Formation of syncytia in human lymphoblastoid cells infected with type C viruses

Abstract

Infection of human lymphoblastoid cells with either of two feline type C viruses (FeLV and RD-114) resulted in the rapid appearance of syncytial cells attributable to cell fusion. Syncytia disappeared from infected cultures in approximately 7 days. By 3–5 wk after infection, a second cycle of syncytia occurred followed by the establishment of chronically infected cultures in the absence of further syncytial formation. The percentage of cells involved in the two cycles of syncytia was dependent on the input virus dose. With high input doses, the initial cycle of syncytia involved 15–20% of the cells, while the second cycle involved 5% or less of the cells. With low virus input doses, the percentage of syncytial cells was greatest during the second cycle. Cultures chronically infected with RD-114 virus were resistant to fusion induced by either RD-114 virus or FeLV. Cultures chronically infected with FeLV were still susceptible to fusion induced by RD-114 virus but not by FeLV. Treatment of RD-114 virus with B-propiolactone (BPL) destroyed the infectivity of the virus when tested in RD (nonlymphoid) cells, although the BPL-inactivated virus could still induce fusion of human lymphoblastoid cells. Surprisingly, lymphoblastoid cells infected with BPL-inactivated RD-114 virus showed a second cycle of syncytia at 3–5 wk after infection which was followed by the appearance of infections virus and the establishment of chronically infected cultures. A small percentage of syncytial cells induced by RD-114 virus showed synthesis of Epstein-Barr (EB) virus antigens. In the case of nonproducer cells (Raji), the synthesis of EB virus-associated early antigen (s) suggested activation of the repressed virus genome following fusion induced by RD-114 virus. Disappearance of syncytia was accompanied by disappearance of EB virus associated antigens. Once established, Raji RD-114 carrier cultures showed no evidence of EB virus antigen synthesis.