Research Progress Report
of Epstein-Barr virus in MS
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.
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
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.
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.
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.
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.
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.
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.
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.