Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) ultimately resulting in severe disability and morbidity. The disease presents with a chronic inflammatory phenotype, and B cells appear to play a major role, being difficult to control. MS is caused by a combination of predisposing genetic factors and promoting environmental factors. Among environmental factors, more and more evidence has accumulated, pointing to a pivotal role of Epstein-Barr virus (EBV), a B cell-tropic human herpes virus. Many of the known clinical characteristics of MS, including intrathecal IgG synthesis and inflammatory foci in the CNS, can be related to the entry of EBV-infected B cells to the CNS followed by entry of T helper cells, stimulating the B cells, and cytotoxic T cells, attempting to eliminate EBV-infected B cells. The result is an inflammatory process, which damages surrounding tissue. Likewise, several known genetic and environmental factors can be connected to the EBV infection process and the ensuing immune response. Many questions remain unanswered in this respect, including the relative role of molecular mimicry, bystander activation, regulatory T cells, and autoimmune reactions. Therefore, more attention needs to be drawn to how EBV orchestrates the pathogenic immune responses in MS development.
This Research Topic will focus on current knowledge and future research on the role of Epstein-Barr Virus in multiple sclerosis, including the subjects outlined below. Within this Research Topic, we welcome the submission of Original Research, Review, Mini Review, and Opinion articles. We welcome submissions based on the following sub-topics (but are not limited to them):
- The immune response to EBV in MS
- EBV immune evasion in relation to MS
- EBV and the role of B cells, T cells, NKT cells, and NK cells in MS
- EBV and current MS therapies
- EBV and future MS therapies
- EBV and MS epidemiology
- EBV tropism and life cycle in relation to MS
- Other (herpes) viruses in MS (compared with EBV)
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) ultimately resulting in severe disability and morbidity. The disease presents with a chronic inflammatory phenotype, and B cells appear to play a major role, being difficult to control. MS is caused by a combination of predisposing genetic factors and promoting environmental factors. Among environmental factors, more and more evidence has accumulated, pointing to a pivotal role of Epstein-Barr virus (EBV), a B cell-tropic human herpes virus. Many of the known clinical characteristics of MS, including intrathecal IgG synthesis and inflammatory foci in the CNS, can be related to the entry of EBV-infected B cells to the CNS followed by entry of T helper cells, stimulating the B cells, and cytotoxic T cells, attempting to eliminate EBV-infected B cells. The result is an inflammatory process, which damages surrounding tissue. Likewise, several known genetic and environmental factors can be connected to the EBV infection process and the ensuing immune response. Many questions remain unanswered in this respect, including the relative role of molecular mimicry, bystander activation, regulatory T cells, and autoimmune reactions. Therefore, more attention needs to be drawn to how EBV orchestrates the pathogenic immune responses in MS development.
This Research Topic will focus on current knowledge and future research on the role of Epstein-Barr Virus in multiple sclerosis, including the subjects outlined below. Within this Research Topic, we welcome the submission of Original Research, Review, Mini Review, and Opinion articles. We welcome submissions based on the following sub-topics (but are not limited to them):
- The immune response to EBV in MS
- EBV immune evasion in relation to MS
- EBV and the role of B cells, T cells, NKT cells, and NK cells in MS
- EBV and current MS therapies
- EBV and future MS therapies
- EBV and MS epidemiology
- EBV tropism and life cycle in relation to MS
- Other (herpes) viruses in MS (compared with EBV)