Host genetics in JCV and EBV infection

Multiple Sclerosis (MS) is a neurodegenerative disease caused by several genetic and environmental factors. In MS, auto-reactive immune cells enter the brain and destroy the myelin leading to neuronal damage and cell death. For patients, this means increasing loss of motor function, as well as impaired cognitive function. In Sweden, MS affects around 1/400.

There are treatments but no cure for MS. Natalizumab is a so called second-line drug given as an infusion once every month. It is very efficient in reducing the number of relapses (periods when the disease is active) but has severe side-effects, such as JC-virus infection of the brain causing progressive multifocal leukoencephalopathy, PML.
PML is a severe disease and often fatal. Therefore it is very important to study the relationship between MS and JC virus infections further, to be able to identify patients at risk and reduce PML incidence.

Another virus that is associated with an increased risk for MS (but not PML) is Epstein-Barr Virus (EBV). Most of us are infected during childhood, but those who are infected during their teens often develop infectious mononucleosis.

We are currently looking at host genetic factors determining the outcome of JC virus and EBV infection in MS patients and controls from Sweden. We have found genes involved in the level of antibodies directed against either JC virus or EBV in our study population.

The aim of the project is to try and replicate these findings, through PCR-based genotyping methods, and statistical analysis.

We are looking for an enthusiastic and motivated student who wants to gain experience in working in a lab and who wants to contribute to our group.

Please contact Emilie Sundqvist (PhD-student) for more information. Formal supervisor will be associate professor Ingrid Kockum (Ingrid.kockum(at)ki.se). Our lab is at the Center for Molecular Medicine, Karolinska university hospital Solna. We need a student for the fall semester 2011, and deadline for application is August 22nd, 2011.