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Increased adherence of human granulocytes to herpes simplex virus type 1 infected endothelial cells
B A Zajac1, K O'Neill, H M Friedman
1Department of Medicine, University of Pennsylvania School of Medicine.
Abstract:
We studied the interaction of human polymorphonuclear leukocytes (PMNs) with umbilical vein endothelial cells infected with herpes simplex virus (HSV) type 1. PMNs labeled with 51Cr were added to endothelial monolayers at varying times after infection and their adherence assessed 1 h later. Granulocyte adherence (GA) to uninfected cells averaged 26.5 +/- 1.9%. Increased adherence began 6 h postinfection and rose to a maximum at 20 to 24 h. HSV-1 glycoproteins seemed to mediate the increase in GA: tunicamycin treatment of infected monolayers for 18 h abolished the increased GA as did incubation of infected cells with F(ab')2 fragments prepared from human antiserum containing HSV-1 antibody.
Insights
Human polymorphonuclear leukocytes (PMNs) show increased adherence to endothelial cells infected with herpes simplex virus (HSV) type 1. This interaction is mediated by HSV-1 glycoproteins, suggesting a role in viral pathogenesis.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Herpes simplex virus (HSV) type 1 infects endothelial cells.
- Polymorphonuclear leukocytes (PMNs) are key immune cells involved in host defense.
Purpose of the Study:
- To investigate the interaction between human PMNs and HSV-1 infected endothelial cells.
- To determine the role of HSV-1 infection in modulating PMN adherence to endothelial cells.
Main Methods:
- Human umbilical vein endothelial cells were infected with HSV-1.
- 51Cr-labeled human PMNs were added to infected endothelial monolayers at various time points.
- Granulocyte adherence (GA) was assessed 1 hour later.
- Tunicamycin treatment and F(ab')2 fragments from HSV-1 antiserum were used to probe the mechanism.
Main Results:
- Basal GA to uninfected cells was 26.5 +/- 1.9%.
- Increased GA to HSV-1 infected cells began at 6 hours post-infection, peaking at 20-24 hours.
- Tunicamycin treatment and HSV-1 specific antibodies significantly reduced the increased GA, indicating mediation by HSV-1 glycoproteins.
Conclusions:
- HSV-1 infection significantly enhances PMN adherence to endothelial cells.
- HSV-1 glycoproteins are critical mediators of this increased granulocyte adherence.
- These findings suggest a potential mechanism by which HSV-1 may influence immune cell interactions during infection.