Herpes simplex virus-infected cells disarm killer lymphocytes

Dennis L. Confer, Gregory M. Vercellotti, Dusan Kotasek, Jesse L. Goodman, Augusto Ochoa, Harry S. Jacob

Research output: Contribution to journalArticlepeer-review

24 Scopus citations

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 h r 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.

Original languageEnglish (US)
Pages (from-to)3609-3613
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume87
Issue number9
DOIs
StatePublished - May 1990

Keywords

  • Herpesvirus hominis
  • Interleukin 2
  • Natural killer cells

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