MS & Epstein-Barr Virus Update – Part 1

Today, we are presenting Part 1 of a two-part update on a role for Epstein-Barr Virus (EBV) in multiple sclerosis (MS).  This first part is going to focus on the evidence of why people think that a link may exist between the two, while Part 2 will look at a new theory as to how it (EBV) might be involved.

THE EVIDENCE (FOR)

A number of studies have provided reasons to suggest that EBV may be involved in the development of MS.  The key points are:

• Very few (to almost zero) people develop MS if they haven’t been previously infected with EBV

• Being infected with EBV, doesn’t necessarily mean that you will develop infectious mononucleosis or glandular fever.  However, people who have glandular fever have almost double the risk of getting MS compared to people who have an EBV infection without symptoms.

• The relative risk of developing MS for people who have been infected with EBV is around 15.  The relative risk for those who were infected with EBV and developed glandular fever is around 30.  This is compared to the strongest known genetic risk factors, the HLA molecules, which have a relative risk of around 3 – 4.

• A recent study in a single individual with secondary progressive MS (SPMS) showed that a treatment aimed at completely clearing the EBV infection provided significant benefits.  This work was completed by Professor Michael Pender in Queensland and his studies are ongoing.

THE EVIDENCE (AGAINST)

There is one main piece of evidence that goes against the link between EBV and MS.  It is estimated that greater than 90% of adults have been previously infected with EBV.  However, the incidence of MS is much, much lower than this.  This has always made it difficult to understand how EBV could be a cause in some people, but not lead to MS in many others.

OUTSIDE-IN OR INSIDE-OUT?

When it comes to autoimmune diseases, there is much debate about how they arise.  There are two main concepts.

OUTSIDE-IN

This is the more commonly accepted theory in autoimmune diseases.  In this theory, an infection triggers an immune response that causes autoreactive T and B cells present in the body to begin to attack self-tissue.

INSIDE-OUT

In this theory, MS would begin with a primary lesion in the central nervous system (CNS).  It is this initial lesion that causes new self-targets for the immune system to be released, which leads to the irregular autoimmune response.

There is a suggestion that the first model has become more popular because of the use of specific-pathogen-free (SPF) mice for research.  It has been proposed by some people that the fact that these animals aren’t exposed to similar environmental conditions to humans may skew the findings.

In Part 2, we will look at findings obtained from a marmoset (monkey) model of EAE, which have been bred under similar environmental conditions to humans.

Stay tuned!