Direct contact with herpes simplex virus-infected cells results in inhibition of lymphokine-activated killer cells because of cell-to-cell spread of virus

David Johnson, David C. Johnson

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Natural killer (NK) and lymphokine-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.

Original languageEnglish (US)
Pages (from-to)1127-1132
Number of pages6
JournalJournal of Infectious Diseases
Volume168
Issue number5
StatePublished - Nov 1993
Externally publishedYes

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Lymphokine-Activated Killer Cells
Simplexvirus
Viruses
Human Herpesvirus 1
Glycoproteins
Infection
Immune Evasion
Virus Internalization
Neutralizing Antibodies
Cell Membrane

ASJC Scopus subject areas

  • Immunology
  • Public Health, Environmental and Occupational Health

Cite this

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title = "Direct contact with herpes simplex virus-infected cells results in inhibition of lymphokine-activated killer cells because of cell-to-cell spread of virus",
abstract = "Natural killer (NK) and lymphokine-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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N2 - Natural killer (NK) and lymphokine-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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