Chromatin organization at the nuclear pore favours HIV replication

Mickaël Lelek, Nicoletta Casartelli, Danilo Pellin, Ermanno Rizzi, Philippe Souque, Marco Severgnini, Clelia Di Serio, Thomas Fricke, Felipe Diaz-Griffero, Christophe Zimmer, Pierre Charneau and Francesca Di Nunzio ()
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Mickaël Lelek: Institut Pasteur, Unité Imagerie et Modélisation, CNRS 3691
Nicoletta Casartelli: Institut Pasteur, Unité Virus et Immunité Unité, CNRS 3015
Danilo Pellin: Vita-Salute San Raffaele University Centre for Statistics in the Biomedical Sciences
Ermanno Rizzi: Institute for Biomedical Technologies (ITB), CNR
Philippe Souque: Institut Pasteur, Unité Virologie Moléculaire et Vaccinologie, CNRS 3569
Marco Severgnini: Institute for Biomedical Technologies (ITB), CNR
Clelia Di Serio: Vita-Salute San Raffaele University Centre for Statistics in the Biomedical Sciences
Thomas Fricke: Albert Einstein College of Medicine
Felipe Diaz-Griffero: Albert Einstein College of Medicine
Christophe Zimmer: Institut Pasteur, Unité Imagerie et Modélisation, CNRS 3691
Pierre Charneau: Institut Pasteur, Unité Virologie Moléculaire et Vaccinologie, CNRS 3569
Francesca Di Nunzio: Institut Pasteur, Unité Virologie Moléculaire et Vaccinologie, CNRS 3569

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: Abstract The molecular mechanisms that allow HIV to integrate into particular sites of the host genome are poorly understood. Here we tested if the nuclear pore complex (NPC) facilitates the targeting of HIV integration by acting on chromatin topology. We show that the integrity of the nuclear side of the NPC, which is mainly composed of Tpr, is not required for HIV nuclear import, but that Nup153 is essential. Depletion of Tpr markedly reduces HIV infectivity, but not the level of integration. HIV integration sites in Tpr-depleted cells are less associated with marks of active genes, consistent with the state of chromatin proximal to the NPC, as analysed by super-resolution microscopy. LEDGF/p75, which promotes viral integration into active genes, stabilizes Tpr at the nuclear periphery and vice versa. Our data support a model in which HIV nuclear import and integration are concerted steps, and where Tpr maintains a chromatin environment favourable for HIV replication.

Date: 2015
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DOI: 10.1038/ncomms7483

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