Microarray Profiling Analysis Uncovers Common Molecular Mechanisms of Rubella Virus, Human Cytomegalovirus, and Herpes Simplex Virus Type 2 Infections in ECV304 Cells

Mo, Xiaoyang; Xu, Luoling; Yang, Qiya; Feng, Hao; Peng, Jinghui; Zhang, Y.; Yuan, Weiming; Wang, Y.; Li, Y.; Deng, Yifan; Wan, Yunxia; Chen, Z.; Li, F.; Wu, Xiujing

doi:10.2174/156652411796268696

Cited by 3 publications

(1 citation statement)

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“…Fu reported latent CMV infection modulated the expression of cellular miRNAs predicted to target the Wnt pathway. Lytic CMV infection increased Wnt2 and WISP2 expression , and may reduce expression of Wnt5a/b, LRP6, Axin1 , CCND1, MYC and DKK1, and may induce the degradation of β‐catenin .…”

Section: Viruses Associated With Human Cancermentioning

confidence: 99%

The Wnt pathway: a key network in cell signalling dysregulated by viruses

Zuylen

Rawlinson

Ford

2016

Reviews in Medical Virology

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Viruses are obligate parasites dependent on host cells for survival. Viral infection of a cell activates a panel of pattern recognition receptors that mediate antiviral host responses to inhibit viral replication and dissemination. Viruses have evolved mechanisms to evade and subvert this antiviral host response, including encoding proteins that hijack, mimic and/or manipulate cellular processes such as the cell cycle, DNA damage repair, cellular metabolism and the host immune response. Currently, there is an increasing interest whether viral modulation of these cellular processes, including the cell cycle, contributes to cancer development. One cellular pathway related to cell cycle signalling is the Wnt pathway. This review focuses on the modulation of this pathway by human viruses, known to cause (or associated with) cancer development. The main mechanisms where viruses interact with the Wnt pathway appear to be through (i) epigenetic modification of Wnt genes; (ii) cellular or viral miRNAs targeting Wnt genes; (iii) altering specific Wnt pathway members, often leading to (iv) nuclear translocation of β-catenin and activation of Wnt signalling. Given that diverse viruses affect this signalling pathway, modulating Wnt signalling could be a generalised critical process for the initiation or maintenance of viral pathogenesis, with resultant dysregulation contributing to virus-induced cancers. Further study of this virus-host interaction may identify options for targeted therapy against Wnt signalling molecules as a means to reduce virus-induced pathogenesis and the downstream consequences of infection. Copyright © 2016 John Wiley & Sons, Ltd.

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Section: Viruses Associated With Human Cancermentioning

confidence: 99%

The Wnt pathway: a key network in cell signalling dysregulated by viruses

Zuylen

Rawlinson

Ford

2016

Reviews in Medical Virology

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An Image-Based Genetic Assay Identifies Genes in T1D Susceptibility Loci Controlling Cellular Antiviral Immunity in Mouse

et al. 2014

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The pathogenesis of complex diseases, such as type 1 diabetes (T1D), derives from interactions between host genetics and environmental factors. Previous studies have suggested that viral infection plays a significant role in initiation of T1D in genetically predisposed individuals. T1D susceptibility loci may therefore be enriched in previously uncharacterized genes functioning in antiviral defense pathways. To identify genes involved in antiviral immunity, we performed an image-based high-throughput genetic screen using short hairpin RNAs (shRNAs) against 161 genes within T1D susceptibility loci. RAW 264.7 cells transduced with shRNAs were infected with GFP-expressing herpes simplex virus type 1 (HSV-1) and fluorescent microscopy was performed to assess the viral infectivity by fluorescence reporter activity. Of the 14 candidates identified with high confidence, two candidates were selected for further investigation, Il27 and Tagap. Administration of recombinant IL-27 during viral infection was found to act synergistically with interferon gamma (IFN-γ) to activate expression of type I IFNs and proinflammatory cytokines, and to enhance the activities of interferon regulatory factor 3 (IRF3). Consistent with a role in antiviral immunity, Tagap-deficient macrophages demonstrated increased viral replication, reduced expression of proinflammatory chemokines and cytokines, and decreased production of IFN-β. Taken together, our unbiased loss-of-function genetic screen identifies genes that play a role in host antiviral immunity and delineates roles for IL-27 and Tagap in the production of antiviral cytokines.

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