EBV is a member of the herpes family of viruses that are common in humans.
The silent infection and the life-long persistence are the keys to the widespread infection of EBV in the human population.
In most individuals, EBV infection occurs early in childhood and goes unnoticed.
In contrast, delayed primary infection during adolescence can lead to infectious mononucleosis (IM) = glandular fever.
EBV primarily targets and remains latent in memory B cells.
Depending on the type of latency, EBV expresses different sets of latent products.
In the latency typically seen in IM, up to 12 viral products, including 6 EBV-encoded nuclear antigens (EBNA-LP, EBNA1, EBNA2, EBNA3A, EBNA3B, and EBNA3C), 3 latent membrane proteins (LMP1, LMP2A, and LMP2B) and large quantities of 2 non-coding RNAs (EBERs) are expressed
A small percentage of latently infected cells intermittently enter the lytic cycle resulting in the release of viral particles
This transition from latency to lytic cycle is triggered by the expression of two immediate early viral proteins, BZLF1 and BRLF1
Almost all MS patients are infected with EBV compared to ~95% non-MS controls.
Thus, EBV seronegative individuals have almost zero risk of developing MS.
However, a dramatic upsurge in MS risk is seen when these individuals seroconvert following EBV infection.
Furthermore, individuals who have a history of EBV-associated IM have also been shown to be at increased risk of developing MS.
In the paper below
Overall, 91/101 (90%) of MS cases were EBV positive by l compared to only 5/21 (24%) non-MS cases