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J Gen Virol 76 (1995), 1317-1325; DOI 10.1099/0022-1317-76-6-1317
© 1995 Society for General Microbiology

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Replication pattern of human immunodeficiency virus type 1 in mature Langerhans cells

Burkhard Ludewig1, Johannes Holzmeister1, Massimo Gentile3, Hans R. Gelderblom1, Katharina Rokos1, Yechiel Becker2 and Georg Pauli1,*

1 Department of Virology, Robert Koch-Institut, Nordufer 20, 13353 Berlin, Germany
2 Department of Molecular Virology, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel
and3 Institute of Virology, University of Rome ‘La Sapienza’, Rome, Italy

Langerhans cells (LC), the dendritic antigen presenting cells of the skin, mature into potent immunostimulatory cells during migration to regional lymph nodes, where they are identified as interdigitating cells (IDC). Since mature Langerhans cells (mLC) resemble IDC in phenotype and immunostimulatory capacity, we examined whether these cells were susceptible to infection with macrophagetropic and lymphotropic strains of human immunodeficiency virus type 1 (HIV-1). Highly purified cell preparations of mLC migrating from human epidermis expressed high amounts of major histocompatibility complex (MHC) class I and II antigens and of the accessory molecules CD40, CD80 and CD86, indicative of the phenotype of potent immunostimulatory cells. CD4 expression was up-regulated on mLC during cultivation, independent of the presence of tumour necrosis factor {alpha} (TNF-{alpha}) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in the culture medium. The macrophagetropic HIV-1 strain SF162 replicated to higher titres in mLC than the lymphotropic strain IIIB. Both strains induced syncytia, with SF162 showing a more rapid cytophathic effect. Addition of TNF-{alpha} enhanced virus production, due to better cell viability under TNF-{alpha} treatment, whereas GM-CSF did not significantly influence viability of cells and replication pattern of the virus. These findings suggest that in the infected individual IDC in lymph nodes may function as target cells for HIV-1.

* Author for correspondence. Fax +49 30 4547 2605.

Received 11 October 1994; accepted 30 January 1995.


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