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 Blood, 1 November 2008, Vol. 112, No. 9, pp. 3772-3776.
Prepublished online as a Blood First Edition Paper on August 14, 2008; DOI 10.1182/blood-2008-04-151761.

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IMMUNOBIOLOGY

Brief Report

Lack of endogenous TRIM5{alpha}-mediated restriction in rhesus macaque dendritic cells

Nathalie J. Arhel1, Sébastien Nisole2, Laetitia Carthagena2, Frédéric Coutant1, Philippe Souque1, Audrey Brussel3, Jérôme Estaquier3, and Pierre Charneau1

1 Molecular Virology and Vectorology Laboratory, Institut Pasteur, Paris; 2 Department of Infectious Diseases, Institut Cochin, Paris; and 3 Physiopathology of Lentiviral Infections Unit, Institut Pasteur, Paris, France

Rhesus macaques are resistant to infection by HIV-1 as a result of an innate cellular restriction mechanism attributable to the expression of rhTRIM5{alpha}, a member of the large tripartite motif (TRIM) protein family. TRIM5{alpha}-mediated restriction, which occurs before reverse transcription through targeting of the HIV-1 capsid, has been identified in a number of macaque primary cells and cell lines and is thought to occur in all macaque cell types. We report, however, that rhesus macaque dendritic cells (DCs) lack TRIM5{alpha}-mediated restriction and are equally permissive to HIV-1 infection as human DCs. Evidence suggests that, although TRIM5{alpha} RNA levels are normal in these cells, the protein may be dysfunctional. We propose that abrogation of TRIM5{alpha}-mediated restriction in DCs, although still operative in cells that replicate HIV-1 (macrophages, T lymphocytes), illustrates the need for innate mechanisms to not inhibit adaptive immune responses to ensure an optimal fight against pathogens.


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