HIV-1 Induces the Formation of Stable Microtubules to Enhance Early Infection

Sabo, Yosef; Walsh, Derek; Barry, Denis; Tinaztepe, Sedef; Santos, Kenia de los; Goff, Stephen P.; Gundersen, Gregg G.; Naghavi, Mojgan H.

doi:10.1016/j.chom.2013.10.012

Cited by 119 publications

(176 citation statements)

References 39 publications

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“…For example, it was reported that HIV-1 intracellular trafficking requires the formation of acetylated and detyrosinated stable MT tracts [78]. The end-binding protein EB1 mediates the virus-induced tubulin acetylation, and HIV-1 matrix protein targets the EB1-binding protein Kif4 to induce MT stabilization.…”

Section: Post-entry and Nuclear Targetingmentioning

confidence: 99%

Cellular defence or viral assist: the dilemma of HDAC6

Zheng

Jiang

et al. 2017

Journal of General Virology

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Histone deacetylase 6 (HDAC6) is a unique cytoplasmic deacetylase that regulates various important biological processes by preventing protein aggregation and deacetylating different non-histone substrates including tubulin, heat shock protein 90, cortactin, retinoic acid inducible gene I and b-catenin. Growing evidence has indicated a dual role for HDAC6 in viral infection and pathogenesis: HDAC6 may represent a host defence mechanism against viral infection by modulating microtubule acetylation, triggering antiviral immune response and stimulating protective autophagy, or it may be hijacked by the virus to enhance proinflammatory response. In this review, we will highlight current data illustrating the complexity and importance of HDAC6 in viral pathogenesis. We will summarize the structure and functional specificity of HDAC6, and its deacetylaseand ubiquitin-dependent activity in key cellular events in response to virus infection. We will also discuss how HDAC6 exerts its direct or indirect histone modification ability in viral lytic-latency switch.

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Section: Post-entry and Nuclear Targetingmentioning

confidence: 99%

Cellular defence or viral assist: the dilemma of HDAC6

Zheng

Jiang

et al. 2017

Journal of General Virology

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“…HIV-1 infection was also shown to induce tubulin post-translational modifications that are associated with the formation of a more stable subset of MTs, thus facilitating translocation of HIV-1 across the cytoplasm (80,91). Virus-induced MT stabilization, which occurs very rapidly after cell entry (within 1-2 h post-infection), was found to involve EB1 (91) and, albeit to a lesser extent, MAP1A/MAP1S proteins (80).…”

Section: Maps Mediate Virus-induced Microtubule Stabilizationmentioning

confidence: 99%

“…Virus-induced MT stabilization, which occurs very rapidly after cell entry (within 1-2 h post-infection), was found to involve EB1 (91) and, albeit to a lesser extent, MAP1A/MAP1S proteins (80). Conversely, HIV-1 infection was impaired by overexpression of moesin, a member of the ezrin, radixin and moesin (ERM) family that negatively regulates the stable MT network (101), thus confirming that MT stabilization favors viral particle trafficking to their site of replication.…”

Section: Maps Mediate Virus-induced Microtubule Stabilizationmentioning

confidence: 99%

“…However, the underlying mechanisms by which many viruses remodel host MT networks and potential roles for MAPs still remain relatively poorly understood. Recent work showed that adenovirus, African swine fever virus (ASFV), influenza A virus, reoviruses, HSV-1, HIV-1, and Ebola virus all induce MT stabilization, often observed with concomitant posttranslational modifications such as acetylation and detyrosination in host cells (90)(91)(92)(93)(94)(95)(96). Specifically, HSV-1 is thought to promote both its trafficking to the nucleus and its egress by multiple mechanisms, including the stabilization and hyper acetylation of MTs by the tegument protein VP22 (94) and viral kinase Us2 (97), binding of the molecular chaperone Hsp90 (98), disruption of the centrosomal nature of the MT-organizing center (MTOC) and its transfer to the trans-Golgi network (97,99,100).…”

Section: Maps Mediate Virus-induced Microtubule Stabilizationmentioning

confidence: 99%

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Role of non-motile microtubule-associated proteins in virus trafficking

Portilho

Persson²,

Arhel

2016

Biomolecular Concepts

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Viruses are entirely dependent on their ability to infect a host cell in order to replicate. To reach their site of replication as rapidly and efficiently as possible following cell entry, many have evolved elaborate mechanisms to hijack the cellular transport machinery to propel themselves across the cytoplasm. Long-range movements have been shown to involve motor proteins along microtubules (MTs) and direct interactions between viral proteins and dynein and/or kinesin motors have been well described. Although less well-characterized, it is also becoming increasingly clear that non-motile microtubule-associated proteins (MAPs), including structural MAPs of the MAP1 and MAP2 families, and microtubule plus-end tracking proteins (+ TIPs), can also promote viral trafficking in infected cells, by mediating interaction of viruses with filaments and/or motor proteins, and modulating filament stability. Here we review our current knowledge on nonmotile MAPs, their role in the regulation of cytoskeletal dynamics and in viral trafficking during the early steps of infection.

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“…Ϫ .E Ϫ HIV-1-based plasmid lacking env and vpr genes and having an mCherry open reading frame (ORF) instead of the nef gene, together with a VSV-G expression plasmid (13). We used a VSV-G envelope to bypass cell entry limitations and to look specifically at postentry events.…”

Section: Transduction Of Primary Cord-derived Cd34mentioning

confidence: 99%

HIV-1 Is Restricted prior to Integration of Viral DNA in Primary Cord-Derived Human CD34 ⁺ Cells

Griffin

Goff

2015

J Virol

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There is currently significant controversy regarding whether human hematopoietic stem cells (HSCs) can become infected with HIV-1; some but not all investigators have detected HIV-1 in human HSCs of infected patients (1, 2). Lentiviruses do successfully infect nondividing cells, but HIV-1 infection of human HSCs in culture is inefficient compared to that in activated T cells (3)(4)(5). A significant body of work has identified postintegration silencing as a major mechanism employed by murine stem cells (MSCs) to restrict retroviruses, but human HSCs may be different. The point in the retroviral replication cycle at which retroviruses are blocked in human HSCs remains unknown, and whether this involves a preintegration block or is due to transcriptional silencing of integrated proviruses has not been studied in detail (6-10).This investigation evaluated infection of primary cord-derived human CD34 ϩ cells, a mixed population composed of true human HSCs (Lin Ϫ 34 ϩ 38 Ϫ 90 ϩ 45RA dim ) as well as several hematopoietic progenitor cell (HPC) types. We identified a block occurring prior to viral DNA integration as a major factor in the nonpermissiveness of cord-derived primary CD34 ϩ cells for HIV-1 infection. Transduction of primary cord-derived CD34؉ cells by lentiviral vectors is inefficient at low MOIs. Primary human cordderived CD34 ϩ cells were used to study the efficiency of lentiviral transduction under various conditions. Each experimental replicate was performed independently with primary human CD34 ϩ cells from different donors. CD34 ϩ cells were isolated with magnetic beads from cord blood samples obtained from the Long Island Blood Service or obtained preisolated from AllCells (11,12). CD34 ϩ cells were put into culture in serum-free VIVO-X 20 medium. These cells were either cultured in the absence of cytokines or prestimulated for 24 h with various cytokines, singly or in combination, prior to exposure to preparations of pseudotyped lentiviral vectors. Vesicular stomatitis virus G (VSV-G)-pseudotyped virus with a modified pNL4.3 HIV-1-based core was prepared by cotransfecting 293T cells with a pNL4.3.mCherry.RϪ .E Ϫ HIV-1-based plasmid lacking env and vpr genes and having an mCherry open reading frame (ORF) instead of the nef gene, together with a VSV-G expression plasmid (13). We used a VSV-G envelope to bypass cell entry limitations and to look specifically at postentry events. Multiplicities of infection (MOIs) were calculated based on viral titers of mCherry transduction units, determined by infection of the permissive 293T cell line with serial dilutions of the virus preparation. The cells were preincubated for 24 h with no cytokines, Flt3 ligand (FLT3L) at 100 ng/ml, stem cell factor (SCF) at 100 ng/ml, thrombopoietin (TPO) at 100 ng/ml, or all three cytokines at 100 ng/ml. These cells were then exposed to pseudotyped virus by spinoculation at 37°C and 2,000 rpm for 60 min. Cells were then left in culture for 72 h at 37°C and evaluated using flow cytometry and PCR. All experiments were performed i...

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HIV-1 Induces the Formation of Stable Microtubules to Enhance Early Infection

Cited by 119 publications

References 39 publications

Cellular defence or viral assist: the dilemma of HDAC6

Cellular defence or viral assist: the dilemma of HDAC6

Role of non-motile microtubule-associated proteins in virus trafficking

HIV-1 Is Restricted prior to Integration of Viral DNA in Primary Cord-Derived Human CD34 ⁺ Cells

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HIV-1 Induces the Formation of Stable Microtubules to Enhance Early Infection

Cited by 119 publications

References 39 publications

Cellular defence or viral assist: the dilemma of HDAC6

Cellular defence or viral assist: the dilemma of HDAC6

Role of non-motile microtubule-associated proteins in virus trafficking

HIV-1 Is Restricted prior to Integration of Viral DNA in Primary Cord-Derived Human CD34 + Cells

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HIV-1 Is Restricted prior to Integration of Viral DNA in Primary Cord-Derived Human CD34 ⁺ Cells