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Journal of Virology, July 2005, p. 8861-8869, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.8861-8869.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Differential Susceptibility to Human Immunodeficiency Virus Type 1 Infection of Myeloid and Plasmacytoid Dendritic Cells

Anna Smed-Sörensen,1* Karin Loré,2 Jayanand Vasudevan,2 Mark K. Louder,3 Jan Andersson,1 John R. Mascola,3 Anna-Lena Spetz,1 and Richard A. Koup2

Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden,1 Immunology Laboratory,2 BSL-3 Virology Laboratory, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland3

Received 30 November 2004/ Accepted 26 March 2005

Human immunodeficiency virus type 1 (HIV-1) infection of dendritic cells (DCs) plays an important role in HIV-1 transmission and pathogenesis. Here, we studied the susceptibility of ex vivo-isolated CD11c+ myeloid DCs (MDCs) and CD123+ plasmacytoid DCs (PDCs) to HIV-1 infection and the function of these cells early after infection. Both DC subsets were susceptible to CCR5- and CXCR4-using HIV-1 isolates (BaL and IIIB, respectively). However, MDCs were more susceptible to HIV-1BaL infection than donor-matched PDCs. In addition, HIV-1BaL infected MDCs more efficiently than HIV-1IIIB, whereas PDCs were equally susceptible to both isolates. While exposure to HIV-1 alone resulted in only weak maturation of DCs, Toll-like receptor 7/8 ligation induced full maturation in both infected and uninfected DCs. Maturation did not increase HIV-1 replication in infected DCs, and infected DCs retained their ability to produce tumor necrosis factor alpha after stimulation. Both HIV-1 isolates induced alpha interferon production exclusively in PDCs, irrespective of productive infection. In conclusion, PDCs and MDCs were susceptible to HIV-1 infection, but neither displayed functional defects as a consequence of infection. The difference in susceptibility of PDCs and MDCs to HIV-1 may have implications for HIV-1 transmission and DC-mediated transfer of HIV-1 to T cells.

* Corresponding author. Mailing address: Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, F59 Huddinge University Hospital, S-141 86 Stockholm, Sweden. Phone: 46 8 585 896 88. Fax: 46 8 746 76 37. E-mail: Anna.Smed.Sorensen{at}medhs.ki.se.

Journal of Virology, July 2005, p. 8861-8869, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.8861-8869.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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