Translational regulation of APOBEC3G mRNA by Vif requires its 5′UTR and contributes to restoring HIV-1 infectivity

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• dc.contributor.author Guerrero, Santiago
• dc.contributor.author Libre, Camille
• dc.contributor.author Batisse, Julien
• dc.contributor.author Mercenne, Gaëlle
• dc.contributor.author Richer, Delphine
• dc.contributor.author Laumond, Géraldine
• dc.contributor.author Decoville, Thomas
• dc.contributor.author Moog, Christiane
• dc.contributor.author Marquet, Roland
• dc.contributor.author Paillart, Jean-Christophe
• dc.date.accessioned 2024-01-22T06:50:02Z
• dc.date.available 2024-01-22T06:50:02Z
• dc.date.issued 2016
• dc.description.abstract The essential HIV-1 viral infectivity factor (Vif) allows productive infection of non-permissive cells expressing cytidine deaminases APOBEC3G (A3G) and A3F by decreasing their cellular level, and preventing their incorporation into virions. Unlike the Vif-induced degradation of A3G, the functional role of the inhibition of A3G translation by Vif remained unclear. Here, we show that two stem-loop structures within the 5′-untranslated region of A3G mRNA are crucial for translation inhibition by Vif in cells, and most Vif alleles neutralize A3G translation efficiently. Interestingly, K26R mutation in Vif abolishes degradation of A3G by the proteasome but has no effect at the translational level, indicating these two pathways are independent. These two mechanisms, proteasomal degradation and translational inhibition, similarly contribute to decrease the cellular level of A3G by Vif and to prevent its incorporation into virions. Importantly, inhibition of A3G translation is sufficient to partially restore viral infectivity in the absence of proteosomal degradation. These findings demonstrate that HIV-1 has evolved redundant mechanisms to specifically inhibit the potent antiviral activity of A3G.
• dc.format.mimetype application/pdf
• dc.identifier.citation Guerrero S, Libre C, Batisse J, Mercenne G, Richer D, Laumond G, et al. Translational regulation of APOBEC3G mRNA by Vif requires its 5′UTR and contributes to restoring HIV-1 infectivity. Sci Rep. 2016 Dec 20;6(1):39507. DOI: 10.1038/srep39507
• dc.identifier.doi http://dx.doi.org/10.1038/srep39507
• dc.identifier.issn 2045-2322
• dc.identifier.uri http://hdl.handle.net/10230/58773
• dc.language.iso eng
• dc.publisher Nature Research
• dc.relation.ispartof Scientific Reports. 2016 Dec 20;6(1):39507
• dc.rights This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.rights.uri http://creativecommons.org/licenses/by/4.0/
• dc.subject.other VIH (Virus)
• dc.subject.other Immunodeficiència
• dc.subject.other ADN -- Dany
• dc.title Translational regulation of APOBEC3G mRNA by Vif requires its 5′UTR and contributes to restoring HIV-1 infectivity
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/publishedVersion