Epstein-Barr virus latency: LMP2, a regulator or means for Epstein-Barr virus persistence?

Like other herpesviruses, Epstein-Barr virus (EBV) persists in its host through an ability to establish a latent infection that periodically reactivates, producing infectious virus that infects naïve hosts. Disease syndromes in humans caused by EBV reflect the cell types that EBV infects, being primarily of lymphoid or epithelial origin. The most notable lymphoid disease, infectious mononucleosis, is a self-limiting lymphoproliferative disease that occurs in normal adolescents on primary infection. Children are normally able to resolve primary EBV infection with few or no symptoms. By the age of 25 most individuals are EBV seropositive. EBV is associated with a variety of hematopoietic cancers such as African Burkitt's lymphoma, Hodgkin's, and adult T-cell leukemia. EBV-associated lymphoproliferative disease occurs in individuals with congenital or acquired cellular immune deficiencies. The two notable epithelial diseases associated with EBV infection are nasopharyngeal cancer, a malignancy endemic to southern China, and oral hairy leukoplakia, an epithelial hyperplasia of the lingual squamous epithelium in AIDS patients. Latent membrane protein 2 (LMP2) is expressed both in normal EBV latency and EBV-associated pathologies. LMP2 may regulate reactivation from latency by interfering with normal B-cell signal transduction processes and in doing so may also provide a survival signal that could be important for viral persistence. Current knowledge about the function of LMP2 is described, defining a new class of regulators of herpesvirus latency.