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Journal of Virology, September 2008, p. 9299-9302, Vol. 82, No. 18
0022-538X/08/$08.00+0 doi:10.1128/JVI.00717-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Viral Immunology Laboratory, School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland,1 ZLB Behring, Wankdorfstrasse 10, 3000 Bern 22, Switzerland,2 National Institute of Biological Standards and Controls, Blanch Lane, South Mimms, Potters Bar, Hertsfordshire EN6 3QG, United Kingdom3
Received 1 April 2008/ Accepted 3 July 2008
Human parainfluenza virus type 3 (HPIV3) is a major respiratory pathogen in humans. Failure to induce immunological memory associated with HPIV3 infection has been attributed to inhibition of lymphocyte proliferation. We demonstrate that the inability of mixed lymphocytes to respond to virally infected antigen-presenting cells is due to an interleukin-2-dependent, nonapoptotic mechanism involving natural killer (NK) cells and their influence is exerted in a contact-dependent manner. These results suggest a novel regulatory mechanism for NK cells during HPIV3 infection, offering an explanation for viral persistence and poor memory responses.
Published ahead of print on 9 July 2008.
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