Inhibition of macrophage inflammatory protein–1α production by Epstein-Barr virus

Authors:
Publisher website
Google Scholar
Abstract
Infection with Epstein-Barr virus (EBV) exerts substantially immunomodulating activities in vitro and in vivo. In this context, EBV-induced chemokine production and the influence of EBV on this highly redundant system of inflammatory proteins have hardly been investigated. This study analyzed the production of interleukin-8, RANTES, monocyte chemotactic protein–1, and macrophage inflammatory protein–1α (MIP-1α) on EBV infection of peripheral blood mononuclear cells from immune EBV-seropositive (EBV+) and noninfected EBV-seronegative (EBV−) individuals. EBV failed to induce the production of MIP-1α in EBV+ as well as EBV− individuals, whereas the other chemokines studied were readily expressed. Moreover, EBV completely down-regulated lipopolysaccharide (LPS)– and phytohemagglutinin–induced MIP-1α production up to 4 hours after induction. Reverse transcription–polymerase chain reaction (RT-PCR) analysis of EBV- and LPS-stimulated cultures revealed that EBV inhibited MIP-1α production on the transcriptional level. This effect was abolished by addition of antiglycoprotein (gp)350/220, a monoclonal antibody against EBV9s major envelope glycoprotein, which mediates binding of the virus to the EBV receptor, CD21. However, recombinant gp350/220 protein alone did not inhibit the LPS-induced MIP-1α production, indicating that infection of the target cell is indispensable for this effect. In summary, we demonstrate a new immunomodulating activity of EBV on the chemokine system that probably helps the virus to evade the host9s immune system favoring lifelong infection.

This publication has 37 references indexed in Scilit: