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Scientists win £800,000 to boost research into fighting viruses

15.03.2005


A team of University of Glasgow scientists have received a grant of £800,000 from the Wellcome Trust to research a mechanism that blocks a critical step in the replication cycle of retroviruses. In the long term, the research could lead to the design of new therapeutic strategies or drugs against retroviruses, which cause diseases such as AIDS and certain leukemias.



Mammals have evolved several mechanisms to fight viral infections, and insight into how humans and animals successfully limit virus spread helps to develop effective anti-viral drugs and vaccines.

The scientists are set to further investigate a mechanism that may be able to stop so-called retroviruses in their tracks. Retroviruses, during their life cycle, spread by permanently inserting their genetic material into healthy cell’s DNA.


The scientists, led by Professor Massimo Palmarini from the University of Glasgow’s Faculty of Veterinary Medicine, are investigating how some endogenous retroviruses (’benign’ retrovirusese present in the genome of all mammals) protect hosts by interfering with the infection by related disease-causing retroviruses.

The new grant will boost the study of how an ’endogenous’ retroviruses (ERV) named enJS56A1 interferes with a pathogenic ’exogenous’ retrovirus (JSRV), the cause of major infectious diseases of sheep. enJS56A1 forms viral particles that ’stick’ together and cannot exit the cell and spread to other cells. JSRV instead forms particles normally able to exit the cell.

However, when JSRV and enJS56A1 are present in the same cell only defective ’sticky particles’ are formed, effectively blocking viral infection. Understanding the mechanisms of enJS56A1-induced block can lay the foundation to develop new drugs that stop production of viruses from infected cells.

The research is set to shed light on how retroviruses evolve and will help explain late steps in the retroviral life cycle. Understanding how enJS56A1 functions could provide a model for designing new anti-retroviral therapies that work on cells already infected by retroviruses. Many current anti-retroviral drugs function only immediately after the virus infects a new cell.

Professor Palamarini, from the University of Glasgow’s Veterinary Faculty, said: ’The grant is set to develop much needed research into viral infections. We need to understand more about how retroviruses work and this work could eventually lead to new treatments to fight retroviruses.’

’Like all viruses, retroviruses insert their genetic material into host cells and then force the host to make copies of the virus. Unlike other viruses, however, retroviruses permanently insert a copy of their genes into the genome of cells they invade. Every sheep on the planet has retroviruses that are present in the genome like every other gene. In fact, all animal species - humans included - have retroviruses that are genetically inherited.’

The University of Glasgow recently recruited Professor Massimo Palmarini, a world-leading expert in viral pathogenesis and lung cancer. Most recently of the University of Georgia, USA, Professor Palmarini now leads a team of molecular cancer specialists and virologists at Glasgow and is set to continue his groundbreaking work into a virus induced type of lung cancer, the disease which led to the demise of Dolly the sheep, the world’s first cloned mammal.

His expertise spans the fields of viral pathogenesis, infectious disease and cancer. The major focus of Professor Palmarini’s research is the study of a naturally occurring contagious lung cancer of sheep, ovine pulmonary adenocarcinoma (OPA) that cannot currently be controlled, and leads to significant economic loss in the UK and beyond. Research into the mechanisms underlying this form of lung cancer could provide strategies to understand the onset and progression of human lung cancer, the leading cause of deaths in cancer patients.

Jenny Murray | alfa
Further information:
http://www.gla.ac.uk:443/newsdesk/pressreleases/stories.cfm?PRID=3216

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