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MUSC study links Lupus, Epstein-Barr virus 

An MUSC study suggests a common viral infection may increase the risk of lupus in African-Americans. Findings also show that a genetic variation may affect the immune response to Epstein-Barr virus in lupus patients.
  
Almost everyone has been infected with Epstein-Barr virus (EBV), a member of the herpes family and one of the most common human viruses. Symptoms range from a typically mild childhood illness with a fever and sore throat to mononucleosis in teenagers or adults. After the initial infection, the virus settles into beta cells in the immune system, where it remains for life, mostly dormant, with occasional bouts of reactivation and replication. 
  
Due to its interference with immune function and promotion of certain antibodies, EBV was implicated in systemic lupus erythematosus (SLE), a chronic, potentially debilitating autoimmune disease that more often affects women and is also more common in blacks. Although the specific cause of lupus is not yet known, both genetic and environmental triggers are likely involved. 
  
“Although EBV was a known risk factor for lupus for more than three decades, this is the first study to show that an interaction between a gene of the immune system (CTLA-4) and environment (EBV) increases the risk by several folds,” said Janardan Pandey, Ph.D., MUSC professor of microbiology and immunology. “In other words, there are inter-individual differences in susceptibility to EBV-associated lupus. In addition to the Carolina Lupus Study, we have shown the involvement of CTLA-4 in patients from Korea. Thus, this gene appears to be an important risk factor for lupus in diverse racial groups. It is important however, not to focus too much on any one gene. Like most human diseases, lupus is the result of interactions among many genes as well as environmental factors.”
  
Published in the April issue of “Arthritis & Rheumatism” (http://www.interscience.wiley.com/journal/arthritis), the results of the study show a strong association of EBV-IgA antibodies with lupus in African- Americans. 
  
In addition, the findings shed new light on variation in a T-cell response gene that might influence immune responsiveness to EBV among lupus patients. Maintaining EBV infection in a latent or quiet state primarily depends on the power of T cells, which play a major role in keeping the immune system functioning properly.
  
Among both lupus patients and controls, blacks had a higher prevalence of EBV-IgG antibodies than white subjects, the telltale sign of a history of EBV infection. However, another antibody, EBV-IgA, seen with repeat or reactivated EBV infection, was also more common in African-Americans with lupus. EBV-IgA was found in 66 percent of black patients, and calculated at increasing the odds for lupus by 5 to 6 fold. Among white lupus patients, the EBV-IgA association was modest, yet increased significantly with age. The association also appeared stronger in older blacks than younger patients. 
  
Among lupus patients, both black and white, researchers also observed a genetic variation in CTLA-4, a protein that works on T cells in regulating immunity, and which significantly increased the risk of lupus associated with EBV-IgA antibodies. This variation was previously linked to risk of lupus in younger African-Americans in the Carolina Lupus Study.
  
“The racial difference in the association between EBV-IgA and SLE is intriguing, especially since African-Americans have a higher risk of SLE,
tend to develop the disease earlier, and often have a more severe course of disease,” said Christine G. Parks, Ph.D., NIEHS, one of the National Institutes of Health in Research Triangle Park, N.C. “One explanation could be that there are more opportunities for re-infection among African-Americans, given the higher population prevalence of infection and likelihood of encountering and becoming infected with new viral strains. Alternatively, other factors independently related to the immune response to EBV and loss of latency could vary by race, with the same difference being related to the differential risk of SLE.” 
 

Friday, April 15, 2005
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