As reviewed by others (
Robinson and Steinman, 2022
;
Sollid, 2022
;
Giovannoni et al., 2022b
;
Läderach and Münz, 2022
;
- Läderach F.
- Münz C.
Altered immune response to the epstein-barr virus as a prerequisite for multiple sclerosis.
Cells. 2022; 11https://doi.org/10.3390/cells11172757
Maple et al., 2022
) and in our prior Editors' commentary (
Giovannoni et al., 2022a
), the evidence that EBV plays a pivotal role in the causal pathway that leads to
MS is now overwhelming. Currently, there are two main competing theories of how EBV
causes MS. On the one hand, is the ‘hit-and-run’ theory that EBV triggers autoimmunity through molecular mimicry, i.e. EBV fools the
immune system into making an immune reaction against its proteins/antigens, in particular,
EBV nuclear antigen-1 (EBNA-1), which then cross-reacts with antigens in the central
nervous system (CNS) to cause focal inflammatory events that is MS (
Läderach and Münz, 2022
). A second theory is that EBV is the ‘driver of MS’ by continually cycling through its latent and lytic infection phases is responsible
for driving MS pathology (
- Läderach F.
- Münz C.
Altered immune response to the epstein-barr virus as a prerequisite for multiple sclerosis.
Cells. 2022; 11https://doi.org/10.3390/cells11172757
Giovannoni et al., 2022b
). This could either be by (1) direct CNS infection, (2) continuously stimulating
autoreactive T and B cells, or (3) upregulating a second virus such as MS-associated
HERVs (human endogenous retroviruses or human herpes virus 6), which in turn cause
tissue damage (
Küry et al., 2018
). This latter is called the ‘dual-viral’ hypothesis of MS (
Giovannoni et al., 2007
).To read this article in full you will need to make a payment
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Publication history
Published online: November 26, 2022
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