DIRECT-CONTACT WITH HERPES-SIMPLEX VIRUS-INFECTED CELLS RESULTS IN INHIBITION OF LYMPHOKINE-ACTIVATED KILLER-CELLS BECAUSE OF CELL-TO-CELL SPREAD OF VIRUS

Natural killer (NK) and lymphokine-activated killer (LAK) cells are di sarmed after contact with herpes simplex virus (HSV)-infected cells. C ells infected with HSV-1 mutants that lack glycoproteins essential for viral entry into cells (gB, gD, gK, gH, and gL) did not inhibit LAK c ells; cells infected with HSV-1 mutants that lack glycoproteins not re quired for virus entry into cells (gE, gl, gG, and gJ) inhibited lysis . LAK cells became infected after contact with target cells infected w ith wild-type HSV-1 but not with a gD- HSV-1, which cannot spread from cell to cell. Because LAK cells were inhibited only by very high conc entrations of cell-free preparations of HSV and because neutralizing a ntibodies did not prevent infection of LAK cells in contact with infec ted cells, infection of LAK cells is probably greatly enhanced by the apposition of the effector and target cell membranes during target rec ognition. Disarming of immune effector cells by infection may be a gen eral strategy for immune evasion by HSV.