Project description:Glioma stem cells derived from patient samples were infected with ZIKV at MOI of 1 for 48hrs, total RNA was extracted and deep sequenced to compare the gene expression profiles between mock and ZIKV infected cells
Project description:Purpose: While type I interferons (IFN) are important for control of viral replication, we see that, upon infection of Ifnar-/- females were crossed to Ifnar+/- males with ZIKV, only Ifnar+/- fetuses are resorbed or develop severe growth restriction. To identify how IFN may be altering placenta development, we performed RNAsequencing on infected and uninfected Ifnar-/- and Ifnar+/- placentas. Methods: Ifnar-/- females were crossed to Ifnar+/- males and infected intravaginally with Cambodian ZIKV at E5.5. Placentas were harvested from infected and uninfected pregnant dams at E10.5. Results/ Conclusions: Comparison of ZIKV-infected Ifnar-/- and Ifnar+/- shows an elevated interferon stimulated gene (ISG) signature in Ifnar+/- placentas but does not reveal any underlying developmental defects that may be causing defects in placenta development.
Project description:An iTRAQ-based quantitative proteomic analysis of ZIKV infected Aedes albopictus C6/36 cells was performed to investigate host proteins involved in ZIKV infection process. A total of 3,544 host proteins were quantified, with 200 being differentially regulated. Bioinformatics analysis on regulated host proteins highlights several ZIKV infection regulated biological processes.
Project description:In this work, we demonstrate that neonatal mice infected with ZIKV via intracranial injection suffers from transient olfactory dysfunction when they grow up to puberty. Moreover, ZIKV exhibits broad cellular tropism and mainly targets the olfactory ensheathing cells (OECs) in the olfactory mucosa (OM) of mice. To decipher the underlying mechanism of the observed olfactory dysfunction in ZIKV infected mice at the molecular level, RNA-Seq analyses of the OM and OB samples from ZIKV infected mice were performed in comparison with that from the control animals.
Project description:To investigate cellular pathway dysregulation upon ZIKV infection, time-resolved phosphoproteomics LC-MS/MS analysis was used. ZIKV-infected SK-N-BE2 cells or mock-treated cells were harvested 24, 48 and 72 hours post virus infection and their phosphoproteome was quantitatively analyzed by label-free LC-MS/MS.
Project description:We repoted the Glioblastoma stem cells(GSCs) infected by two strains of ZIKA virus, the Brazil and Dakar strains. The ZIKV was added into the medium of GSCs for 48 hours, the RNA was harvested after ZIKV infection. We found that the GSCs up-regulated the Type 1&2 interferons after infected by ZIKV
Project description:Brain abnormalities and congenital malformations have been linked to the circulating strain of Zika virus (ZIKV) in Brazil since 2016 during the microcephaly outbreak; however, the molecular mechanisms behind several of these alterations and differential viral molecular targets have not been fully elucidated. Here we explore the proteomic alterations induced by ZIKV by comparing the Brazilian (Br ZIKV) and the African (MR766) viral strains, in addition to comparing them to the molecular responses to the Dengue virus (DENV). Neural stem cells (NSCs) derived from induced pluripotent stem (iPSCs) were cultured both as monolayers and in suspension (resulting in neurospheres), which were then infected with ZIKV (Br ZIKV or ZIKV MR766) or DENV to assess alterations within neural cells. Large-scale proteomic analyses allowed the comparison not only between viral strains but also regarding the two- and three-dimensional cellular models of neural cells derived from iPSCs, and the effects on their interaction. Altered pathways and biological processes were observed, related to cell death, cell cycle dysregulation, and neurogenesis. These results reinforce already published data and provide further information regarding the biological alterations induced by ZIKV and DENV.