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EBV suppresses prostaglandin E2 biosynthesis in human monocytes
M Savard1, C Bélanger, M J Tremblay
1Laboratories of Viral Immunology, Hospitalier de l'Université Laval, Université Laval, Québec, Canada.
Journal of Immunology (Baltimore, Md. : 1950)
|June 8, 2000
Summary
Epstein-Barr virus (EBV) inhibits prostaglandin E2 (PGE2) production in monocytes by suppressing cyclooxygenase-2 (COX-2) expression. This viral immune evasion strategy may contribute to EBV pathogenicity.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Epstein-Barr virus (EBV) employs immune evasion strategies, including binding to monocytes and altering inflammatory mediator expression.
- Previous studies show EBV affects monocyte inflammatory mediator expression (IL-1, IL-6, TNF-alpha, leukotrienes) and phagocytosis.
Purpose of the Study:
- To investigate the effect of EBV on prostaglandin E2 (PGE2) biosynthesis in monocytes.
- To elucidate the molecular mechanisms by which EBV influences PGE2 production.
Main Methods:
- Monocytes were exposed to EBV.
- Expression of cyclooxygenase (COX) isoforms (COX-1 and COX-2) was analyzed at transcriptional and translational levels.
- NF-kappaB activation pathway was assessed.
- Experiments were conducted with and without phosphonoacetic acid, a herpesvirus DNA polymerase inhibitor.
Main Results:
- EBV suppresses the biosynthesis of PGE2, an immunomodulatory molecule.
- This suppression involves the inhibition of inducible COX-2 expression, but not constitutive COX-1.
- EBV impacts the NF-kappaB activation pathway, crucial for COX-2 induction.
- Inhibition of PGE2 was reversed by phosphonoacetic acid, suggesting viral replication/proteins are involved.
Conclusions:
- EBV actively suppresses PGE2 biosynthesis in monocytes.
- The mechanism involves down-regulation of COX-2 via the NF-kappaB pathway.
- This inhibition of PGE2 represents a novel immune evasion mechanism contributing to EBV pathogenicity.