HSV1 MicroRNA Modulation of GPI Anchoring and Downstream Immune Evasion

Enk, Jonatan; Levi, Assi; Weisblum, Yiska; Yamin, Rachel; Charpak-Amikam, Yoav; Wolf, Dana; Mandelboim, Ofer

doi:10.1016/j.celrep.2016.09.077

Cited by 37 publications

(23 citation statements)

References 42 publications

(61 reference statements)

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“…Among these pathways, the GPI-anchor is considered to play an important role in the infection and pathogenesis of many viruses. For example, Enk et al found that the herpes simplex virus (HSV)-1-encoded miR H8 could target the GPI anchoring pathway, which further reduced the expression levels of several immune-modulating proteins and finally enhanced viral spread and enabled evasion of elimination by natural killer cells [6]. Amet et al demonstrated that a deficiency of GPI-anchor could inhibit the production of infectious HIV-1 and render virions sensitive to complement attack [1].…”

Section: Discussionmentioning

confidence: 99%

Transcriptome analysis following enterovirus 71 and coxsackievirus A16 infection in respiratory epithelial cells

Liu

et al. 2020

Arch Virol

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Enterovirus 71 (EV-A71) and coxsackievirus A16 (CV-A16) are the major pathogens responsible for hand, foot and mouth disease (HFMD), but the mechanism by which these viruses cause disease remains unclear. In this study, we used transcriptome sequencing technology to investigate changes in the transcriptome profiles after infection with EV-A71 and CV-A16 in human bronchial epithelial (16HBE) cells. Using systematic bioinformatics analysis, we then searched for useful clues regarding the pathogenesis of HFMD. As a result, a total of 111 common differentially expressed genes were present in both EV-A71-and CV-A16-infected cells. A trend analysis of these 111 genes showed that 91 of them displayed the same trend in EV-A71 and CV-A16 infection, including 49 upregulated genes and 42 downregulated genes. These 91 genes were further used to conduct GO, pathway, and coexpression network analysis. It was discovered that enriched GO terms (such as histone acetylation and positive regulation of phosphorylation) and pathways (such as glycosylphosphatidylinositol (GPI)anchor biosynthesis and DNA replication) might be closely associated with the pathogenic mechanism of these two viruses, and key genes (such as TBCK and GPC) might be involved in the progression of HFMD. Finally, we randomly selected 10 differentially expressed genes for qRT-PCR to validate the transcriptome sequencing data. The experimental qRT-PCR results were roughly in agreement with the results of transcriptome sequencing. Collectively, our results provide clues to the mechanism of pathogenesis of HFMD induced by EV-A71 and CV-A16.

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Section: Discussionmentioning

confidence: 99%

Transcriptome analysis following enterovirus 71 and coxsackievirus A16 infection in respiratory epithelial cells

Liu

et al. 2020

Arch Virol

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“…HHV-1 encodes for miR-H8, which reduces the surface levels of ULBP2 and ULBP3. 98 The EBV-miR-BART2-5p directly targets MICB, 99 while EBV-miR-BART7 targets MICA. 100 MICB expression is also repressed by the CMV-miR-UL122 101 and by KSHV-miR-K12-7.…”

Section: Viral-encoded Mirs Enable Immune Evasion By Targeting Nkg2d-mentioning

confidence: 99%

Molecular mechanisms of human herpes viruses inferring with host immune surveillance

Jasinski‐Bergner

Mandelboim

Seliger

2020

J Immunother Cancer

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Several human herpes viruses (HHVs) exert oncogenic potential leading to malignant transformation of infected cells and/or tissues. The molecular processes induced by viral-encoded molecules including microRNAs, peptides, and proteins contributing to immune evasion of the infected host cells are equal to the molecular processes of immune evasion mediated by tumor cells independently of viral infections. Such major immune evasion strategies include (1) the downregulation of proinflammatory cytokines/chemokines as well as the induction of anti-inflammatory cytokines/chemokines, (2) the downregulation of major histocompatibility complex (MHC) class Ia directly as well as indirectly by downregulation of the components involved in the antigen processing, and (3) the downregulation of stress-induced ligands for activating receptors on immune effector cells with NKG2D leading the way. Furthermore, (4) immune modulatory molecules like MHC class Ib molecules and programmed cell death1 ligand 1 can be upregulated on infections with certain herpes viruses. This review article focuses on the known molecular mechanisms of HHVs modulating the above-mentioned possibilities for immune surveillance and even postulates a temporal order linking regular tumor immunology with basic virology and offering putatively novel insights for targeting HHVs.

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“…Although most identified targets of the 27 mature HSV-1 miRNAs are viral transcripts, recent research has described roles for these viral miRNAs in targeting cellular transcripts to promote immune evasion, viral replication, cell proliferation, and pathogenesis [ 82 , 83 ]. One such example is the targeting of PIGT by miR-H8.…”

Section: Herpesvirusesmentioning

confidence: 99%

“…PIGT is an important component of the glycosylphosphatidylinositol anchoring pathway that allows proteins to be presented on the cell surface. MiR-H8 represses PIGT expression resulting in a reduction in presentation of many immune-related proteins, including NK-cell ligands and the viral restriction factor, tetherin [ 83 ]. Thus, by targeting PIGT, miR-H8 efficiently counteracts the host immune response at several key points.…”

Section: Herpesvirusesmentioning

confidence: 99%

The Diverse Roles of microRNAs at the Host–Virus Interface

Bernier

Sagan

2018

Viruses

107

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MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression at the post-transcriptional level. Through this activity, they are implicated in almost every cellular process investigated to date. Hence, it is not surprising that miRNAs play diverse roles in regulation of viral infections and antiviral responses. Diverse families of DNA and RNA viruses have been shown to take advantage of cellular miRNAs or produce virally encoded miRNAs that alter host or viral gene expression. MiRNA-mediated changes in gene expression have been demonstrated to modulate viral replication, antiviral immune responses, viral latency, and pathogenesis. Interestingly, viruses mediate both canonical and non-canonical interactions with miRNAs to downregulate specific targets or to promote viral genome stability, translation, and/or RNA accumulation. In this review, we focus on recent findings elucidating several key mechanisms employed by diverse virus families, with a focus on miRNAs at the host–virus interface during herpesvirus, polyomavirus, retroviruses, pestivirus, and hepacivirus infections.

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HSV1 MicroRNA Modulation of GPI Anchoring and Downstream Immune Evasion

Cited by 37 publications

References 42 publications

Transcriptome analysis following enterovirus 71 and coxsackievirus A16 infection in respiratory epithelial cells

Transcriptome analysis following enterovirus 71 and coxsackievirus A16 infection in respiratory epithelial cells

Molecular mechanisms of human herpes viruses inferring with host immune surveillance

The Diverse Roles of microRNAs at the Host–Virus Interface

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