Similar Datasets
Project description:ZIKV infection increases HUVECs endothelial barrier permeability and activates inflammatory cytokines
| PRJNA488555 | ENA
Project description:In this project, we aimed to explore the role of extracellular vesicles (EVs) in Zika virus (ZIKV) infection. We preferred antibody capture to ltracentrifugation for exosome isolation. The EVs derived from naive HUVEc cells or ZIKV-infected HUVEc cells were harvested and analyzed by mass spectrometry. The protein profile data understand the relationship between the ZIKV and EVs.
2023-01-19 | PXD039152 | Pride
Project description:The objective of this assay was to determine the effect of ZIKV on host cellular pathways
2017-09-01 | GSE103114 | GEO
Project description:Zika virus (ZIKV) infection causes microcephaly and has been linked to other brain abnormalities. How ZIKV impairs brain development and function remains elusive. Here we systematically profiled transcriptomes of human neural progenitor cells (hNPCs) and astrocytes exposed to Asian ZIKVC, African ZIKVM, and Dengue virus (DENV). DENV causes distinct gene expression changes; and ZIKV has a broader impact on the expression of gene involved in DNA replication and repair. While overall expression profiles are similar, ZIKVC, but not ZIKVM, induces upregulation of viral response genes. Upon ZIKV infection, astrocytes exhibit more prominent transcriptome changes than hNPCs, particularly enriching genes related to inflammatory response and cytokine production pathways. Our analyses reveal cell-type- and strain-specific molecular signatures associated with ZIKV infection, and identify astrocytes as a major direct target of ZIKV. Further investigation of ZIKV-host interactions based our transcriptomic datasets may help to illuminate neural virulence determinants of ZIKV in patients. Gene Expression Analyses of the cells infected with different flaviviruses
2016-08-23 | E-GEOD-80434 | biostudies-arrayexpress
Project description:C20 were pre-treated with metformin at specified concentration (5 mM) for 2 h, followed by ZIKV infection at MOI 3. After infection of 1.5 h, cells were washed three times with PBS. Medium containing metformin was again supplemented and maintained during the culture. The total RNA of samples at 16 and 48 h were extracted for RNA-seq analysis. We then performed differential expression analysis using data obtained by RNA-seq of ZIKV infection and metformin treatment (16 h and 48 h).
2023-05-03 | GSE231200 | GEO
Project description:To determine the effect of Zika virus infection on pre-implantation embryonic development, we performed single blastocyst RNA-Seq on MOCK and ZIKV infected embryos. ZIKV infection results in an increased risk of spontaneous abortion and poor intrauterine growth although the mechanisms underlying fetal loss remain undetermined. Little is known about the impact of ZIKV infection during the earliest stages of pregnancy, or pre- and peri-implantation, because most current studies of ZIKV infection in pregnancy models focus on post-implantation stages. Here, we demonstrate that trophectoderm cells of pre-implantation human and mouse embryos can be efficiently infected with ZIKV, and that trophectoderm can propagate virus causing cell death of neural progenitors. These findings were corroborated by our demonstration that hESC-derived trophectoderm cells are infected by ZIKV in a dose dependent manner. RNAseq of single blastocysts revealed key transcriptional changes in cellular and physiologic functions upon ZIKV infection, including nervous system development and function, prior to commitment to the neural cell lineage. Finally, the pregnancy rate of mice infected pre-implantation was > 50% lower than females infected at E4.5. These results demonstrate that pre-implantation ZIKV infection of trophectoderm leads to miscarriage or spontaneous abortion. Moreover, pre- and peri-implantation ZIKV infects trophectoderm cells that propagate virus over time causing cell death in neural progenitors. Cumulatively, these data demonstrate that vertical pre- and peri-implantation ZIKV infection of trophectoderm impairs fetal development and causes neural progenitor cell death, elucidating a previously unappreciated association of pre- and peri-implantation ZIKV infection and microcephaly.
2019-08-16 | GSE133254 | GEO
Project description:We previously demonstrated that 25HC (25-hydroxycholesterol, a derivative of cholesterol) blocks KSHV (Kaposi Sarcoma-associated Herpesvirus/ Human Herpesvirus-8) de novo infection of primary endothelial cells at a post-entry step and decreases viral gene expression. Herein we sought to determine transcriptomic changes associated with 25HC treatment of primary endothelial cells and primary B cells using RNA sequencing. To understand how 25HC inhibits KSHV infection, we examined global gene expression changes induced by 25HC in HUVECs, with or without KSHV infection. We pre-treated HUVEC with 25HC or vehicle control, then infected with KSHV (four conditions: -/+ 25HC, -/+ infection). At 2 days post-infection (dpi), we harvested RNA and performed RNA-seq to determine differentially expressed genes. We found that 25HC treatment inhibited KSHV gene expression globally and induced several inflammatory cytokines (CXCL8, IL1?), AP-1 components, and innate immunity receptors (RIG-I, TLR2) . Likewise, we also observed 25HC to block EBV de novo infection by inducing apoptosis and blocking transformation into lymphoblastoid cell lines. To determine transcriptomic changes that contributes to this, we purified B cells from healthy donors and infected them with EBV after 25HC pre-treatment with 4 similar conditions mentioned above. Samples were sent for RNA-Seq at 10-12 dpi. In contrast to KSHV infection, we found that only a subset of EBV viral transcripts are downregulated in the 25HC-treated samples. LMP1, which is the primary oncogenic factor, was suppressed and several downstream host targets that would prevent apoptosis during infection were likewise dysregulated. Additionally, several viral noncoding RNAs were also highly downregulated. Further analyses revealed that some 25HC-induced genes in our KSHV data set overlap with antiviral genes that were previously identified in various published screens involving other viruses, demonstrating the broad activity of 25HC. Together, these results answer some important questions about a widely acting antiviral (25HC), with implications for multiple viral and bacterial infections.
2021-11-24 | GSE165328 | GEO
Project description:ZIKV alters transcriptional responses of infected cells to avoid immune detection. We have compared the transcriptional responses of ZIKV-infected hBMECs and mock-infected hBMECs. Examination of transcriptional responses of ZIKV-infected hBMECs versus mock-infected hBMECs
2017-07-15 | GSE98889 | GEO
Project description:Zika virus (ZIKV) infection causes microcephaly and has been linked to other brain abnormalities. How ZIKV impairs brain development and function remains elusive. Here we systematically profiled transcriptomes of human neural progenitor cells (hNPCs) exposed to Asian ZIKVC, African ZIKVM, and Dengue virus (DENV). DENV causes distinct gene expression changes; and ZIKV has a broader impact on the expression of gene involved in DNA replication and repair. While overall expression profiles are similar, ZIKVC, but not ZIKVM, induces upregulation of viral response genes. Our analyses reveal virus- and strain-specific molecular signatures associated with ZIKV infection. Further investigation of ZIKV-host interactions based our transcriptomic datasets may help to illuminate neural virulence determinants of ZIKV in patients.
2016-08-23 | GSE80434 | GEO
Project description:ZIKV strain sequencing including African strains
| PRJEB39677 | ENA