Epstein-Barr and Lupus
A. G. Moore 8/22
As pieces to the lupus puzzle are discovered and rearranged, the role of a viral antagonist comes to the fore. Among the several specific viruses which have been associated with systemic lupus, one of the most consistent actors has been Epstein-Barr. While as much as 95% of the population (in the U.S., anyway) eventually is affected by this virus, in most cases infection is an event without noticeable consequence. For some people, however, Epstein-Barr can be a serious illness.
Mononucleosis afflicts about 2% of those who contract Epstein-Barr (see:Students Still Getting Mono After all these Years, http://www.nytimes.com/ref/health/healthguide/esn-mono-ess.html). And systemic lupus, according to the NIH, can actually be induced by infection with Epstein-Barr (see: Epstein-Barr virus infection induces lupus autoimmunity, (http://www.ncbi.nlm.nih.gov/pubmed/17121489).
To be clear about what this means, let me restate the case for an Epstein-Barr/Lupus link: Epstein-Barr infection has been shown to be one provocation of the immune system which can eventually lead to systemic disease. Epstein-Barr can cause lupus in a susceptible person; by susceptible, I mean someone who has a genetic predisposition to develop lupus. The process by which this immune system antagonism takes place is spelled out in the NIH article cited above. According to that article, “the first lupus-specific autoantibodies arise from particular antibodies directed against Epstein-Barr virus Nuclear Antigen-1 (EBNA-1) and that infection with Epstein-Barr virus (EBV) is an environmental risk factor for lupus.”
Understanding how someone goes from having normal immunity to having autoimmunity is critical in unraveling the lupus puzzle. The researchers at NIH believe they have insight into the path from normal immunity to autoimmunity, at least when it comes to infection with Epstein-Barr. The researchers posit that the presence of Epstein-Barr stimulates the production of an antibody called “anti-EBNA-1”. Anti-EBNA-1 apparently attaches itself to “lupus-specific autoantigens (Sm or Ro)”. In a person susceptible to lupus, the autoimmune trigger has, in effect, been pulled. After the Anti-EBNA-1 antibodies and the lupus-specific-autoantigens meet up, a cascade of immune system events occurs which leads to the development of lupus.
Of course, the NIH article which spells out the Epstein-Barr/lupus association is laden with terms like “suggest” and “seems”. Much like Agatha Christy’s dogged detective, Hercule Poirot, NIH scientists are on a trail. The clues they have assembled are persuasive, persuasive enough for them to conclude, “In aggregate, these results are consistent with an immune response against Epstein-Barr virus being important in at least some patients for the initiation of lupus autoimmunity”. That’s a pretty compelling statement, considering the usual semantic reserve of the research-oriented scientific community.
What does all of this mean to someone who has lupus? As in every instance where an association between lupus and an antagonist is established, we may not know if this connection explains our individual experience. What we do know, though, is that in the future others, perhaps members of our own families who share our genetic make-up, may benefit from the understanding that comes from sorting the various clues to the lupus puzzle.