Effects of herpes simplex virus type 1 infection on immune functions of human neutrophils. 
Herpesviruses may play roles in the development of periodontal diseases.  This study analyzed the effects of herpes simplex virus type 1 (HSV-1) infection on neutrophil function.  The effects of lipopolysaccharide (LPS) from the periodontal pathogen, Porphyromonas gingivalis, during HSV-1 infection were also determined.  Purified HSV-1 was pretreated with buffer containing no serum, with HSV-1 immunoglobulin G (IgG)-positive serum (HSV-1 antiserum) or with control serum.  Neutrophils were mock-infected or infected with the pretreated HSV-1.  Viral binding and phagosome formation were detected using immunostaining.  Intracellular reactive oxygen species (ROS) were determined using 2',7'-dichlorofluorescin diacetate and fluorometry.  Leukotriene B(4) (LTB(4)) and interleukin-8 (IL-8) were detected using enzyme immunoassays.  Release of matrix metalloproteinase-9 (MMP-9) was examined using gelatin zymography.  Phosphorylation of Akt/glycogen synthase kinase-3 (GSK-3) was determined using western blotting.  HSV-1 bound directly to neutrophils and enhanced the release of MMP-9.  HSV-1 immune complexes, formed in the HSV-1 antiserum, bound neutrophils and induced the formation of early phagosome more effectively than did HSV-1 alone.  The relative levels of ROS and phosphorylation of Akt/GSK-3 were increased significantly in neutrophils after infection with HSV-1 immune complexes.  Infection with HSV-1 and HSV-1 immune complexes also stimulated the production of inflammatory mediators, LTB(4) and IL-8.  Moreover, LPS enhanced the HSV-1-stimulatory production of IL-8.  This study demonstrated differences in neutrophils infected with HSV-1 alone or with HSV-1 immune complexes, suggesting that opsonization of HSV-1 might enhance its effects on neutrophils.  The in vitro findings suggest that HSV-1 infection may induce the inflammatory response and affect periodontal health.