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      ZIKV infection differentially affects the transcriptional profiles in HTR8 and U251 cells

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          Highlights

          • ZIKV has a different infection pattern for placental trophoblasts and human brain cells.

          • ZIKV infection induced interferons, inflammatory cytokines, and chemokine production.

          • TNF-α neutralisation could promote ZIKV infection between HTR8 and U251 cells.

          Abstract

          The mechanism by which Zika virus (ZIKV) causes severe birth defects in pregnant women remains unclear. Cell tropisms in placenta and brain play a crucial role in ZIKV pathogenesis, leading to congenital Zika syndrome (CZS). To identify the host factors involved in ZIKV infection, we compared the transcriptional profiles of ZIKV-infected human first-trimester placental trophoblast cells HTR8/SVneo and a human glioblastoma astrocytoma cell line U251. Our results demonstrated that ZIKV exhibited lower rates of mRNA replication and protein expression in HTR8 than in U251 cells, while showing a higher release of infectious viral particles. However, a greater number of differentially expressed genes (DEGs) were found in ZIKV-infected U251 cells than in ZIKV-infected HTR8 cells. Several of these DEGs were enriched in distinct biological processes related to the characteristics of each cell type that may contribute to foetal damage. Both cell types exhibited activation of common interferons, inflammatory cytokines, and chemokine production upon ZIKV infection. Moreover, the neutralization of tumour necrosis factor-alpha (TNF-α) promoted ZIKV infection in both trophoblasts and glioblastoma astrocytoma cells. Overall, we identified multiple DEGs associated with ZIKV pathogenesis.

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          Most cited references56

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          Cytoscape: a software environment for integrated models of biomolecular interaction networks.

          Cytoscape is an open source software project for integrating biomolecular interaction networks with high-throughput expression data and other molecular states into a unified conceptual framework. Although applicable to any system of molecular components and interactions, Cytoscape is most powerful when used in conjunction with large databases of protein-protein, protein-DNA, and genetic interactions that are increasingly available for humans and model organisms. Cytoscape's software Core provides basic functionality to layout and query the network; to visually integrate the network with expression profiles, phenotypes, and other molecular states; and to link the network to databases of functional annotations. The Core is extensible through a straightforward plug-in architecture, allowing rapid development of additional computational analyses and features. Several case studies of Cytoscape plug-ins are surveyed, including a search for interaction pathways correlating with changes in gene expression, a study of protein complexes involved in cellular recovery to DNA damage, inference of a combined physical/functional interaction network for Halobacterium, and an interface to detailed stochastic/kinetic gene regulatory models.
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            ClueGO: a Cytoscape plug-in to decipher functionally grouped gene ontology and pathway annotation networks

            Summary: We have developed ClueGO, an easy to use Cytoscape plug-in that strongly improves biological interpretation of large lists of genes. ClueGO integrates Gene Ontology (GO) terms as well as KEGG/BioCarta pathways and creates a functionally organized GO/pathway term network. It can analyze one or compare two lists of genes and comprehensively visualizes functionally grouped terms. A one-click update option allows ClueGO to automatically download the most recent GO/KEGG release at any time. ClueGO provides an intuitive representation of the analysis results and can be optionally used in conjunction with the GOlorize plug-in. Availability: http://www.ici.upmc.fr/cluego/cluegoDownload.shtml Contact: jerome.galon@crc.jussieu.fr Supplementary information: Supplementary data are available at Bioinformatics online.
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              Zika virus outbreak on Yap Island, Federated States of Micronesia.

              In 2007, physicians on Yap Island reported an outbreak of illness characterized by rash, conjunctivitis, and arthralgia. Although serum from some patients had IgM antibody against dengue virus, the illness seemed clinically distinct from previously detected dengue. Subsequent testing with the use of consensus primers detected Zika virus RNA in the serum of the patients but no dengue virus or other arboviral RNA. No previous outbreaks and only 14 cases of Zika virus disease have been previously documented. We obtained serum samples from patients and interviewed patients for information on clinical signs and symptoms. Zika virus disease was confirmed by a finding of Zika virus RNA or a specific neutralizing antibody response to Zika virus in the serum. Patients with IgM antibody against Zika virus who had a potentially cross-reactive neutralizing-antibody response were classified as having probable Zika virus disease. We conducted a household survey to estimate the proportion of Yap residents with IgM antibody against Zika virus and to identify possible mosquito vectors of Zika virus. We identified 49 confirmed and 59 probable cases of Zika virus disease. The patients resided in 9 of the 10 municipalities on Yap. Rash, fever, arthralgia, and conjunctivitis were common symptoms. No hospitalizations, hemorrhagic manifestations, or deaths due to Zika virus were reported. We estimated that 73% (95% confidence interval, 68 to 77) of Yap residents 3 years of age or older had been recently infected with Zika virus. Aedes hensilli was the predominant mosquito species identified. This outbreak of Zika virus illness in Micronesia represents transmission of Zika virus outside Africa and Asia. Although most patients had mild illness, clinicians and public health officials should be aware of the risk of further expansion of Zika virus transmission. 2009 Massachusetts Medical Society
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                Author and article information

                Contributors
                Journal
                Virus Res
                Virus Res
                Virus Research
                Elsevier
                0168-1702
                1872-7492
                07 July 2023
                September 2023
                07 July 2023
                : 334
                : 199166
                Affiliations
                [a ]School of Public Health (Shenzhen), Shenzhen Campus of Sun Yat-sen University, Shenzhen 518107, PR China
                [b ]School of Public Health (Shenzhen), Sun Yat-sen University, Guangzhou 510275, PR China
                [c ]Huizhou Municipal Central Hospital, Huizhou 516001, PR China
                [d ]Cancer Hospital Chinese Academy of Medical Sciences, Shenzhen Center, Shenzhen 518172, PR China
                [e ]The Emergency Department, Eighth People's Hospital of Nanyang City, Nanyang 473000, PR China
                [f ]Shaoxing Center for Disease Control and Prevention, Shaoxing 312075, PR China
                [g ]Shenzhen Nanshan Center for Disease Control and Prevention, Shenzhen 518054, PR China
                [h ]Shenzhen Center for Disease Control and Prevention, Shenzhen 518073, PR China
                [i ]Institute of Pathogen Biology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100176, PR China
                [j ]Key Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, PR China
                Author notes
                [* ]Corresponding author at: School of Public Health (Shenzhen), Shenzhen Campus of Sun Yat-sen University, No. 66, Gongchang Road, Guangming District, Shenzhen, Guangdong 518107, PR China. luohle@ 123456mail.sysu.edu.cn
                [1]

                These authors contributed equally to this work.

                Article
                S0168-1702(23)00128-4 199166
                10.1016/j.virusres.2023.199166
                10410584
                5e03e203-86ce-4dfe-a8b3-b3d1b1c90ba5
                © 2023 The Authors. Published by Elsevier B.V.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 29 December 2022
                : 27 June 2023
                : 28 June 2023
                Categories
                Article

                Microbiology & Virology
                zika virus (zikv),rna-sequence,transcriptional profile,differentially expressed genes (degs),tumour necrosis factor-alpha (tnf-α)

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