Various plus unique: Viral protein U as a plurifunctional protein for HIV-1 replication

Soper, Andrew; Juarez-Fernandez, Guillermo; Aso, Hirofumi; Moriwaki, Miyu; Yamada, Eri; Nakano, Yoshiaki; Koyanagi, Yoshio; Sato, Kei

doi:10.1177/1535370217697384

Cited by 9 publications

(4 citation statements)

References 112 publications

(214 reference statements)

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“…Thus, Vpu-mediated antagonism of antiviral factors seems to involve both proteasomal degradation and alterations in clathrin-dependent trafficking pathways (27,(29)(30)(31). The effects of Vpu on CD4, tetherin, and nuclear factor kappa B (NF-κB), as well as its potential impact on Nef function and viral pathogenesis, have been previously reviewed (24,(32)(33)(34)(35). The main focus of this review is to discuss how these well-established and more recently reported Vpu activities cooperate to ensure the continued production and release of fully infectious HIV-1 particles, while preventing superinfection and elimination of productively infected cells.…”

Section: Figurementioning

confidence: 99%

Small but Highly Versatile: The Viral Accessory Protein Vpu

Volcic

Wiesmüller²,

Kirchhoff

2023

Annual Review of Virology

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Human and simian immunodeficiency viruses (HIVs and SIVs, respectively) encode several small proteins (Vif, Vpr, Nef, Vpu, and Vpx) that are called accessory because they are not generally required for viral replication in cell culture. However, they play complex and important roles for viral immune evasion and spread in vivo. Here, we discuss the diverse functions and the relevance of the viral protein U (Vpu) that is expressed from a bicistronic RNA during the late stage of the viral replication cycle and found only in HIV-1 and closely related SIVs. It is well established that Vpu counteracts the restriction factor tetherin, mediates degradation of the primary viral CD4 receptors, and inhibits activation of the transcription factor nuclear factor kappa B. Recent studies identified additional activities and provided new insights into the sophisticated mechanisms by which Vpu enhances and prolongs the release of fully infectious viral particles. In addition, it has been shown that Vpu prevents superinfection not only by degrading CD4 but also by modulating DNA repair mechanisms to promote degradation of nuclear viral complementary DNA in cells that are already productively infected. Expected final online publication date for the Annual Review of Virology, Volume 10 is September 2023. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

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Section: Figurementioning

confidence: 99%

Small but Highly Versatile: The Viral Accessory Protein Vpu

Volcic

Wiesmüller²,

Kirchhoff

2023

Annual Review of Virology

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“…Vpu is a multifunctional type I transmembrane protein [reviewed in Ref. ( 68 )] and sequesters tetherin molecules from the cell surface to endosomal compartments through transmembrane domain-mediated interaction ( 69 – 72 ). Additionally, the DSGXXS motif in the cytoplasmic tail of Vpu interacts with BTRC1 (beta-transducin repeat containing E3 ubiquitin protein ligase; also known as β-TrCP1 and Fbxw1), a subunit of E3 ubiquitin ligase.…”

Section: Restriction Factors (Rfs): Isgs Potently Control Hiv-1 Replimentioning

confidence: 99%

Type I Interferon Responses by HIV-1 Infection: Association with Disease Progression and Control

et al. 2018

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Human immunodeficiency virus type 1 (HIV-1) is the causative agent of acquired immunodeficiency syndrome and its infection leads to the onset of several disorders such as the depletion of peripheral CD4+ T cells and immune activation. HIV-1 is recognized by innate immune sensors that then trigger the production of type I interferons (IFN-Is). IFN-Is are well-known cytokines eliciting broad anti-viral effects by inducing the expression of anti-viral genes called interferon-stimulated genes (ISGs). Extensive in vitro studies using cell culture systems have elucidated that certain ISGs such as APOBEC3G, tetherin, SAM domain and HD domain-containing protein 1, MX dynamin-like GTPase 2, guanylate-binding protein 5, and schlafen 11 exert robust anti-HIV-1 activity, suggesting that IFN-I responses triggered by HIV-1 infection are detrimental for viral replication and spread. However, recent studies using animal models have demonstrated that at both the acute and chronic phase of infection, the role of IFN-Is produced by HIV or SIV infection in viral replication, spread, and pathogenesis, may not be that straightforward. In this review, we describe the pluses and minuses of HIV-1 infection stimulated IFN-I responses on viral replication and pathogenesis, and further discuss the possibility for therapeutic approaches.

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“…Неструктурные белки ВИЧ-1 практически не содержатся в вирусной частице, однако в значительных количествах производятся инфицированной клеткой, поступают в кровоток, поглощаются другими инфицированными и неинфицированными клетками различных тканей организма, изменяют процессы функционирования как производящих, так и поглотивших их клеток, активно участвуя в репликации вируса и формируя защиту вируса от иммунной системы хозяина [53][54][55][56][57][58]. В связи с этим в настоящее время неструктурные белки ВИЧ-1 являются мишенями для разработки антиретровирусных препаратов и терапевтических вакцин [59][60][61][62][63][64][65].…”

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The role of HIV-1 polymorphism in the pathogenesis of the disease

Kuznetsova

2023

VIČ-infekc. immunosupr.

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High genetic variability is one of the defining HIV-1 properties. It contributes to the appearance of drug resistance and to the formation of various HIV variants. In the world, the different variants of HIV-1 are distributed unevenly. In Russia there are circulating unique virus variants which are characteristic for our country and some countries of the former USSR and which are difference from HIV-1 variants circulating in other countries of the world. For many years, the studies aimed on the analysis of the influence of various HIV-1 variants on pathogenesis have been conducted. Within the framework of these studies, the polymorphism mutations in different subtypes and recombinant forms have been detected. Currently the main objects of antiretroviral therapy are HIV-1 structural proteins, mainly enzyme proteins, thus polymorphic mutations in which could affect the degree of virus sensitivity to antiretroviral therapy. Non-structural HIV-1 proteins are involved in virus replication and virus protection from the host immune system, enter the bloodstream and tissues, causing the development of inflammation. The polymorphic mutations in non-structural proteins could affect the degree of HIV infection progression and the development of concomitant somatic diseases. Today, nonstructural proteins are considered as objects for the creation of therapeutic agents, thus the identification of polymorphic mutations in nonstructural proteins in different HIV-1 variants is a basis for such developments. Thus, the study of polymorphism of both structural and non-structural HIV-1 proteins is a promising area of research in the future.

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Various plus unique: Viral protein U as a plurifunctional protein for HIV-1 replication

Cited by 9 publications

References 112 publications

Small but Highly Versatile: The Viral Accessory Protein Vpu

Small but Highly Versatile: The Viral Accessory Protein Vpu

Type I Interferon Responses by HIV-1 Infection: Association with Disease Progression and Control

The role of HIV-1 polymorphism in the pathogenesis of the disease

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