They found that EBV does persist within self and polyreactive B cells, but found no evidence that it favoured the survival of pathogenic autoreactive B cells. On the contrary, EBV+ memory B cells express lower levels of self-reactive and especially polyreactive antibodies than their uninfected counterparts. This work suggests that EBV has only a modest effect on the GC process, which allows it to access and persist within a subtly unique niche of the memory compartment characterized by relatively low levels of self and polyreactivity. They suggest this might reflect an active process of the virus to minimize the risk of autoimmune disease
"This paper questions one of the hypotheses put forward the EBV causes MS by immortalising autoreactive B cells, i.e. B cells that produce antibodies against self or B cells that stimulate T cells, to attack self proteins that these antibodies bind to."
"One of the unsolved mysteries in MS is how and when does EBV trigger MS? What is the biology of this process? If we understood this we could target this process or processes to treat or prevent MS."