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• W2125830488 abstract "The HIV-1 accessory proteins, Viral Infectivity Factor (Vif) and the pleiotropic Viral Protein R (Vpr) are important for efficient virus replication. While in non-permissive cells an appropriate amount of Vif is critical to counteract APOBEC3G-mediated host restriction, the Vpr-induced G2 arrest sets the stage for highest transcriptional activity of the HIV-1 long terminal repeat.We identified a G run localized deep in the vpr AUG containing intron 3 (GI3-2), which was critical for balanced splicing of both vif and vpr non-coding leader exons. Inactivation of GI3-2 resulted in excessive exon 3 splicing as well as exon-definition mediated vpr mRNA formation. However, in an apparently mutually exclusive manner this was incompatible with recognition of upstream exon 2 and vif mRNA processing. As a consequence, inactivation of GI3-2 led to accumulation of Vpr protein with a concomitant reduction in Vif protein. We further demonstrate that preventing hnRNP binding to intron 3 by GI3-2 mutation diminished levels of vif mRNA. In APOBEC3G-expressing but not in APOBEC3G-deficient T cell lines, mutation of GI3-2 led to a considerable replication defect. Moreover, in HIV-1 isolates carrying an inactivating mutation in GI3-2, we identified an adjacent G-rich sequence (GI3-1), which was able to substitute for the inactivated GI3-2.The functionally conserved intronic G run in HIV-1 intron 3 plays a major role in the apparently mutually exclusive exon selection of vif and vpr leader exons and hence in vif and vpr mRNA formation. The competition between these exons determines the ability to evade APOBEC3G-mediated antiviral effects due to optimal vif expression." @default.
• W2125830488 created "2016-06-24" @default.
• W2125830488 creator A5024349567 @default.
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• W2125830488 creator A5057907622 @default.
• W2125830488 creator A5086888386 @default.
• W2125830488 date "2014-08-29" @default.
• W2125830488 modified "2023-09-24" @default.
• W2125830488 title "A functional conserved intronic G run in HIV-1 intron 3 is critical to counteract APOBEC3G-mediated host restriction" @default.
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• W2125830488 doi "https://doi.org/10.1186/s12977-014-0072-1" @default.
• W2125830488 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4163160" @default.
• W2125830488 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25169827" @default.
• W2125830488 hasPublicationYear "2014" @default.
• W2125830488 type Work @default.
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