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Augmentation of B7 expression by herpes simplex virus antigen
Rekha Singh1, Ashok Kumar, Francisco Diaz-Mitoma
1Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada. singh_rek@yahoo.com
Human Immunology
|July 25, 2003
Summary
Herpes simplex virus-2 (HSV-2) infection impacts monocyte B7-1 and B7-2 expression. It blocks interferon-gamma (IFN-gamma) effects while independently increasing B7 expression, potentially influencing recurrent HSV disease.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- B7 costimulation is crucial for herpes simplex virus (HSV) immunity.
- Monocytes play a key role in the immune response to HSV infections.
Purpose of the Study:
- To investigate the effects of HSV-2 infection, immunoregulatory cytokines (IFN-gamma, IL-10), and HSV antigens on B7-1 (CD80) and B7-2 (CD86) expression on monocytes.
- To elucidate the dual impact of HSV-2 on B7 isoform expression.
Main Methods:
- Flow cytometry was utilized to analyze B7-1 and B7-2 expression on monocytes.
- Monocytes were exposed to HSV-2 antigens and cytokines (IFN-gamma, IL-10).
Main Results:
- HSV-2 infection abrogated the IFN-gamma-induced upregulation of B7-1 and B7-2 on monocytes.
- HSV-2 infection independently augmented B7-1 and B7-2 expression on monocytes via an IFN-gamma-independent pathway.
- These opposing effects on B7 expression were observed during HSV-2 infection.
Conclusions:
- HSV-2 infection exerts dual, opposing effects on B7-1 and B7-2 expression on monocytes.
- These complex immunomodulatory effects may contribute to the pathogenesis of recurrent HSV disease in immunocompetent individuals.