The Wistar Institute's Paul M. Lieberman, Ph.D.
, and lab team led by senior staff scientist and first author, Samantha Soldan, Ph.D., have demonstrated how B cells infected with the Epstein-Barr virus (EBV) can contribute to a pathogenic, inflammatory phenotype that contributes to multiple sclerosis (MS); the group has also shown how these problematic B cells can be selectively targeted in a way that reduces the damaging autoimmune response of multiple sclerosis.
The lab's findings were published in Nature Microbiology in the paper, "Multiple sclerosis patient derived spontaneous B cells have distinct EBV and host gene expression profiles in active disease." EBV -; a usually inactive, or latent, herpesvirus -; affects most of the human population; more than 90% of people carry the virus as a passive, typically symptomless infection. However, EBV infection has been linked to several diseases, including MS: an incurable, chronic autoimmune disease that causes the body's immune system to attack the myelin sheath of neurons in the brain and nervous system.
Because myelin sheathing facilitates fast nervous system signaling (the fatty insulation of myelin along a neuron's axon allows electrical impulses to travel through neuronal networks faster), its degradation can cause a wide variety of symptoms in both type and severity that may include motor control disruption, sensory issues, and speech difficulties. Though researchers know that EBV can contribute to the development of MS, t.
