Claudin-6 and Occludin Natural Variants ...
Type de document :
Compte-rendu et recension critique d'ouvrage
PMID :
Titre :
Claudin-6 and Occludin Natural Variants Found in a Patient Highly Exposed but Not Infected with Hepatitis C Virus (HCV) Do Not Confer HCV Resistance In Vitro
Auteur(s) :
Fénéant, Lucie [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Ghosn, Jade [Auteur]
Infection à VIH, réservoirs, diversité génétique et résistance aux antirétroviraux (ARV) [EA 7327]
Hôpital Hôtel-Dieu [Paris]
Fouquet, Baptiste [Auteur]
Physiopathologie et traitement des maladies du foie
Helle, Francois [Auteur]
CHU Amiens-Picardie
Belouzard, Sandrine [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Vausselin, Thibaut [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Seron, Karin [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Delfraissy, François [Auteur]
Hôpital Bicêtre [AP-HP, Le Kremlin-Bicêtre]
Dubuisson, Jean [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Misrahi, Micheline [Auteur]
Université Paris-Sud - Paris 11 [UP11]
Physiopathologie et traitement des maladies du foie
Cocquerel, Laurence [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Ghosn, Jade [Auteur]
Infection à VIH, réservoirs, diversité génétique et résistance aux antirétroviraux (ARV) [EA 7327]
Hôpital Hôtel-Dieu [Paris]
Fouquet, Baptiste [Auteur]
Physiopathologie et traitement des maladies du foie
Helle, Francois [Auteur]
CHU Amiens-Picardie
Belouzard, Sandrine [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Vausselin, Thibaut [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Seron, Karin [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Delfraissy, François [Auteur]
Hôpital Bicêtre [AP-HP, Le Kremlin-Bicêtre]
Dubuisson, Jean [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Misrahi, Micheline [Auteur]
Université Paris-Sud - Paris 11 [UP11]
Physiopathologie et traitement des maladies du foie
Cocquerel, Laurence [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Titre de la revue :
PLoS ONE
Pagination :
e0142539
Éditeur :
Public Library of Science
Date de publication :
2015
ISSN :
1932-6203
Mot(s)-clé(s) en anglais :
Flow cytometry
Luciferase
Hepatocytes
Reporter genes
Tight junctions
Mutation databases
Hepatitis C virus
293T cells
Luciferase
Hepatocytes
Reporter genes
Tight junctions
Mutation databases
Hepatitis C virus
293T cells
Discipline(s) HAL :
Sciences du Vivant [q-bio]/Médecine humaine et pathologie/Maladies infectieuses
Sciences du Vivant [q-bio]/Immunologie/Immunité innée
Sciences du Vivant [q-bio]/Médecine humaine et pathologie/Hépatologie et Gastroentérologie
Sciences du Vivant [q-bio]/Microbiologie et Parasitologie/Virologie
Sciences du Vivant [q-bio]/Immunologie/Immunité innée
Sciences du Vivant [q-bio]/Médecine humaine et pathologie/Hépatologie et Gastroentérologie
Sciences du Vivant [q-bio]/Microbiologie et Parasitologie/Virologie
Résumé en anglais : [en]
The clinical course of Hepatitis C Virus (HCV) infection is highly variable between infected individual hosts: up to 80% of acutely HCV infected patients develop a chronic infection while 20% clear infection spontaneously. ...
Lire la suite >The clinical course of Hepatitis C Virus (HCV) infection is highly variable between infected individual hosts: up to 80% of acutely HCV infected patients develop a chronic infection while 20% clear infection spontaneously. Spontaneous clearance of HCV infection can be predicted by several factors, including symptomatic acute infection, favorable IFNL3 polymorphisms and gender. In our study, we explored the possibility that variants in HCV cell entry factors might be involved in resistance to HCV infection. In a same case patient highly exposed but not infected by HCV, we previously identified one mutation in claudin-6 (CLDN6) and a rare variant in occludin (OCLN), two tight junction proteins involved in HCV entry into hepatocytes. Here, we conducted an extensive functional study to characterize the ability of these two natural variants to prevent HCV entry. We used lentiviral vectors to express Wildtype or mutated CLDN6 and OCLN in different cell lines and primary human hepatocytes. HCV infection was then investigated using cell culture produced HCV particles (HCVcc) as well as HCV pseudoparticles (HCVpp) expressing envelope proteins from different genotypes. Our results show that variants of CLDN6 and OCLN expressed separately or in combination did not affect HCV infection nor cell-to-cell transmission. Hence, our study highlights the complexity of HCV resistance mechanisms supporting the fact that this process probably not primarily involves HCV entry factors and that other unknown host factors may be implicated.Lire moins >
Lire la suite >The clinical course of Hepatitis C Virus (HCV) infection is highly variable between infected individual hosts: up to 80% of acutely HCV infected patients develop a chronic infection while 20% clear infection spontaneously. Spontaneous clearance of HCV infection can be predicted by several factors, including symptomatic acute infection, favorable IFNL3 polymorphisms and gender. In our study, we explored the possibility that variants in HCV cell entry factors might be involved in resistance to HCV infection. In a same case patient highly exposed but not infected by HCV, we previously identified one mutation in claudin-6 (CLDN6) and a rare variant in occludin (OCLN), two tight junction proteins involved in HCV entry into hepatocytes. Here, we conducted an extensive functional study to characterize the ability of these two natural variants to prevent HCV entry. We used lentiviral vectors to express Wildtype or mutated CLDN6 and OCLN in different cell lines and primary human hepatocytes. HCV infection was then investigated using cell culture produced HCV particles (HCVcc) as well as HCV pseudoparticles (HCVpp) expressing envelope proteins from different genotypes. Our results show that variants of CLDN6 and OCLN expressed separately or in combination did not affect HCV infection nor cell-to-cell transmission. Hence, our study highlights the complexity of HCV resistance mechanisms supporting the fact that this process probably not primarily involves HCV entry factors and that other unknown host factors may be implicated.Lire moins >
Langue :
Anglais
Vulgarisation :
Non
Source :
Fichiers
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4643007/pdf
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- efaa2b32ceca9caed06a8b4da64be7ec.pdf
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