Vascular Endothelial Growth Factor A Promotes Vaccinia Virus Entry into Host Cells via Activation of the Akt Pathway

Hiley, Crispin; Chard, Louisa S.; Gangeswaran, Rathi; Tysome, James R.; Briat, Arnaud; Lemoine, Nick R.; Wang, Yaohe

doi:10.1128/jvi.00854-12

Cited by 30 publications

(18 citation statements)

References 49 publications

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“…PIKfyve facilitates Rab7a‐independent fusion of LEs with each other and with LYs 30. In addition, the PIKfyve‐activating kinase, Akt, previously implicated in VACV entry 70, 71, was a hit in our screen. Interestingly, Akt has been reported to phosphorylate PIKfyve to facilitate lysosomal trafficking and degradation of EGFR 72.…”

Section: Discussionmentioning

confidence: 93%

Vaccinia Virus Infection Requires Maturation of Macropinosomes

Rizopoulos

Balistreri

Kilcher

et al. 2015

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The prototypic poxvirus, vaccinia virus (VACV), occurs in two infectious forms, mature virions (MVs) and extracellular virions (EVs). Both enter HeLa cells by inducing macropinocytic uptake. Using confocal microscopy, live‐cell imaging, targeted RNAi screening and perturbants of endosome maturation, we analyzed the properties and maturation pathway of the macropinocytic vacuoles containing VACV MVs in HeLa cells. The vacuoles first acquired markers of early endosomes [Rab5, early endosome antigen 1 and phosphatidylinositol(3)P]. Prior to release of virus cores into the cytoplasm, they contained markers of late endosomes and lysosomes (Rab7a, lysosome‐associated membrane protein 1 and sorting nexin 3). RNAi screening of endocytic cell factors emphasized the importance of late compartments for VACV infection. Follow‐up perturbation analysis showed that infection required Rab7a and PIKfyve, confirming that VACV is a late‐penetrating virus dependent on macropinosome maturation. VACV EV infection was inhibited by depletion of many of the same factors, indicating that both infectious particle forms share the need for late vacuolar conditions for penetration.

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Section: Discussionmentioning

confidence: 93%

Vaccinia Virus Infection Requires Maturation of Macropinosomes

Rizopoulos

Balistreri

Kilcher

et al. 2015

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“…Another gene found in tumor cells that can influence OV therapy is VEGF. Our group has demonstrated that VEGF-A increases VV internalization and in turn replication levels ( 135 ). Therefore, oncolytic VV can take advantage of the increased expression of VEGF by tumor cells to increase delivery of therapeutic genes which in turn increases the efficacy and potency of the treatment.…”

Section: Tumor Cell Biology and Viral Therapymentioning

confidence: 99%

Oncolytic Viruses—Interaction of Virus and Tumor Cells in the Battle to Eliminate Cancer

et al. 2017

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Oncolytic viruses (OVs) are an emerging treatment option for many cancer types and have recently been the focus of extensive research aiming to develop their therapeutic potential. The ultimate aim is to design a virus which can effectively replicate within the host, specifically target and lyse tumor cells and induce robust, long lasting tumor-specific immunity. There are a number of viruses which are either naturally tumor-selective or can be modified to specifically target and eliminate tumor cells. This means they are able to infect only tumor cells and healthy tissue remains unharmed. This specificity is imperative in order to reduce the side effects of oncolytic virotherapy. These viruses can also be modified by various methods including insertion and deletion of specific genes with the aim of improving their efficacy and safety profiles. In this review, we have provided an overview of the various virus species currently being investigated for their oncolytic potential and the positive and negative effects of a multitude of modifications used to increase their infectivity, anti-tumor immunity, and treatment safety, in particular focusing on the interaction of tumor cells and OVs.

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“…CCL chemokines (CCL2, CCL3, CCL4, CCL5, and CCL11) were found in acute ZIKV infection. The role of CCL5 in the arbovirus-induced immunopathology remains a controversial issue, but this chemokine along with CCL2 and CCL3 were previously linked to severity of dengue and Japanese encephalitis virus infections, including neurological diseases and impairment of neuronal survival [23][24][25][26][27].…”

Section: Discussionmentioning

confidence: 99%

Analysis of the immunological biomarker profile during acute Zika virus infection reveals the overexpression of CXCL10, a chemokine already linked to neuronal damage

Naveca

Pontes

Chang

et al. 2017

Preprint

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Infection with Zika virus (ZIKV) manifests in a broad spectrum of disease ranging from mild illness to severe neurological complications. To define immunologic correlates of ZIKV infection, we characterized the levels of circulating cytokines, chemokines and growth factors in 54 infected patients of both genders, at five different time-points after symptoms onset using microbeads multiplex immunoassay; statistical analysis and data mining compared to 100 age-matched controls. ZIKV-infected patients present a striking systemic inflammatory response with high levels of pro-inflammatory mediators. Despite the strong inflammatory pattern, IL-1Ra and IL-4 are also induced during acute infection. Interestingly, the inflammatory cytokines, IL-1β, IL-13, IL-17, TNF-α, IFN-γ; chemokines, CXCL8, CCL2, CCL5; and the growth factor G-CSF display a bimodal distribution accompanying viremia. While this is the first manuscript to document bimodal distributions of viremia in ZIKV infection, bimodal viremia has been documented in other viral infections with primary viremia peaks during mild systemic disease and a secondary viremia with distribution of the virus to organs and tissues. Moreover, biomarker network analysis demonstrated distinct dynamics in consonance with the bimodal viremia profiles at different time-points during ZIKV infection. Such robust cytokine and chemokine response has been associated with blood-brain barrier permeability and neuroinvasiveness in other flaviviral infections. High-dimensional data analysis further established CXCL10, a chemokine involved in fetal neuron apoptosis and Guillain-Barré syndrome, as the most promising biomarker of acute ZIKV infection for a potential clinical application.Author SummaryInfection with Zika virus manifests in a broad spectrum of disease ranging from mild illness to severe neurological complications. This study characterized the levels of circulating cytokines, chemokines and growth factors in Zika-infected patients showing an inflammatory immune response. Specifically, this study identified a chemokine, CXCL10, known to be involved in fetal neuron apoptosis and Guillain-Barré syndrome, as the most promising biomarker to characterize acute Zika virus infection.

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Vascular Endothelial Growth Factor A Promotes Vaccinia Virus Entry into Host Cells via Activation of the Akt Pathway

Cited by 30 publications

References 49 publications

Vaccinia Virus Infection Requires Maturation of Macropinosomes

Vaccinia Virus Infection Requires Maturation of Macropinosomes

Oncolytic Viruses—Interaction of Virus and Tumor Cells in the Battle to Eliminate Cancer

Analysis of the immunological biomarker profile during acute Zika virus infection reveals the overexpression of CXCL10, a chemokine already linked to neuronal damage

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