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<dc:title xml:lang="fr">Etude du rôle des protéines cellulaires RACK1 et TIP47 dans l'infection par le virus de l'hépatite C</dc:title>
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<dc:subject xml:lang="fr">VHC</dc:subject>
<dc:subject xml:lang="fr">RACK1</dc:subject>
<dc:subject xml:lang="fr">Traduction</dc:subject>
<dc:subject xml:lang="fr">IRES</dc:subject>
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<dc:subject xml:lang="fr">Assemblage</dc:subject>
<dc:subject xml:lang="fr">Gouttelettes lipidiques</dc:subject>
<dc:subject xml:lang="fr">Export</dc:subject>
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<dc:subject xml:lang="en">RACK1</dc:subject>
<dc:subject xml:lang="en">Translation</dc:subject>
<dc:subject xml:lang="en">IRES</dc:subject>
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<dcterms:abstract xml:lang="fr">Le virus de l’hépatite C (VHC) dépend de facteurs cellulaires pour accomplir son cycle viral et persister dans l’hôte. L’une des stratégies de notre laboratoire consiste à étudier de manière approfondie le réseau d’interactions virus-hôte, afin d’identifier de nouvelles cibles thérapeutiques cellulaires et de développer des antiviraux plus efficaces pour vaincre la résistance virale. Durant ma thèse j’ai étudié deux facteurs cellulaires importants pour le VHC. Le premier est la protéine ribosomale RACK1. Nous avons montré que cette protéine est spécifiquement requise pour la traduction IRES-dépendante du VHC, et non pour la traduction coiffe-dépendante. Le deuxième facteur est une protéine de surface des gouttelettes lipidiques appelée TIP47. Nous avons montré que cette protéine est importante à la fois pour l’assemblage et pour l’export des particules virales. L’ensemble de ces travaux montre que de nouvelles cibles thérapeutiques pourraient être envisagées pour lutter contre le VHC.</dcterms:abstract>
<dcterms:abstract xml:lang="en">The hepatitis C virus (HCV) relies on cellular factors to complete its life cycle and persist in its host. One of the strategies employed by our laboratory is the in-depth study of the network of virus-host interactions to identify new therapeutic cellular targets and develop more effective antivirals to overcome viral resistance.During my PhD, I studied two cellular factors involved in the HCV life cycle. The first factor is the ribosomal protein RACK1. We have shown that this protein is specifically required for the HCV IRES-mediated translation but not for the cap-mediated translation. The second factor is the lipid droplets binding protein TIP47. We have shown that this protein is important for both assembly and export of viral particles. This work shows that new therapeutic targets could be considered in the fight against HCV.</dcterms:abstract>
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