Inhibition of herpes simplex virus type 1-induced interferon synthesis by monoclonal antibodies against viral glycoprotein D and by lysosomotropic drugs.
Components of herpes simplex virus remained bound to the diploid cell membrane after nucleocapsid penetration into the cytosol. These components enabled the infected cells to induce interferon-alpha (IFN-alpha) in peripheral blood mononuclear cells even when the infected cells were fixed by glutaraldehyde. Monoclonal antibodies directed against the major viral glycoprotein D could neutralize their IFN-alpha-inducing capacity. Thus, the process of IFN induction does not require uptake and penetration of the inducer into the effector cells. The process was, however, sensitive to lysosomotropic drugs. These data suggest that a membrane receptor is involved in the IFN-alpha induction mechanism.
D000643:Ammonium Chloride / Q000494:pharmacology; D000911:Antibodies, Monoclonal / Q000276:immunology; D000914:Antibodies, Viral / Q000276:immunology; D000956:Antigens, Viral / Q000276:immunology; D002462:Cell Membrane / Q000276:immunology; D002738:Chloroquine / Q000494:pharmacology; D006561:Herpes Simplex / Q000276:immunology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007370:Interferon Type I / Q000096:biosynthesis*; D008247:Lysosomes / Q000187:drug effects; D018139:Simplexvirus / Q000276:immunology*; D014759:Viral Envelope Proteins; D014764:Viral Proteins / Q000276:immunology*
D000911:Antibodies, Monoclonal; D000914:Antibodies, Viral; D000956:Antigens, Viral; D007370:Interferon Type I; D014759:Viral Envelope Proteins; D014764:Viral Proteins; C039447:glycoprotein D, Human herpesvirus 1; D000643:Ammonium Chloride; D002738:Chloroquine