title: Epstein-Barr virus: exploiting the immune system.
abstract: In vitro, Epstein-Barr virus (EBV) will infect any resting B cell, driving it out of the resting state to become an activated proliferating lymphoblast. Paradoxically, EBV persists in vivo in a quiescent state in resting memory B cells that circulate in the peripheral blood. How does the virus get there, and with such specificity for the memory compartment? An explanation comes from the idea that two genes encoded by the virus--LMP1 and LMP2A--allow EBV to exploit the normal pathways of B-cell differentiation so that the EBV-infected B blast can become a resting memory cell.
authors.affiliation: Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA. david.thorley-lawson@tufts.edu
authors.forename: D A
authors.initials: DA
authors.lastname: Thorley-Lawson
mesh_terms: D001402:B-Lymphocytes / Q000276:immunology*; D019013:CD40 Antigens / Q000378:metabolism; D020031:Epstein-Barr Virus Infections / Q000276:immunology; D005814:Genes, Viral; D004854:Herpesvirus 4, Human / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity*; D006801:Humans; D007156:Immunologic Memory; D008213:Lymphocyte Activation; D018448:Models, Immunological; D011947:Receptors, Antigen, B-Cell / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology; D014763:Viral Matrix Proteins / Q000235:genetics / Q000276:immunology
chemical_list: D019013:CD40 Antigens; C037662:EBV-associated membrane antigen, Epstein-Barr virus; D011947:Receptors, Antigen, B-Cell; D014763:Viral Matrix Proteins