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Review
.2020:35:159-194.
doi: 10.21775/cimb.035.159. Epub 2019 Aug 18.

Ubiquitination and SUMOylation in HIV Infection: Friends and Foes

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Review

Ubiquitination and SUMOylation in HIV Infection: Friends and Foes

Marta Colomer-Lluch et al. Curr Issues Mol Biol.2020.

Abstract

As intracellular parasites, viruses hijack the cellular machinery to facilitate their replication and spread. This includes favouring the expression of their viral genes over host genes, appropriation of cellular molecules, and manipulation of signalling pathways, including the post-translational machinery. HIV, the causative agent of AIDS, is notorious for using post-translational modifications to generate infectious particles. Here, we discuss the mechanisms by which HIV usurps the ubiquitin and SUMO pathways to modify both viral and host factors to achieve a productive infection, and also how the host innate sensing system uses these post-translational modifications to hinder HIV replication.

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Figures

Figure 24.1
Figure 24.1
Progression of the HIV infection to AIDS in the presence and absence of cART. The graph displays the HIV viral loads as RNA copies/ml of plasma, and CD4+ T cell counts as number of cells/μl. The levels of these variables in the absence of cART are represented in black and dark blue lines, while these elements are depicted in grey and light blue lines under conditions of cART adherence.
Figure 24.2
Figure 24.2
The HIV virion and its genome. (A) Schematic illustration of a HIV particle. (B) Representation of the HIV-1 and HIV-2 genomes as dsDNA. CA: capsid. IN: integrase. MA, matrix; NC, nucleocapsid; PR, protease; RT, reverse transcriptase.
Figure 24.3
Figure 24.3
The HIV replication cycle. The diagram illustrates how HIV infects and produces progeny in CD4+ cells. The different steps in the life cycle of HIV are indicated in bold blue and the virus proteins are labelled in grey. PIC, pre-integration complex; RT, reverse transcription; RTC, reverse transcribing complex.
Figure 24.4
Figure 24.4
Ubiquitination and SUMOylation of HIV dependency factors. The figure illustrates the impact of ubiquitination and SUMOylation of cellular proteins on the replication of HIV. Negative effects are indicated in red boxes. Positive effects are shown in green boxes. The characteristics of these PTMs are also illustrated: moiety (if known) is indicated in red, and the amino acid position where these chains are attached in black anditalics. Virus proteins are labelled in grey. PIC: pre-integration complex.
Figure 24.5
Figure 24.5
Ubiquitination and SUMOylation as a mechanism of innate defence against HIV. The illustration shows how SUMOylation and ubiquitination are commonly used to restrict HIV replication. The red boxes indicate ubiquitination and SUMOylation events that decrease virus replication. Residues where SUMO and ubiquitin chains are attached are indicated in black anditalics. The moiety of these PTMs (if known) is indicated in red. Virus proteins are labelled in grey. Question marks represent events that remain to be elucidated.
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