TY - JOUR
T1 - Direct Contact with Herpes Simplex Virus-Infected Cells Results in Inhibition of Lymphokine-Activated Killer Cells because of Cell-to-Cell Spread of Virus
AU - Johnson, David C.
AU - York, Ian A.
N1 - Funding Information:
Received 24 March 1993; revised 4 June 1993. Financial support: Medical Research Council of Canada and National Cancer Institute of Canada (D.C.J. is a senior research scholar). Reprints or correspondence: Dr. David C. Johnson. Room 4H30. Faculty of Health Sciences. McMaster University. 1200 Main St. W.. Hamilton. Ontario. Canada L8N 3Z5.
PY - 1993/12
Y1 - 1993/12
N2 - Natural killer (NK) and Iymphokine-activated killer (LAK) cells are disarmed after contact with herpes simplex virus (HSV)-infected cells. Cells infected with HSV-1 mutants that lack glycoproteins essential for viral entry into cells (gB, gD, gK, gH, and gL) did not inhibit LAK cells; cells infected with HSV-1 mutants that lack glycoproteins not required for virus entry into cells (gE, gI, gG, and gJ) inhibited lysis. LAK cells became infected after contact with target cells infected with 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 concentrations of cell-free preparations of HSV and because neutralizing antibodies did not prevent infection of LAK cells in contact with infected cells, infection of LAK cells is probably greatly enhanced by the apposition of the effector and target cell membranes during target recognition. Disarming of immune effector cells by infection may be a general strategy for immune evasion by HSV.
AB - Natural killer (NK) and Iymphokine-activated killer (LAK) cells are disarmed after contact with herpes simplex virus (HSV)-infected cells. Cells infected with HSV-1 mutants that lack glycoproteins essential for viral entry into cells (gB, gD, gK, gH, and gL) did not inhibit LAK cells; cells infected with HSV-1 mutants that lack glycoproteins not required for virus entry into cells (gE, gI, gG, and gJ) inhibited lysis. LAK cells became infected after contact with target cells infected with 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 concentrations of cell-free preparations of HSV and because neutralizing antibodies did not prevent infection of LAK cells in contact with infected cells, infection of LAK cells is probably greatly enhanced by the apposition of the effector and target cell membranes during target recognition. Disarming of immune effector cells by infection may be a general strategy for immune evasion by HSV.
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U2 - 10.1093/infdis/168.5.1127
DO - 10.1093/infdis/168.5.1127
M3 - Article
C2 - 8228345
AN - SCOPUS:0027489328
SN - 0022-1899
VL - 168
SP - 1127
EP - 1132
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 5
ER -