It is likely that EBV-induced HERV-K18 env SAg activity is also minimal in vivo, sufficient for the EBV-infected B cells to receive T cell help without overt stimulation of the immune system. This scenario fits very well with the fact that EBV persists in humans throughout our lifetime, causing problems only when the immune system is suppressed. Epstein-Bar virus (EBV) is widespread within the human population with over 90% of adults being infected. In response to primary EBV infection, the host mounts an antiviral immune response comprising both innate and adaptive effector functions. Although the immune system can control EBV infection to a large extent, the virus is not cleared.
With the virus hiding undetected in your organs, your body assumes it's won the war and the invader has been destroyed. Your immune system returns to its normal state, your mononucleosis ends, and your doctor tells you that you're healthy. Unfortunately, the Epstein-Barr virus has barely begun its voyage through your body.Objective. Understanding the cellular and molecular mechanisms underpinning inefficient surveillance of EBV-infected B cells is required to understand disease in patients with PIK3CD GOF mutations, identify key molecules required for cell-mediated immunity against EBV, and develop immunotherapeutic interventions for the treatment of this and other EBV-opathies.