HERPES-SIMPLEX VIRUS TYPE-1 LONG-TERM PERSISTENCE, LATENCY, AND REACTIVATION IN INFECTED BURKITT-LYMPHOMA CELLS

The two herpes simplex virus type 1 (HSV-1) strains F and AK which differ in virus-cell interaction and in DNA organization, were used to establish persistently productive infections in Burkitt lymphoma-derived cell lines BJAB and Raji. Four such lines could be maintained over a period of three years. Like the uninfected parental lines, the persistently infected cells display a cyclic pattern of cell proliferation. The expression of HSV-1-specific antigens proved to be variable. As a consequence, virus yields also vary within a subcultivation period. Pooled human HSV antisera, when continuously present, suppress virus production (inducible latency) and support cell proliferation to higher rates. By contrast, removal of the antiserum after a certain period of cultivation leads to virus reactivation with a delay of 8 to 20 days. After cultivation periods of more than 3 to 12 weeks, replacement of HSV antiserum does no longer result in virus reactivation and even inducers fail to reactivate.