PHILADELPHIA, PA — Salient medical exploration at The Wistar Institute may have shed light on the role of the Epstein-Barr Virus (EBV) in the development of multiple sclerosis (MS). Paul M. Lieberman, Ph.D., and Samantha Soldan, Ph.D., along with their team, have uncovered how EBV-infected B cells may fuel an inflammatory reaction contributing to MS. Furthermore, they have presented a promising method to selectively target these B cells, mitigating the harmful autoimmune response associated with MS.
Here’s a brief background: EBV, a typically latent herpesvirus, resides in the bodies of over 90% of humans without causing any symptoms. However, this seemingly harmless virus has been associated with numerous diseases, including MS, an incurable, chronic autoimmune disease where the immune system attacks the myelin protective covering of brain and nervous system neurons.
While the link between EBV and MS has been recognized, the exact influence of the virus in the disease’s development is not fully understood. To unravel this mystery, Lieberman and his team collaborated with Steven Jacobson, Ph.D., from the National Institute of Neurological Disorders and Stroke. The researchers examined spontaneous lymphoblastoid cell line (SLCL) samples from healthy individuals, patients with active MS, and patients with stable MS.
Why are B cells noteworthy here? As pivotal participants in the immune system, B cells determine which biological signals warrant an immune response. Upon infection with EBV, these cells become ‘immortalized’, meaning they can continue to divide indefinitely, becoming LCLs. This potential for endless division occurs spontaneously in the body due to EBV infection.
After examining the collected samples, Dr. Lieberman and his team determined that the MS-positive samples displayed a higher level of genes associated with active EBV and inflammatory signaling, and more notably, an increase in the expression of the FOXP1 protein, which promotes EBV gene expression. This revelation provides a possible mechanism for active EBV’s contribution to inflammation and disease in MS.
The team didn’t stop there. They tested multiple antiviral compounds on the SLCL samples and found one, TAF, which decreased active EBV gene expression without killing the cells. TAF also notably reduced the expression of inflammatory cytokines in the active MS patient SLCLs. Experimentation revealed that administering TAF in combination with antiviral T cells reduced the T cell response, a significant factor in MS’s autoimmune dysfunction.
“We’ve shown that problematic inflammation from active EBV can be selectively targeted, reducing damaging immune responses,” said Dr. Lieberman. This shines a ray of hope on potentially discovering whether TAF or other EBV inhibitors could be an effective treatment for MS, halting autoimmune damage without causing widespread and perilous cell death.
The research underway at The Wistar Institute could have enormous implications for the future of MS treatment and care. With the potential to stop the autoimmune damage without causing harmful cell death, this breakthrough could revolutionize how we manage this debilitating disease. This could mean a new lease of life for millions of people living with MS worldwide. One virus may, in time, hold the key to treating one of the most complex diseases known to humanity.
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