Study suggests a common viral infection may increase risk of lupus in African Americans. Findings also show that 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 of initial infection 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 the cells of the immune system called B cells, where it remains for life, mostly dormant, with occasional bouts of reactivation and replication. Maintaining EBV infection in a latent or quiet state primarily depends on the power of another kind of immune cell, known as T cells. T cells play a major role in keeping the immune system functioning properly. Due to its interference with immune function and promotion of certain antibodies, EBV has been implicated in systemic lupus erythematosus (SLE), commonly referred to as lupus. Lupus is a chronic, potentially debilitating autoimmune disease that more often affects women and is also more common in African Americans. Although the specific cause of lupus is not yet known, both genetic and environmental triggers are likely to be involved.
To determine if there is an association between Epstein-Barr virus and lupus, researchers in North and South Carolina compared the prevalence of EBV antibodies in blood samples from lupus patients with those from healthy controls. Published in the April 2005 issue of Arthritis & Rheumatism, the results of the National Institute of Environmental Health Sciences (NIEHS) study show a strong association of EBV-IgA antibodies with lupus in African Americans. In addition, their findings shed new light on variation in a T-cell response gene that might influence immune responsiveness to EBV among lupus patients.
Amy Molnar | EurekAlert!
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