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Journal of Virology, September 2008, p. 8900-8905, Vol. 82, No. 17
0022-538X/08/$08.00+0 doi:10.1128/JVI.00196-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Rod S. Daniels,3
Thomas C. Greenough,4
Frank Kirchhoff,5 and
Barbara Schmidt1*
Institute of Clinical and Molecular Virology, German National Reference Centre for Retroviruses, University of Erlangen-Nürnberg, Erlangen, Germany,1 Department of Microbiology, University of Pennsylvania, Philadelphia, Pennsylvania,2 Virology Division, MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London, United Kingdom,3 Department of Pediatrics, University of Massachusetts Medical School, Worcester, Massachusetts,4 Institute of Virology, University of Ulm, Ulm, Germany5
Received 28 January 2008/ Accepted 11 June 2008
Plasmacytoid dendritic cells (PDC) are major producers of type I interferons (IFN) in response to human immunodeficiency virus type 1 (HIV-1) infection. To better define the underlying mechanisms, we studied the magnitude of alpha IFN (IFN-
) induction by recombinant viruses containing changes in the Env protein that impair or disrupt CD4 binding or expressing primary env alleles with differential coreceptor tropism. We found that the CD4 binding affinity but not the viral coreceptor usage is critical for the attachment of autofluorescing HIV-1 to PDC and for subsequent IFN-
induction. Our results illustrate the importance of the gp120-CD4 interaction in determining HIV-1-induced immune stimulation via IFN-
production.
Published ahead of print on 25 June 2008.
Present address: Integral Molecular, Philadelphia, PA.
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