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Research Article Free access | 10.1172/JCI118557

Human herpesvirus-6 enhances natural killer cell cytotoxicity via IL-15.

L Flamand, I Stefanescu, and J Menezes

Pediatric Research Center, University of Montreal, Quebec, Canada.

Find articles by Flamand, L. in: JCI | PubMed | Google Scholar

Pediatric Research Center, University of Montreal, Quebec, Canada.

Find articles by Stefanescu, I. in: JCI | PubMed | Google Scholar

Pediatric Research Center, University of Montreal, Quebec, Canada.

Find articles by Menezes, J. in: JCI | PubMed | Google Scholar

Published March 15, 1996 - More info

Published in Volume 97, Issue 6 on March 15, 1996
J Clin Invest. 1996;97(6):1373–1381. https://doi.org/10.1172/JCI118557.
© 1996 The American Society for Clinical Investigation
Published March 15, 1996 - Version history
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Abstract

The marked tropism of human herpesvirus-6 (HHV-6) for natural killer (NK) cells and T lymphocytes has led us to investigate the effect of HHV-6 on cellular cytotoxicity. We describe here how HHV-6 infection of peripheral blood mononuclear cells (PBMC) leads to upregulation of their NK cell cytotoxicity. The induction of NK cell activity by HHV-6 was abrogated by monoclonal antibodies (mAbs) to IL-15 but not by mAbs to other cytokines (IFN-alpha, IFN-gamma, TNF-alpha, TNF-beta, IL-2, IL-12) suggesting that IL-15 secreted in response to viral infection was responsible for the observed effect. Furthermore, NK activation by HHV-6 was blocked with mAb to CD122, as well as by human anti-HHV-6 neutralizing antibodies. Using RT-PCR, we were able to detect IL-15 mRNA upregulation in purified monocyte and NK cell preparations. IL-15 protein synthesis was increased in response to HHV-6. Finally, addition of IL-15 to PBMC cultures was found to severely curtail HHV-6 expression. Taken together, our data suggest that enhanced NK activity in response to viral infection represent a natural anti-viral defense mechanism aimed at rapidly eliminating virus-infected cells.

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  • Version 1 (March 15, 1996): No description

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