Transcriptomic Analysis of Hofbauer Cells from Human Placental Tissue Infected with HIV, CMV, and ZIKV
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PROVIDER: PRJNA1146376 | ENA |
REPOSITORIES: ENA
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Project description:This study involves the isolation of Hofbauer cells from human placental tissue at different gestation periods and their infection with HIV, CMV, and ZIKV. The transcriptomic profiles of these infected cells were analyzed using RNA-sequencing to identify differentially expressed genes and pathways.
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Project description:Here we studied the transcriptional profile of virus specific CD8 T cells to gain molecular insights in CD8 T cell functionality in HIV infection. HIV- and CMV-specific CD8 T cells were isolated from HIV infected individuals participating in the Amsterdam Cohort Studies (HIV progressors, long-term non-progressors (LTNP; HLA-B*57 and non-HLA-B*57) and individuals carrying the MAVS minor genotype) and CMV seropositive blood donors (BD). The transcription profile of HIV-specific CD8 T cells of LTNP groups was associated with increased protein/RNA metabolism pathways, indicating that immune control of HIV infection in these individuals is associated with increased functionality. In contrast, CMV-specific CD8 T cells from progressors showed increased expression of genes related to effector functions and suggests recent CMV reactivation. Our study provides novel insights into molecular mechanisms involved in HIV and CMV control in chronic HIV infection.
2024-10-09 | GSE197333 | GEO
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
2018-05-26 | GSE114907 | GEO
Project description:The transplacental transfer of maternal IgG to the developing fetus is critical for infant protection against infectious pathogens in the first year of life. However, factors that modulate the transplacental transfer efficiency of maternal IgG that could be harnessed for maternal vaccine design remain largely undefined. HIV-infected women have impaired placental IgG transfer, yet the mechanism underlying this impaired transfer is unknown, presenting an opportunity to explore factors that contribute to the efficiency of placental IgG transfer. We measured the transplacental transfer efficiency of maternal HIV and other pathogen-specific IgG in historical U.S. (n=120) and Malawian (n=47) cohorts of HIV-infected mothers and their HIV58 exposed uninfected and HIV-infected infants. We then examined the role of maternal HIV disease progression, infant factors, placental Fc receptor expression, and IgG Fc region subclass and glycan signatures and their association with transplacental transfer efficiency of maternal antigen-specific IgG. We established 3 distinct phenotypes of placental IgG transfer efficiency in HIV-infected women, including: 1) efficient transfer of the majority of antigen-specific IgG populations; 2) generally poor IgG transfer phenotype that was strongly associated with maternal CD4+ T cell counts, hypergammaglobulinemia, and frequently yielded non-protective levels of vaccine-specific IgG; and 3) variable transfer of IgG across distinct antigen specificities. Interestingly, maternal IgG characteristics, such as binding to placentally expressed Fc receptors FcgRIIa and FcgRIIIa, IgG subclass frequency, and Fc region glycan profiles were associated with placental IgG transfer efficiency. These maternal IgG transplacental transfer determinants were distinct among different antigen-specific IgG populations. Our findings suggest that in HIV-infected women, both maternal disease progression and Fc region characteristics modulate the selective placental transfer of distinct IgG subpopulations, with implications for both the health of HIV-exposed uninfected infants and maternal vaccine design.
2019-09-11 | GSE129272 | GEO
Project description:We analyzed the gene expression profile of the PBMC from -2dpi, 2dpi, and 6dpi ZIKV-infected treeshrew
2018-07-31 | GSE115093 | GEO
Project description:Here we use a proteomic approach to study the role of the placenta in ZIKV-induced microcephaly and the mechanisms of ZIKV to cross the placental barrier. Samples were separated into three groups: an uninfected control group (ZIKV-CZS-), a group of placentas infected by ZIKV with normal neonates (ZIKV+CZS-), and a group of placentas infected by ZIKV that developed microcephaly in newborns (ZIKV+CZS+). Zika virus causes DNA damage and impairs gene expression and mRNA translation during infection of the placenta. Processes related to viral transcytosis, like endocytosis, autophagy and disruption of actin filament were also observed in CZS-infected placentas, which could lead to a higher virus infiltration. Unncontrolled maternal immune response as well as greater expression of cellular adhesion proteins in the decidua could lead to a disruption of tolerance during pregnancy and induction of neurological malformation of the neonates
2024-07-02 | PXD023777 | Pride
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.
2017-12-31 | GSE98423 | GEO
Project description:Using HIV-1 SortSeq, we identified HIV-1-infected cells containing inducible HIV-1 for RNAseq from resting CD4+ T cells treated with PMA/ionomycin for 16 hours from HIV-1-infected, antiretroviral therapy treated, virally suppressed individuals. Using custom bioinformatic pipeline, we identified HIV-1 genomic RNA, host RNA and HIV-1-host chimeric RNA junctions.
2020-05-15 | GSE126230 | GEO
Project description:The clonal expansion of HIV-1-infected CD4+ T cells is a major barrier to cure. Using single-cell ECCITE-seq, we examined the transcriptional landscape, upstream immune regulators, HIV-1 RNA expression, and T cell clonal expansion dynamics of 215,458 CD4+ T cells (267 HIV-1 RNA+ cells and 68 expanded HIV-1 RNA+ T cell clones) from six HIV-1-infected individuals (during viremia and after suppressive antiretroviral therapy) and two uninfected individuals, in unstimulated conditions and after CMV and HIV-1 antigen stimulation. We found that despite antiretroviral therapy, antigen and TNF responses persisted and shaped T cell clonal expansion. HIV-1 resided in Th1 polarized, antigen-responding T cells expressing Bcl-2 family anti-apoptotic genes. HIV-1 RNA+ T cell clones were larger in clone size, established during viremia, persistent after viral suppression, and enriched in GZMB+ cytotoxic effector memory Th1 cells. Targeting HIV-1-infected cytotoxic CD4+ T cells and drivers of clonal expansion provides a new direction for HIV-1 eradication.
2022-03-21 | GSE187515 | GEO
Project description:Zika Virus (ZIKV) infection has been associated with fetal abnormalities by compromising placental integrity. Flavivirus have shown deregulation of the host proteome, specially extracellular matrix (ECM) proteins. Our hypothesis is that ZIKV infection of placental tissue deregulates specific ECM proteome, allowing a mechanism of persistent infection and loss of placental integrity. Using nine different placental samples from Puerto Rico collected during 2016 ZIKV epidemic, we compared the proteome of five ZIKV infected samples with uninfected controls. Quantitative proteomics was performed using tandem mass tag TMT10plex™ Isobaric Label Reagent Set followed by Q Exactive™ Hybrid Quadrupole Orbitrap Mass Spectrometry. Identification of proteins was performed by Proteome Discover 2.1, and protein fold change in both groups was compared using Limma software. Differentially expressed proteins were analyzed with STRING and Ingenuity Pathway using both the fold change and p-value. TMT analysis showed that ZIKV infected placentas had 94 reviewed differentially abundant proteins, 32 More abundant and 62 Less abundant. STRING analysis results indicate that 45 of the deregulated proteins are cellular components of the ECM and 16 play a role in its structure and organization. Some of the significantly More abundant proteins were Fibrinogen, Vitronectin and Fibronectin. The results we observed in the samples from naturally infected pregnant women may contribute to the understanding of the mechanism (s) employed by ZIKV during placental infection and give insight on novel targets used to disrupt placental function.
2022-06-09 | PXD023964 | Pride