The nucleolus and herpesviral usurpation

Ni, Liwen; Wang, Shuai; Zheng, Chunfu

doi:10.1099/jmm.0.045963-0

Cited by 10 publications

(9 citation statements)

References 85 publications

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“…Upon infection with herpes simplex type 1 (HSV-1), profound alterations of nucleolar morphology of the host cell occur. Nucleolin, B23 and UBF proteins leave the nucleolus to accumulate into the viral DNA replication centres (VRCs) [23] , [24] , [25] , [26] . In addition, ribosomal protein L9 interacts with the mouse mammary tumor virus (MMTV) Gag protein in the nucleolus of the cells and knockdown of the endogenous L9 cause an impairment of virus production [27] .…”

Section: Discussionmentioning

confidence: 99%

HIV-1 Infection Causes a Down-Regulation of Genes Involved in Ribosome Biogenesis

et al. 2014

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HIV-1 preferentially infects CD4+ T cells, causing fundamental changes that eventually lead to the release of new viral particles and cell death. To investigate in detail alterations in the transcriptome of the CD4+ T cells upon viral infection, we sequenced polyadenylated RNA isolated from Jurkat cells infected or not with HIV-1. We found a marked global alteration of gene expression following infection, with an overall trend toward induction of genes, indicating widespread modification of the host biology. Annotation and pathway analysis of the most deregulated genes showed that viral infection produces a down-regulation of genes associated with the nucleolus, in particular those implicated in regulating the different steps of ribosome biogenesis, such as ribosomal RNA (rRNA) transcription, pre-rRNA processing, and ribosome maturation. The impact of HIV-1 infection on genes involved in ribosome biogenesis was further validated in primary CD4+ T cells. Moreover, we provided evidence by Northern Blot experiments, that host pre-rRNA processing in Jurkat cells might be perturbed during HIV-1 infection, thus strengthening the hypothesis of a crosstalk between nucleolar functions and viral pathogenesis.

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Section: Discussionmentioning

confidence: 99%

HIV-1 Infection Causes a Down-Regulation of Genes Involved in Ribosome Biogenesis

et al. 2014

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“…This is also observed for a combined knockdown of HSV-1 glycoproteins gB and gH that are also components of the final envelope [15,16]. However, as herpesviruses commonly co-opt host proteins [17,18] and cellular vesicle fusion requires many players [19,20], it has been suggested that host proteins might cooperate with viral proteins for efficient nuclear egress [21]. Several cellular proteins have been reported to be involved, including CD98 heavy chain, its binding partner β-integrin, and p32.…”

Section: Introductionmentioning

confidence: 89%

Host Vesicle Fusion Protein VAPB Contributes to the Nuclear Egress Stage of Herpes Simplex Virus Type-1 (HSV-1) Replication

Saiz-Ros

Czapiewski

Epifano

et al. 2019

Cells

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The primary envelopment/de-envelopment of Herpes viruses during nuclear exit is poorly understood. In Herpes simplex virus type-1 (HSV-1), proteins pUL31 and pUL34 are critical, while pUS3 and some others contribute; however, efficient membrane fusion may require additional host proteins. We postulated that vesicle fusion proteins present in the nuclear envelope might facilitate primary envelopment and/or de-envelopment fusion with the outer nuclear membrane. Indeed, a subpopulation of vesicle-associated membrane protein-associated protein B (VAPB), a known vesicle trafficking protein, was present in the nuclear membrane co-locating with pUL34. VAPB knockdown significantly reduced both cell-associated and supernatant virus titers. Moreover, VAPB depletion reduced cytoplasmic accumulation of virus particles and increased levels of nuclear encapsidated viral DNA. These results suggest that VAPB is an important player in the exit of primary enveloped HSV-1 virions from the nucleus. Importantly, VAPB knockdown did not alter pUL34, calnexin or GM-130 localization during infection, arguing against an indirect effect of VAPB on cellular vesicles and trafficking. Immunogold-labelling electron microscopy confirmed VAPB presence in nuclear membranes and moreover associated with primary enveloped HSV-1 particles. These data suggest that VAPB could be a cellular component of a complex that facilitates UL31/UL34/US3-mediated HSV-1 nuclear egress.

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“…Interactions have been described to enable the exploitation of nucleolar proteins to facilitate specific processes in viral replication or of nucleoli as structural platforms for virus assembly (Hiscox, 2007;Sonntag et al, 2010;Salvetti and Greco, 2014). Nucleolar targeting by nuclear viruses has been the subjects of several reviews (Hiscox, 2007;Greco, 2009;Hiscox et al, 2010;Wang et al, 2010a;Ni et al, 2012;Salvetti and Greco, 2014) and a number of known/hypothesized functions are summarized in Table 1.…”

Section: Viral Targeting Of the Nucleolusmentioning

confidence: 99%

The nucleolar interface of RNA viruses

Rawlinson

Moseley

2015

Cell Microbiol

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SummaryIn recent years, understanding of the nucleolus has undergone a renaissance. Once considered primarily as the sites of ribosome biogenesis, nucleoli are now understood to be highly dynamic, multifunctional structures that participate in a plethora of cellular functions including regulation of the cell cycle, signal recognition particle assembly, apoptosis and stress responses. Although the molecular/mechanistic details of many of these functions remain only partially resolved, it is becoming increasingly apparent that nucleoli are also common targets of almost all types of viruses, potentially allowing viruses to manipulate cellular responses and the intracellular environment to facilitate replication and propagation. Importantly, a number of recent studies have moved beyond early descriptive observations to identify key roles for nucleolar interactions in the viral life cycle and pathogenesis. While it is perhaps unsurprising that many viruses that replicate within the nucleus also form interactions with nucleoli, the roles of nucleoli in the biology of cytoplasmic viruses is less intuitive. Nevertheless, a number of positivestranded RNA viruses that replicate exclusively in the cytoplasm are known to express proteins that enter the nucleus and target nucleoli, and recent data have indicated similar processes in several cytoplasmic negative-sense RNA viruses. Here, we review this emerging aspect of the virus-host interface with a focus on examples where virusnucleolus interactions have been linked to specific functional outcomes/mechanistic processes in infection and on the nucleolar interfaces formed by viruses that replicate exclusively in the cytoplasm.

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The nucleolus and herpesviral usurpation

Cited by 10 publications

References 85 publications

HIV-1 Infection Causes a Down-Regulation of Genes Involved in Ribosome Biogenesis

HIV-1 Infection Causes a Down-Regulation of Genes Involved in Ribosome Biogenesis

Host Vesicle Fusion Protein VAPB Contributes to the Nuclear Egress Stage of Herpes Simplex Virus Type-1 (HSV-1) Replication

The nucleolar interface of RNA viruses

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