The potentially oncogenic Epstein-Barr virus (EBV) is carried by almost all humans in a well equilibrated coexistence. The phenotype of the cells that carry EBV genomes is determined by virally-encoded and cellular proteins. B lymphocyte is the main target of the virus and latent infection of this cell induces proliferation. Nine virus-encoded genes participate in the "growth program" that is expressed in a narrow differentiation window of the B cell. Such cells have the potential to develop malignant proliferations. However, several control mechanism eliminate this danger and the general chronic virus carrier state is most often asymptomatic. One mechanism exploits the normal regulation in the immune system, the T cell mediated modulation of the B cell differentiation state. Another is based on cognate recognition and elimination of the infected cells. The expression of EBV encoded genes in B lymphocytes can be also "restricted," they do not express all components of the viral growth program. Here, we discuss a rare viral expression in B cells that has not been connected with malignant transformation yet.
Keywords: EBNA-2; EBV; LMP-1; Type II; Type IIa; Type IIb.