Herpes simplex virus-infected cells disarm killer lymphocytes. |
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| Authors: | D L Confer G M Vercellotti D Kotasek J L Goodman A Ochoa H S Jacob |
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| Affiliation: | Department of Medicine, University of Minnesota, Minneapolis 55455. |
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| Abstract: | 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. |
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