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Jun 2014
Predicting MS in children
Oct 2014
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Breakthrough study shows great promise

Research Progress Report

Immune control of Epstein-Barr virus in MS  

Professor Michael Pender at the University of Queensland has for many years been researching the relationship between the Epstein Barr Virus (EBV) and the immune system, and its role in MS. In 2013, he received further funding from the Trish MS Research Foundation in partnership with Foundation 5 Million Plus and MS Research Australia to continue these investigations.        

There is a large body of evidence from both Australian and international research indicating that infection with the Epstein-Barr virus (EBV) may play a role in the cause of MS. EBV is an extremely common virus, causing very mild symptoms in childhood, but often causing glandular fever when contracted in adolescence or adulthood.  

Around 95% of all adults have evidence of a previous EBV infection, however, at least 99% of people with MS have had EBV, suggesting that EBV, together with other environmental and genetic risk factors, is a key piece in the MS puzzle.  

EBV infects the B cells of the immune system, and once the initial active infection is brought under control by other cells of the immune system, the virus persists inside B-cells in a latent, or resting, state.  

In his previous work, Professor Pender has shown that people with MS have decreased numbers of a particular type of immune cell known as CD8 T cells which may potentially allow the accumulation of EBV-infected cells in the brain.  

In this first year, Professor Pender has already been able to show that the deficiency in CD8 T cells in people with MS is specifically due to reduced numbers of a sub-group of CD8 T Cells called CD8 effector memory T cells. These cell types retain a memory of pathogens that they have ‘seen’ before and can immediately mount a response to clear infected cells.  

Professor Pender has also examined blood samples from a large number of people with all forms of MS including the earliest signs of MS, known as Clinically Isolated Syndrome (CIS). The CD8 effector memory cell deficiency is present in all of these stages and types of the disease, including the very earliest stage, CIS, suggesting that is a cause, rather than a consequence, of the disease.  

In the coming two years, Professor Pender will continue to tease apart the mechanism by which this deficiency may lead to inadequate control of EBV infection, and how this may lead to MS, including the genetic factors that may be involved.  

This work is vitally important for the development of new therapies aimed at preventing and treating MS by controlling EBV infection. An exciting development in this direction was revealed earlier this year, when Professor Pender and his colleagues published the promising results for a patient with secondary progressive MS who was treated with CD8 cells primed to recognise EBV. In parallel with continuing his work in the laboratory, Professor Pender is now working towards an early stage clinical trial to test this treatment in more patients with secondary progressive MS.  

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