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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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Submitted April 14, 2008
Accepted June 17, 2008

Lack of endogenous TRIM5alpha-mediated restriction in rhesus macaque dendritic cells

Nathalie J Arhel, Sebastien Nisole, Laetitia Carthagena, Frederic Coutant, Philippe Souque, Audrey Brussel, Jerome Estaquier, and Pierre Charneau*

Virology Department, Institut Pasteur, Paris, France
Department of Infectious Diseases, Institut Cochin, INSERM U567, Paris, France
Physiopathology of Lentiviral Infections, Institut Pasteur, Paris, France
INSERM U841, Faculte Creteil Henri Mondor, Creteil, France

* Corresponding author; email: charneau{at}pasteur.fr.

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 (DC) lack TRIM5{alpha}-mediated restriction and are equally permissive to HIV-1 infection as human DC. 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 DC, while still operative in cells that replicate HIV-1 (macrophages, T lymphocytes), illustrates the need for innate mechanisms to not inhibit adaptive immune responses in order to ensure an optimal fight against pathogens.


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