carrier state is almost general in men. The virus induces B lymphocyte
but this is counteracted
immune response. Therefore, EBV-induced malignancies occur only when the immune
response is impaired, e.g. in transplant recipients. The versatility of the viral gene expression strategy
secures the consistent maintainance of the virus in healthy individuals. The
viral proteins required for transformation render the cell immunogenic.
Expression of the transforming genes leads to rejection, but these genes are
not required for the maintenance of the viral genome. EBV is an important
contributor for malignant transformation, even when it does not directly induce
cell proliferation. Several mechanisms have been unravelled in EBV-associated
tumors whereby the virus may modify the cellular phenotype and may influence
the interaction of tumor cells with their microenvironment. The virus carrier
state can lead to the evasion of apoptosis and can intensify the response to
growth promoting signals, too.