening,” said Wills.

“We’ve also found that latently infected cells are producing a number of viral proteins,” added Wills. “That’s a dangerous strategy for the virus, because these proteins could be presented on the surface of the cells they’re hiding in, which would attract immune cells like T cells to kill them. Our initial research showed that there are T-cell responses – so why aren’t the viral cells being eliminated? It’s paradoxical.” In further investigations, they uncovered another mechanism in which the virus was promoting a certain subtype of T cell that suppresses the immune system. “So now we’re working to remove the immunosuppressive component of that immune response by either removing or neutralising the function of the immunosuppressive T-cell subtype, to enable the other components of the body’s immune response to target the infected cells,” added Wills.

By targeting latent infection, this work holds great promise for developing better methods of treatment for HCMV and for the design of a vaccine. “If you intervene just before a transplant, and use this immunotherapeutic technique to target the latently infected cells, in combination with the drugs, you can purge the infected cells,” said Sinclair. “This massively reduces the potential that HCMV will reactivate in the person receiving the transplant, because effectively you’re not giving them the virus,” he added.

They have proved this concept in the laboratory and their new MRC grant will enable them to trial its effectiveness in a model system as a stepping stone to human clinical trials. “A decade ago we couldn’t have even contemplated doing this type of work,” said Sinclair, “but now we have worked out what’s going on during latent infection, we can try to target these changes. Being able to clear the latent infection is key to eradicating much of the disease caused by HCMV that we see in the clinic.”

Many of us are infected with a virus we’ll never clear. While we’re healthy, it’s nothing to worry about, but when our immune system is suppressed it could kill us.

̽��ֱ��virus is deliberately trying to evade the immune system by manipulating it

Mark Wills

̽��ֱ��District

HCMV

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Offensive manoeuvres in the war against HIV

lw355 — Mon, 25 Feb 2013 10:31:53 +0000

It was in Los Angeles in 1981 that the first report emerged of an unusual cluster of patients whose immune systems appeared to have failed. This report is now acknowledged as the first scientific account of an infectious disease that was to become the HIV/AIDS global epidemic, infecting 60 million people and killing 25 million to date

Three decades later, and with more than 20 antiretroviral drugs to combat HIV, treatment can now significantly prolong life and reduce the rate of viral transmission. For some patients, life expectancy with uninterrupted treatment is now similar to that of someone who is not infected with HIV – not the death sentence it once was – and the global rate of new infections is at last declining.

Yet, current therapies do not fully restore health and, in resource-poor settings, patients often lack access to antiretroviral drugs. Moreover, because the virus has the ability to insert its genetic material into the genetic material of the patient’s cells, ‘latent’ viruses can re-emerge at any point, necessitating lifelong drug treatment.

“There is no imminent prospect of a vaccine, and there may not be one in the way that we have for measles and mumps, where our own immune system can clear the virus,” explained Andrew Lever, Professor of Infectious Diseases in the Department of Medicine and Honorary Consultant Physician at Addenbrooke’s Hospital. “ ̽��ֱ��bottom line is 60 million immune systems have had a crack at eradicating HIV and all have failed.”

̽��ֱ��virus is both adaptable and versatile, escaping drug treatment by mutating the structure of its proteins. Patients require combinations of drugs – an approach known as highly active antiretroviral therapy (HAART) – because this reduces the chance that a virus will mutate sufficiently to escape all.

Continued research efforts are therefore urgently required, as Lever explained: “ ̽��ֱ��big areas in HIV research are finding new drugs to complement the ones we’ve got already, so as to outrun the virus in terms of resistance, and finding a means to eradicate the latent virus.”

Lever’s research, which has been investigating the mechanisms of HIV infection for almost 25 years, is helping to tackle both of these challenges.

Structural traps

Anti-HIV drugs typically target viral proteins that are involved in the process of entering or exiting the cell. But, as Lever explained, this lies at the heart of resistance to the virus: “Proteins are very adaptable. Time and again the virus escapes the drug by altering its protein structure so that it still functions but the drug no longer recognises it. We decided instead to target the virus’ RNA genetic material.”

Lever’s previous studies had provided fundamental insights into the way in which RNA is packaged, a process that he realised could provide a remarkable opportunity for a completely new type of antiretroviral therapeutic.

For the virus RNA to be packaged and released from the cell as an intact virus particle, it must twist itself into a three-dimensional knot-like structure. It was this structure which Lever and colleagues discovered is used as a packaging signal by the virus. To form the structure, the sequence of the RNA must be highly conserved between viruses. As a result, opportunities for ‘escape mutation’ are limited. A virus protein called Gag uses the knot-like structure to pick out the viral RNA from the thousands of cellular RNAs that are an integral part of the process by which a cell translates the information in its DNA into molecules that enable the cell to function.

Interfering with Gag binding can potentially stop the virus spreading from cell to cell. In collaboration with Professor Shankar Balasubramanian and Dr Neil Bell in the Department of Chemistry, and researchers at the ̽��ֱ�� of Sussex, Lever is now using this phenomenon as the basis for designing novel antiviral drugs. In parallel, work with Professor David Klenerman in the Department of Chemistry is providing the first high-resolution data on the precise conformation of the RNA structure.

̽��ֱ��goal is to create a ‘structural trap’ in which small-molecule drugs lock the RNA in a conformation that can no longer interact properly with Gag. Targeting the function of RNA through its 3D structure is a new direction for antiviral drug discovery, and sufficiently challenging to receive funding from the Medical Research Council Milstein Fund – specifically intended for ‘high-risk, high-reward’ studies.

Using an assay they developed for measuring the interaction between Gag and RNA, the team is now screening a library of small drug-like molecules for those with potential to interfere with the process. “Although it’s very early stages, the molecular hypothesis that we started with for targeting this structure has taken us to a situation where we have molecules that look like they are doing something interesting in the assay,” said Balasubramanian. “Being able to target RNA in this way would be a paradigm shift in terms of new therapeutics for HIV, and other infectious diseases.”

Will RNA-directed therapeutics overcome viral resistance? “It’s a good question and untested,” added Balasubramanian. “Once we find a good small molecule that disrupts binding and packaging then we can address exactly this question.”

Curing HIV

Drug discovery is a key area for the future. However, the scientists also have their eyes on an even bigger prize – a cure for HIV – and a new collaboration between five UK Biomedical Research Centres (BRCs) is now working towards understanding how to rid the body of latent virus.

“Because latent virus exists only as genetic material, essentially indistinguishable from the genetic material of the patient’s cells, it’s effectively hidden. ̽��ֱ��patient’s immune system can’t see these infected cells and the drugs can’t target them,” explained Lever. “ ̽��ֱ��reservoir of infection sits there for years because it’s in very long-lived immune cells. Even if you suppress the virus right down using drug treatment, as soon as you stop the drugs it bounces right back with viruses that, based on their genetic sequence, are historically very old, so these have been latent for a long time.”

̽��ֱ��new project, CHERUB (Collaborative HIV Eradication of Viral Reservoirs: UK BRC), funded by the National Institute for Health Research, brings together researchers from Imperial College, King’s College Biobank, ̽��ֱ�� of Cambridge, ̽��ֱ�� College London and ̽��ֱ�� of Oxford, and is the first pan-BRC cooperative project to compete internationally in a new field of biomedical research.

Lever leads the Cambridge contribution along with Dr Mark Wills and Dr Axel Fun from the Department of Medicine. “Until we learn how to eradicate the latent virus then all we can do is contain it,” Lever explained. “CHERUB will work in collaboration with NHS Trusts and the pharmaceutical industry to recruit new patient cohorts for studies that range from fundamental laboratory research through to large-scale clinical trials of novel agents.”

̽��ֱ��Cambridge researchers will develop an assay to detect latent virus that will be used to provide a measure of the relative success of drugs, as well as expand current research areas to learn new ways to rouse the virus from its latency.

“All HIV patients have latent virus – it’s a fact of life,” added Lever. “You can suppress active viruses with current conventional drugs so that the patient’s immune system recovers but you can’t get rid of the latent virus. ̽��ֱ��aim now is to suppress the virus to the point where the immune system recovers but at the same time to wake up and eradicate the virus from the latently infected cells. And then we are talking about a cure.”

For more information, please contact Louise Walsh at the ̽��ֱ�� of Cambridge Office of External Affairs and Communications.

Although anti-HIV drugs can significantly prolong life, patients must take the drugs for the rest of their lives. New approaches to therapeutics may hold the answer to finding a cure for HIV.

̽��ֱ��bottom line is 60 million immune systems have had a crack at eradicating HIV and all have failed.

Andrew Lever

Cynthia Goldsmith, Centers for Disease Control and Prevention

HIV-1 budding from a cultured cell

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