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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 1990 May;87(9):3609–3613. doi: 10.1073/pnas.87.9.3609

Herpes simplex virus-infected cells disarm killer lymphocytes.

D L Confer 1, G M Vercellotti 1, D Kotasek 1, J L Goodman 1, A Ochoa 1, H S Jacob 1
PMCID: PMC53951  PMID: 2159156

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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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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