Epstein-Barr virus (EBV) is a herpes virus otherwise known of as human herpesvirus 4 (HHV-4). It is most well known for causing glandular fever but research shows that EBV infection is also linked to an increased risk for various autoimmune conditions including rheumatoid arthritis, dermatomyositis and multiple sclerosis.
Multiple sclerosis is an autoimmune, inflammatory disorder in which the body's own immune system attacks the myelin sheath that forms a protective coating around nerves in the brain and spinal cord and also aids the conduction of nerve signals to the rest of the body. This causes a wide range of problems and disturbances in balance, movement and vision that can become severe over time.
Evidence suggests that herpes viruses may play a role in the pathology of demyelination and studies have shown that individuals who have never had EBV have a reduced risk for developing multiple sclerosis compared with individuals who have been infected. In addition, those infected with EBV during adolescence are at less risk of developing multiple sclerosis than those infected at a younger age.
In 2009, an Italian team of researchers presented their findings that brain lesions from individuals with multiple sclerosis contained B lymphocytes infected with an abnormal accumulation of EBV. The researchers also demonstrated that the B lymphocytes in the brain are targeted in an immune response that is mounted against them, which causes inflammation and in turn, tissue destruction. Another study currently being carried out at the university of Birmingham in the UK is trying to establish whether or not the immune response to EBV really does cause autoimmune destruction of myelin.
Another study looked at the expression of EBV markers in the brains of deceased multiple sclerosis patients. In almost all of the cases examined (21 of 22) , there was evidence of EBV infiltrating B cells and plasma cells in a significant proportion of the brain. In some cases of secondary progressive multiple sclerosis, B cell follicles forming in the cerebral meninges were found to be sites where EBV had persisted.
Latent viral proteins were a regular occurrence in the samples overall, but actual reactivation of the viral particles seemed to be confined to these newly formed B cell follicles. Furthermore, activated cytotoxic T cells were observed along with signs of plasma cell cytotoxicity at these major sites of EBV infection.
Although it is unclear whether EBV-infected B cells in the central nervous system cause the development of multiple sclerosis or whether this occurs as result of another unknown disease process, many researchers believe that EBV persistence and reactivation is an important contributor to the pathology of multiple sclerosis.