H
Hichem Lahouassa
Researcher at French Institute of Health and Medical Research
Publications - 13
Citations - 1069
Hichem Lahouassa is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: SAMHD1 & Ubiquitin ligase. The author has an hindex of 10, co-authored 13 publications receiving 960 citations. Previous affiliations of Hichem Lahouassa include University of Würzburg & Paris Descartes University.
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Journal ArticleDOI
SAMHD1 restricts the replication of human immunodeficiency virus type 1 by depleting the intracellular pool of deoxynucleoside triphosphates.
Hichem Lahouassa,Waaqo Daddacha,Henning Hofmann,Diana Ayinde,Diana Ayinde,Diana Ayinde,Eric C. Logue,Loïc Dragin,Loïc Dragin,Loïc Dragin,Nicolin Bloch,Claire Maudet,Claire Maudet,Claire Maudet,Matthieu Bertrand,Matthieu Bertrand,Matthieu Bertrand,Thomas Gramberg,Gianfranco Pancino,Stéphane Priet,Bruno Canard,Nadine Laguette,Monsef Benkirane,Catherine Transy,Catherine Transy,Catherine Transy,Nathaniel R. Landau,Baek Kim,Baek Kim,Florence Margottin-Goguet,Florence Margottin-Goguet,Florence Margottin-Goguet +31 more
TL;DR: It is found that SAMHD1 restricted infection by hydrolyzing intracellular deoxynucleoside triphosphates (dNTPs), lowering their concentrations to below those required for the synthesis of the viral DNA by reverse transcriptase (RT).
Journal ArticleDOI
p21-mediated RNR2 repression restricts HIV-1 replication in macrophages by inhibiting dNTP biosynthesis pathway.
Awatef Allouch,Annie David,Sarah M. Amie,Hichem Lahouassa,Loïc Chartier,Florence Margottin-Goguet,Francoise Barre-Sinoussi,Baek Kim,Baek Kim,Asier Sáez-Cirión,Gianfranco Pancino +10 more
TL;DR: It is shown that p21 impairs the reverse transcription of HIV-1 and other primate lentiviruses, including the simian immunodeficiency virus (SIV)mac, by blocking the synthesis of cellular deoxynucleotides (dNTP) that are used by retroviral reverse transcriptase for viral DNA synthesis.
Journal ArticleDOI
HIV-2/SIV viral protein X counteracts HUSH repressor complex.
Ghina Chougui,Ghina Chougui,Ghina Chougui,Soundasse Munir-Matloob,Soundasse Munir-Matloob,Soundasse Munir-Matloob,Roy Matkovic,Roy Matkovic,Roy Matkovic,Michaël M Martin,Michaël M Martin,Michaël M Martin,Marina Morel,Marina Morel,Marina Morel,Hichem Lahouassa,Hichem Lahouassa,Hichem Lahouassa,Marjorie Leduc,Bertha Cecilia Ramirez,Bertha Cecilia Ramirez,Bertha Cecilia Ramirez,Lucie Etienne,Lucie Etienne,Lucie Etienne,Florence Margottin-Goguet,Florence Margottin-Goguet,Florence Margottin-Goguet +27 more
TL;DR: The results suggest the HUSH complex as a restriction factor, active in primary CD4+ T cells and counteracted by Vpx, therefore providing a molecular link between intrinsic immunity and epigenetic control.
Journal ArticleDOI
Interferon block to HIV-1 transduction in macrophages despite SAMHD1 degradation and high deoxynucleoside triphosphates supply.
Loic Dragin,Loic Dragin,Loic Dragin,Laura A. Nguyen,Hichem Lahouassa,Hichem Lahouassa,Hichem Lahouassa,Adèle Sourisce,Adèle Sourisce,Adèle Sourisce,Baek Kim,Bertha Cecilia Ramirez,Bertha Cecilia Ramirez,Bertha Cecilia Ramirez,Florence Margottin-Goguet,Florence Margottin-Goguet,Florence Margottin-Goguet +16 more
TL;DR: The results suggest that the early antiviral effect of IFN-α results from a mechanism independent of nucleotide depletion in MDMs, and indicate that the macrophage-like THP-1 cell line may provide a system to characterize an IFn-α-induced cell response that inhibits Vpx-mediated SAMHD1 degradation.
Journal ArticleDOI
HIV-1 Vpr Induces the Degradation of ZIP and sZIP, Adaptors of the NuRD Chromatin Remodeling Complex, by Hijacking DCAF1/VprBP
Claire Maudet,Adèle Sourisce,Loïc Dragin,Hichem Lahouassa,Jean-Christophe Rain,Serge Bouaziz,Serge Bouaziz,Bertha Cecilia Ramirez,Bertha Cecilia Ramirez,Bertha Cecilia Ramirez,Florence Margottin-Goguet,Florence Margottin-Goguet,Florence Margottin-Goguet +12 more
TL;DR: Two transcriptional regulators, ZIP and sZIP, are identified as Vpr-binding proteins degraded in the presence of Vpr, highlighting the existence of two host transcription factors inactivated by Vpr.