27 Aug 2015

Summer School at IGH

In July we hosted our very first Science Summer School for a group of seven local pupils aged 16-19. This was a pilot project supported by the Wellcome Trust's Institutional Strategic Support Fund. Our aim was to provide a structured week-long work experience programme for STEM students through a mix of meetings, talks and practical experiences across all three of our Institute locations. Matthew Davies from St Edward's College took part and here he tells us about his week.

IGH Science Summer School - class of 2015!
This summer I took part in the Institute of Infection and Global Health's Summer Science School with several other students interested in biology and chemistry. It took place from Monday to Friday and included a variety of activities every day. After introducing ourselves and getting to know each other on the Monday, the activities started on the Tuesday.We were split up into groups and in the morning, we started with Western blotting and in the afternoon, cell counting. The majority of the week was spent in the institute's Ronald Ross building but on Wednesday, some of us went to the IC2 building and some went to the Leahurst campus. I went to the IC2 and what a fun, jam-packed day this was! While we were there, we learned about why there was a snail culture room, looked at some rhino worms under a microscope and watched a diagnostic test for worms in rabbits! On Thursday, we returned to the Ronald Ross building. After a demonstration of the ELISA test in the morning, we extracted DNA from Pseudomonas bacteria in the afternoon. This was the most exciting and interesting part of the week! Finally, on Friday, in our groups we gave presentations on what each of us did during the week. Overall, I thought the week was extremely fun and gave me a valuable insight into some of the techniques regularly used in laboratories. Also, I found the regular meetings with PhD students very helpful too. Thank you to everyone involved for such a great week!

Matthew Davies 

12 Aug 2015

How to get the most out of veterinary work experience

A-level student Miles Huglin tells us about his week of veterinary work experience here with us at the University of Liverpool.

Anyone hoping to get anywhere in the veterinary world needs work placements. Sites for animal care vary massively, from vet practices to slaughter houses, and to ensure you’re up for the job, it’s necessary to visit as many of these as possible.  That’s why teachers, parents and lecturers stress the importance of work experience so much to students from such a young age – the sooner you start, the better it looks on your CV. But what does that mean?

No matter how impressive it might be on paper, absent-mindedly staring in the direction of a bunch of adults doing their jobs isn’t gaining experience; it’s wasting it. And as an A level student myself, I know many of us are guilty of this. A week at University of Liverpool's School of Veterinary Science and Institute of Infection and Global Health, however, has taught me how much more valuable these opportunities can be, and how to make the most of every second you get; it’s not only about building your CV, it’s about learning how the network behind veterinary medicine works, and how you can be a part of it.

A dog being assessed at the small animal teaching hospital

Taking your pet to the vet, you meet a receptionist and a practitioner. Volunteering there, you meet the nurses and students, clean out the cages and think you’ve seen it all. But where do those blood samples go? Where do the results come from? How have the surgical and medical procedures you watch been developed? These are easy questions to overlook while making tea and glancing at the clock every minute until lunch, but why not ask?

While working at my local vet in Hatfield, I saw animal samples being taken sent off and witnessed decisions being made based on the test results that came back. It never once occurred to me that somewhere in the country it was someone’s job to sift through the skin tags, blood and faeces to obtain these vital data;  Paul Gilmore, of Test-a-Pet diagnostics, talked me through how the company analyses samples, ranging from tortoise toes from Birmingham to rabbit droppings from London. While I was with him, a dog’s blood was being tested for Lyme disease, with the owner of this animal somewhere else in the country having no idea where this small sample of their beloved pet was; this simple fact was what made me realise just how much of this medical process goes on in the background.

Lyme disease, as I discovered, is caused by a type of bacteria of the ‘borelia’ genus, closely related to the species which was being studied by my next lecturer at Liverpool, Dr Nick Evans (one of the single most enthusiastic scientists I have ever met). This researcher was investigating Bovine Digital Dermatitis – a problem affecting the back legs of cows and sheep which lowers their milk yields and fertility. Having identified the bacterium he believed to be the cause, Nick was looking into how the disease is spread (from calf hoof to calf hoof), and effective solutions: medications and drugs are all potentially viable, but simply raising awareness seemed to him the most important factor. He told me that many farmers clip their cows’ hooves to prevent the spread without even disinfecting their clippers between cattle, and 90% of these tools were found to be contaminated with the treponema which causes the disease! As with any disease investigation, however, a major hurdle in this research was posed by the fundamental basis of proving that the bacterium in question caused the disease, so that farmers would listen. It’s fascinating to think that your pet’s infection was once a non-diagnosable enigma with no known cause, until someone like Nick did something about it.

Dr Nick Evans
Dr Nick Evans
With this thought I was brought to technicians Catherine Hartley and Jenna Dawson, who were growing cow hoof tissue in culture and planning on introducing Nick’s treponemal bacteria to analyse the results. To prove his hypothesis, they hoped to observe a pathogenic response from the bacteria, and if this occurred then the testing could be progressed to cows themselves; the closer to the animals you do your research, the more conclusive the results tend to be, but the team wanted an indication of the likelihood of positive results before they moved to live cattle trials.

Staff working in a laboratory
In the lab
I was astounded. All this work was to make a tiny bit of progress in the understanding of one disease, but with scientists around the country investigating and developing cures for so many others we are gaining a better understanding of a huge number of the diseases affecting our animals every year; I was only catching a tiny glimpse of this in the hours I spent learning about this one cattle disease.

Much of this might be difficult to relate to, but what stands out is clear: opportunities in the veterinary world are endless. With a rapidly growing human population to feed and so many diseases like Ebola and Avian Flu being identified as zoonotic (spreading from animals to humans), research into our animals’ diseases is more important than ever. And why stop there? A degree in veterinary medicine not only lends itself to a practical career, but also to one in scientific research and experimentation. At a university like Liverpool, the diseases facing us today are being fought by scientists, doctors and vets working hand in hand.

I went to Liverpool hoping to see veterinary students at work, and left with my eyes opened to all the possibilities that follow; sitting back, watching surgeries and keeping questions to myself simply wasn’t an option, and I can’t keep the experience to myself. The network of scientific minds behind every prescription, every operation and every routine practised by vets around the country is much more extensive than we can ever comprehend.

So, given the opportunity to scratch the surface of such a limitlessly fascinating scientific world, why bother doing veterinary work experience if all you’re learning to do is make the perfect cup of tea?

Miles HuglinMiles Huglin is an A-level student from Hertfordshire who spent a week at the University of Liverpool on a work experience placement earlier this year. For more information about work experience opportunities at the University please visit www.liv.ac.uk/working/jobvacancies/workexperience

10 Aug 2015

When we understand how HIV replicates despite drug therapy, then we can stop it

Anna Maria Geretti, University of Liverpool
The last two decades has seen great advances in the treatment of human immunodeficiency virus (HIV). Therapy can now be tailored to the patient, ensuring patients’ bodies can tolerate it and making the drugs extremely effective.

Those diagnosed with HIV before the virus has caused significant damage to their immune system can now expect to live long and healthy lives, similar even to those of people without the infection. This is simply an amazing success story for modern medicine. So what’s stopping us from eradicating the virus altogether?

HIV infects white blood cells called CD4 T-lymphocytes, important immune cells that protect the body against infections and cancers. Without treatment, HIV makes new copies of itself within each infected cell – new viruses that then leave the CD4 cells and infect new cells, starting the process over again. Eventually the loss of CD4 cells and damage to the immune defences are so severe that disease develops.

Treatment stops HIV production within the CD4 cells, preventing damage to the immune system and further progression of the disease. This works very well – provided the anti-HIV drugs are continuously present in the body. This means medication must be taken regularly and without missing doses for therapy to remain successful.

From left to right: a red blood cell, a platelet and a T-lymphocyte, pictured using a scanning electron micrograph. NCI-Frederick

HIV is a stealthy opponent

A preferable solution would be to eradicate HIV and cure the infection once and for all. However current HIV therapy, while remarkably successful in stopping virus production, cannot cure the infection and must therefore be carried out throughout a patient’s life. For those who are diagnosed with HIV in their thirties, this currently means around 40 years of uninterrupted daily therapy.
We have long understood that during treatment the HIV virus hides inside the CD4 T-lymphocytes, by inserting, or “integrating”, its own genetic information into the DNA of the CD4 cells. The integrated virus is invisible to both drugs and immune defences, and as soon as therapy is interrupted it fuels new virus production.

Research, such as my recent study, shows that the integrated HIV “reservoir” in the CD4 cells doesn’t diminish during treatment – even over a period of 14 years.

Why is the HIV reservoir so stable, even when the virus isn’t replicating itself during therapy and any integrated virus is expected to die with the host CD4 cell when it dies naturally? Understanding this is key to finding a cure for HIV.

How does HIV survive therapy?

We are making progress. The mechanism is relatively simple: whenever something stimulates the CD4 cells to multiply, any integrated HIV will also be split across the new cells with the rest of the cell DNA, a sort of silent HIV growth that does not require the cells to actually produce and release new viruses. So whenever a CD4 cell multiplies to produce more cells, it copies itself and the HIV at the same time, automatically incorporating the HIV at the birth of the new cell.

My research provides more evidence for this view, by showing that the amount of integrated HIV in CD4 cells is not a product of active virus replication. Instead, it’s associated with the body’s natural immune response, which stimulates CD4 T-lymphocytes to multiply – carrying the virus with them.

Finding a cure

In recent years there have been serious efforts from academia and pharmaceutical companies to find a way to eradicate HIV infection. One strategy is to stimulate immune cells in such a way that they are better able to fight the virus. However this study’s findings cast doubts on this strategy: stimulating the immune system may simply cause CD4 T-lymphocytes to multiply, expanding the virus reservoir as they do so.

Other strategies appear more promising: they aim to gently stimulate CD4 cells in such a way that active HIV production is started, so that the virus is recognised by both the drugs and the body’s natural immune responses, or perhaps by infusion of antibodies, and is killed off. This “kick and kill” strategy is currently being tested both in the laboratory and in clinical trials, and initial results are encouraging.

HIV is a clever virus, and clever strategies will be required to eradicate it – but recent research findings offer hope that a HIV cure may one day be possible.

The Conversation
Anna Maria Geretti is Professor of Virology & Infectious Diseases at University of Liverpool.
This article was originally published on The Conversation. Read the original article.
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