Systemic lupus erythematosus is a common, debilitating autoimmune disease in which components of the body’s own cells are targeted and attacked by the immune system. The origins of the disease are still unclear, but it is known that genetic, environmental, and hormonal factors are all involved in causing lupus. We are studying the interactions of genetic risk factor and the putative environmental factor Epstein-Barr virus (EBV). Considerable evidence indicates that EBV infection is associated with lupus. The major question with this finding is that nearly ev¬eryone has been infected with EBV, while very few of those people will go on to develop lupus. The genetic background of the person may play a key role in deciding the outcome of the infection.
Although there is a strong genetic component to lupus, not much is known about how genes influence the development of the disease. We are fo¬cusing on lupus-associated variations in the IRF5 gene. The IRF5 protein is a key intermediary in the response to viral infection, and interacts with EBV during the course of the EBV infection. We hypothesize that the modifica¬tions to the IRF5 gene associated with lupus cause aberrant activation of EBV and heightened response to EBV infection, potentially leading to the altered immune response to EBV seen in lupus patients and people at risk for lupus.
Through studying these interactions, we hope to identify markers for peo¬ple who are at high risk for lupus, and early indicators that autoimmunity is devel¬oping. Early intervention in the disease has shown promise in slowing its effects.
