Hypothesis of development of SLE from EBV infection. Genetic insufficiencies may result in poor control and thereby more frequent reactivation of the latent EBV infection. The increased number of EBV-infected cells will, upon apoptosis, initiate an innate and adaptive immune response against the released cellular antigens and EBV antigens due to defective removal of waste products. This will result in production of autoantibodies and EBV antibodies as an attempt to control the virus-induced inflammation. Furthermore, activation of both autoreactive and EBV-reactive T cells will occur. The response from the immune system cause organ and tissue damage leading to development of SLE.