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dc.date.accessioned2020-05-27T19:16:12Z
dc.date.available2020-08-06T22:46:24Z
dc.date.created2020-01-27T14:47:34Z
dc.date.issued2019
dc.identifier.citationPlissonnier, Marie-Laure Cottarel, Jessica Piver, Eric Kullolli, Majlinda Centonze, Federica Grazia Pitteri, Sharon Farhan, Hesso Meunier, Jean-Christophe Zoulim, Fabien Parent, Romain . LARP1 binding to hepatitis C virus particles is correlated with intracellular retention of viral infectivity. Virus Research. 2019
dc.identifier.urihttp://hdl.handle.net/10852/76354
dc.description.abstractHepatitis C virus (HCV) virions contain a subset of host liver cells proteome often composed of interesting virus-interacting factors. A proteomic analysis performed on double gradient-purified clinical HCV highlighted the translation regulator LARP1 on these virions. This finding was validated using post-virion capture and immunoelectron microscopy, as well as immunoprecipitation applied to in vitro (Huh7.5 liver cells) grown (Gt2a, JFH1 strain) and patient-derived (Gt1a) HCV particles. Upon HCV infection of Huh7.5 cells, we observed a drastic transfer of LARP1 to lipid droplets, inducing colocalization with core proteins. RNAi-mediated depletion of LARP1 using the C911 control approach decreased extracellular infectivity of HCV Gt1a (H77), Gt2a (JFH1), and Gt3a (S52 chimeric strain), yet increased their intracellular infectivity. This latter effect was unrelated to changes in the hepatocyte secretory pathway, as evidenced using a functional RUSH assay. These results indicate that LARP1 binds to HCV, an event associated with retention of intracellular infectivity.
dc.languageEN
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.titleLARP1 binding to hepatitis C virus particles is correlated with intracellular retention of viral infectivity
dc.typeJournal article
dc.creator.authorPlissonnier, Marie-Laure
dc.creator.authorCottarel, Jessica
dc.creator.authorPiver, Eric
dc.creator.authorKullolli, Majlinda
dc.creator.authorCentonze, Federica Grazia
dc.creator.authorPitteri, Sharon
dc.creator.authorFarhan, Hesso
dc.creator.authorMeunier, Jean-Christophe
dc.creator.authorZoulim, Fabien
dc.creator.authorParent, Romain
cristin.unitcode185,51,12,17
cristin.unitnameCellesignalering
cristin.ispublishedtrue
cristin.fulltextpostprint
cristin.qualitycode1
dc.identifier.cristin1783250
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Virus Research&rft.volume=&rft.spage=&rft.date=2019
dc.identifier.jtitleVirus Research
dc.identifier.volume271
dc.identifier.doihttps://doi.org/10.1016/j.virusres.2019.197679
dc.identifier.urnURN:NBN:no-79442
dc.type.documentTidsskriftartikkel
dc.type.peerreviewedPeer reviewed
dc.source.issn0168-1702
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/76354/2/VIRO-S-18-00863_new.pdf
dc.type.versionAcceptedVersion
cristin.articleid197679


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