Herpesvirvses are significant human pathogens and cause a variety of disease syndromes which range in severity from inapparent infection to life-threatening disease. A hallmark of herpesvirvses is their ability to establish persistent infection. This ability is especially evident in diseases such as oral or genital herpes simplex virus infections, in which periods of latency are punctuated with episodes of active, localized lesions. Very little is known about the alterations in virus/cell interactions which result in herpesviral persistent infection rather than productive, lytic infection. As a model system for persistent infection by a cytocidal herpesvirus, persistently infected/oncogenically transformed cell lines were developed by infection of primary hamster embryo cells with equine herpesvirus type I (EHV-1) preparations rich in defective interfering particles (DIPs). Small populations (
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