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Journal of Virology, November 2007, p. 12086-12090, Vol. 81, No. 21
0022-538X/07/$08.00+0 doi:10.1128/JVI.00800-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Departments of Dermatology and Venereology and of Microbiology and Molecular Medicine, University Hospital and Medical School of Geneva, Geneva, Switzerland,1 MRC Centre for Medical Molecular Virology, Department of Infection, Royal Free and University College Medical School, UCL, London W1T4JF, United Kingdom2
Received 13 April 2007/ Accepted 18 August 2007
Dendritic cells are central to the early events of human immunodeficiency virus type 1 (HIV-1) transmission, but HIV-1 infects dendritic cells inefficiently in vitro compared to activated CD4+ T cells. There is a strong postentry restriction of HIV-1 infection in dendritic cells, partly mediated by the cellular restriction factor APOBEC3G. Here, we reveal that arsenic trioxide markedly increases HIV infection of immature and mature dendritic cells as well as blood-derived myeloid dendritic cells in an APOBEC3G- and TRIM5
-independent way. Our data suggest the presence of powerful, arsenic-sensitive antiviral activities in primary human immune cells of the dendritic cell lineage.
Published ahead of print on 29 August 2007.
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