Herpes simplex virus-infected cells disarm killer lymphocytes.
Human endothelial cells or human foreskin fibroblasts infected with herpes simplex viruses (HSVs) potently inhibit the lytic activity of natural killer cells and interleukin 2-activated killer cells. The inhibition occurs after as little as 8 hr of viral infection and requires contact between effector cells and HSV-infected targets. Inhibition evidently stems from direct blockade of killer cell function because killer cells placed atop HSV-infected targets rapidly become incapable of lysing subsequently added HL-60 or K-562 cells. The impairment of killer cell function is prevented when protein glycosylation in HSV-infected cells is blocked with tunicamycin. These studies may be relevant for understanding the persistence of herpes simplex virus infections and, further, suggest a mechanism for failed immune surveillance.
Confer
D L
DL
Department of Medicine, University of Minnesota, Minneapolis 55455.
Vercellotti
G M
GM
Kotasek
D
D
Goodman
J L
JL
Ochoa
A
A
Jacob
H S
HS
D000260:Adenoviruses, Human / Q000235:genetics / Q000276:immunology; D002472:Cell Transformation, Viral; D002478:Cells, Cultured; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D004730:Endothelium, Vascular / Q000276:immunology; D006801:Humans; D066298:In Vitro Techniques; D015979:Killer Cells, Lymphokine-Activated / Q000187:drug effects / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology*; D008297:Male; D018139:Simplexvirus / Q000235:genetics* / Q000276:immunology; D012867:Skin / Q000276:immunology; D014415:Tunicamycin / Q000494:pharmacology
D014415:Tunicamycin