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Results from a 2005 study, conducted by researchers at the National Institute of Environmental Health Sciences, suggested a strong association between Epstein-Barr virus (EBV) and increased risk of lupus, particularly for African Americans. The study of 230 patients with lupus and matched controls assessed the seroprevalence of EBV antibodies. One particular antibody, EBV-IgA, was linked to a five times greater risk of SLE in African Americans. The association was not as strong for whites, but increased with age (patients over 50 years of age had four times higher risk.)
The researchers also observed that a genetic variation in CTLA-4, a protein that helps regulate T-cell immune system response, appeared to modify the risk of lupus associated with EBV-IgA antibodies. The Epstein-Barr virus settles into B cells after initial infection and can become dormant for long periods of time. T-cells trigger an immune response and help fight reactivation of infection. Therefore, an individual’s CTLA-4 genotype could determine the immune system’s responsiveness in fighting repeat episodes of EBV infection.
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Some research suggests that different viruses may imprint specific types of SLE. For instance cytomegalovirus may affect blood vessels and cause problems such as Raynaud's phenomenon or blood abnormalities, but may not affect the kidney as much. These are speculations, however, and not a proven association.
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Sunlight. Ultraviolet (UV) rays found in sunlight are important SLE triggers. When they bombard the skin, they can alter the structure of DNA in cells below the surface. The immune system may perceive these altered skin cells as foreign and trigger an autoimmune response against them. UV light is categorized as UVB or UVA depending on the length of the wave.
- UVB are short waves (280 to 320 nm). The shorter the wavelengths, the more damage they do.
- UVA are longer waves (320 to 400 nm). Some research suggets that UVA wavelengths in the longest range, known as UVA1 (340 to 400 nm), may actually repair DNA and normalize immune responses.
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