APOBEC3F/G and Vif: Action and Counteractions

Libre, Camille; Batisse, Julien; Guerrero, Santiago; Marquet, Roland; Paillart, Jean-Christophe

doi:10.1007/978-1-4614-9610-6_376-1

Encyclopedia of AIDS 2015

DOI: 10.1007/978-1-4614-9610-6_376-1

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APOBEC3F/G and Vif: Action and Counteractions

Camille Libre¹,

Julien Batisse²,

Santiago Guerrero³

et al.

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2016

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Cited by 2 publications

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References 33 publications

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“…Vif reduces the intracellular A3G levels and its incorporation into viral particles by several mechanisms2424. First, it has now been well documented that Vif recruits an E3 ubiquitin ligase complex that polyubiquitinates A3G/A3F proteins and targets them for proteasomal degradation342526.…”

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

Guerrero

Libre

Batisse

et al. 2016

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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.

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confidence: 99%

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

Guerrero

Libre

Batisse

et al. 2016

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“…Vif behaves as a cofactor by stimulating the binding of reverse transcriptase and primer 13 , increasing the polymerization rate of the reverse transcriptase 14 , facilitating the bypass of abasic sites 14 and modulating the post-penetration stability of the RNP complex 15 16 . The major role of Vif relies in the neutralization of a potent intracellular innate defense factor that protects mammals from viral DNA invasion in their genome 17 . By counteracting the antiviral activity of cellular cytidine deaminases, mainly APOBEC3G (A3G) and A3F, Vif prevents the newly made DNA from an intense deamination during RT that is associated with a strong reduction of viral infectivity 18 19 20 21 22 .…”

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Requirements for nucleocapsid-mediated regulation of reverse transcription during the late steps of HIV-1 assembly

Racine

Chamontin

Rocquigny

et al. 2016

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HIV-1 is a retrovirus replicating within cells by reverse transcribing its genomic RNA (gRNA) into DNA. Within cells, virus assembly requires the structural Gag proteins with few accessory proteins, notably the viral infectivity factor (Vif) and two copies of gRNA as well as cellular factors to converge to the plasma membrane. In this process, the nucleocapsid (NC) domain of Gag binds to the packaging signal of gRNA which consists of a series of stem-loops (SL1-SL3) ensuring gRNA selection and packaging into virions. Interestingly, mutating NC activates a late-occurring reverse transcription (RT) step in producer cells, leading to the release of DNA-containing HIV-1 particles. In order to decipher the molecular mechanism regulating this late RT, we explored the role of several key partners of NC, such as Vif, gRNA and the cellular cytidine deaminase APOBEC3G that restricts HIV-1 infection by targeting the RT. By studying combinations of deletions of these putative players, we revealed that NC, SL1-SL3 and in lesser extent Vif, but not APOBEC3G, interplay regulates the late RT.

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APOBEC3F/G and Vif: Action and Counteractions

Cited by 2 publications

References 33 publications

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

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

Requirements for nucleocapsid-mediated regulation of reverse transcription during the late steps of HIV-1 assembly

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