A proinflammatory peptide from herpes simplex virus type 2 glycoprotein G affects neutrophil, monocyte, and NK cell functions.
We have identified a synthetic peptide derived from the secreted portion of HSV type 2 glycoprotein G, denoted gG-2p20, which has proinflammatory properties in vitro. The gG-2p20 peptide, corresponding to aa 190-205 of glycoprotein G-2, was a chemoattractant for both monocytes and neutrophils in a dose-dependent fashion, and also induced the release of reactive oxygen from these cells. The receptor mediating the responses was identified as the formyl peptide receptor. The gG-2p20-induced activation of phagocytes had a profound impact on NK cell functions. The reactive oxygen species produced by gG-2p20-activated phagocytes both inhibited NK cell cytotoxicity and accelerated the apoptotic cell death in NK cell-enriched lymphocyte populations. Hence, we have for the first time been able to identify a potential function of the secreted portion of HSV-2 glycoprotein G. We propose that the proinflammatory gG-2p20 peptide identified could contribute to a reduced function and viability of NK cells during HSV-2 infection due to its ability to recruit and activate phagocytic cells.
Bellner
Lars
L
Department of Rheumatology and Inflammation Research, Göteborg University, Göteborg, Sweden.
Thorén
Fredrik
F
Nygren
Erik
E
Liljeqvist
Jan-Ake
JA
Karlsson
Anna
A
Eriksson
Kristina
K
D000595:Amino Acid Sequence; D017209:Apoptosis / Q000276:immunology; D002634:Chemotaxis, Leukocyte / Q000276:immunology; D003602:Cytotoxicity, Immunologic / Q000276:immunology; D004790:Enzyme Induction / Q000276:immunology; D018258:Herpesvirus 2, Human / Q000276:immunology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000138:chemical synthesis / Q000276:immunology; D018836:Inflammation Mediators / Q000138:chemical synthesis / Q000502:physiology*; D007694:Killer Cells, Natural / Q000276:immunology* / Q000473:pathology / Q000821:virology; D008262:Macrophage Activation / Q000276:immunology; D008969:Molecular Sequence Data; D009000:Monocytes / Q000276:immunology* / Q000473:pathology / Q000821:virology; D019255:NADPH Oxidases / Q000096:biosynthesis / Q000378:metabolism; D018375:Neutrophil Activation / Q000276:immunology; D009504:Neutrophils / Q000201:enzymology / Q000276:immunology* / Q000473:pathology / Q000821:virology; D010446:Peptide Fragments / Q000138:chemical synthesis / Q000502:physiology*; D037342:Pertussis Toxin / Q000494:pharmacology; D010586:Phagocytes / Q000201:enzymology / Q000276:immunology / Q000473:pathology / Q000821:virology; D017382:Reactive Oxygen Species / Q000378:metabolism; D044042:Receptors, Formyl Peptide / Q000502:physiology; D014759:Viral Envelope Proteins / Q000138:chemical synthesis / Q000502:physiology*
D007166:Immunosuppressive Agents; D018836:Inflammation Mediators; D010446:Peptide Fragments; D017382:Reactive Oxygen Species; D044042:Receptors, Formyl Peptide; D014759:Viral Envelope Proteins; C045464:glycoprotein G, herpes simplex virus type 2; D019255:NADPH Oxidases; D037342:Pertussis Toxin