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Quantitative proteomic analysis of ZIKV infected C6/36 cells

ABSTRACT: 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.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Aedes Albopictus

TISSUE(S): Early Embryonic Cell

DISEASE(S): Zika Fever

SUBMITTER: Lei-Ke Zhang

LAB HEAD: Lei-Ke Zhang

PROVIDER: PXD004727 | Pride | 2017-04-21

REPOSITORIES: Pride

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			Action	DRS
	20160603_BP_iTRAQ_1-1.wiff	Wiff
	20160603_BP_iTRAQ_1-1.wiff.scan	Wiff
	20160603_BP_iTRAQ_1-10-1__FDR.xlsx	Xlsx
	20160603_BP_iTRAQ_10-1.wiff	Wiff
	20160603_BP_iTRAQ_10-1.wiff.scan	Wiff

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Publications

Quantitative Proteomic Analysis of Mosquito C6/36 Cells Reveals Host Proteins Involved in Zika Virus Infection.

Xin Qi-Lin QL Deng Cheng-Lin CL Chen Xi X Wang Jun J Wang Shao-Bo SB Wang Wei W Deng Fei F Zhang Bo B Xiao Gengfu G Zhang Lei-Ke LK

Journal of virology 20170526 12

Zika virus (ZIKV) is an emerging arbovirus belonging to the genus Flavivirus of the family Flaviviridae During replication processes, flavivirus manipulates host cell systems to facilitate its replication, while the host cells activate antiviral responses. Identification of host proteins involved in the flavivirus replication process may lead to the discovery of antiviral targets. The mosquitoes Aedes aegypti and Aedes albopictus are epidemiologically important vector ...[more]

PMID: 28404849

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Paracrine IFN response limits ZIKV infection in human Sertoli cells

Project description:Zika virus (ZIKV) is unique among mosquito-borne flaviviruses in its ability to be sexually transmitted. The testes have been implicated as sites of long-term ZIKV replication, and our previous studies have identified Sertoli cells (SC), the nurse cells of the seminiferous epithelium that govern spermatogenesis, as major targets of ZIKV infection. To improve our understanding of the host-ZIKV interaction within human testicular cells, we analyzed ZIKV-induced proteome changes in SC and mixed seminiferous tubule cells (STC) using high-throughput liquid chromatography-tandem mass spectrometry (LC-MS/MS). We found that ZIKV infection in SC and STC induced distinct IFN-stimulated proteins and impacted pathways and functional networks associated with innate antiviral defense. IFN signaling was the most significantly enriched pathway and MX1 was the most abundant IFN-stimulated protein in both SC and STC. Increased levels of MX1 at later time points of infection coincided with diminished propagation of ZIKV in SC, whereas silencing of MX1 and IFIT1 enhanced peak ZIKV titers in SC. Furthermore, although downstream IFN-I signaling was found to be functional and restricted ZIKV replication in SC, in comparison to A549 cells, SC exhibited dampened expression of IFN-I/III-stimulated genes despite higher levels of virus progeny and IFN-I/III transcripts. Together, this study highlights the IFN-I/III response as a driver of the antiviral state that limits ZIKV infection in SC and suggests that delayed and reduced robustness of innate antiviral defense in SC may contribute to ZIKV persistence in the testes.

2021-09-10 | PXD025133 | Pride

RNA-seq of embryonic fibroblasts cell lines derived from CC001, CC071 and C57BL/6J mouse strains infected with ZIKV virus

Project description:Embryonic fibroblasts cell lines derived from CC001, CC071 and C57BL/6J mouse strains were infected with ZIKV virus.

2023-09-06 | E-MTAB-12765 | biostudies-arrayexpress

LC-MS of small extracellular vesicles (sEVs) secreted by mock- vs. Zika virus (ZIKV)-infected JEG-3 cells

Project description:Proteomics profiling of small extracellular vesicles secreted by mock- vs. ZIKV (PRVABC59)-infected JEG-3 cells.

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ZIKV-infected human NPCs LC-MS

Project description:In this study, proteomic analysis on ZIKV-infected primary human fetal neural progenitor cells (NPCs) revealed that virus infection altered levels of cellular proteins involved in NPC proliferation, differentiation and migration.

2018-06-25 | PXD009343 | Pride

Guillain-Barré syndrome following Zika virus infection is associated with a diverse spectrum of peripheral nerve reactive antibodies

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2023-03-10 | PXD028476 | Pride

Time-resolved phosphoproteomic analysis of ZIKV-infected cells

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.

2018-09-03 | PXD009560 | Pride

Analysis of Zika Virus gene expression by Ribosome profiling and RNA sequencing

Project description:Ribosome profiling (Ribo-Seq) (maps positions of translating ribosomes on the transcriptome) and RNA-Seq (quantifies the transcriptome) analysis of African green monkey (Vero E6) cells and Aedes albopictus (C6/36) cells infected with Zika Virus (ZIKV) strain PE243. Cells were harvested at 24 h post infection (p.i.) and Ribo-Seq and RNA-Seq libraries were prepared and deep sequenced.

2018-06-30 | E-MTAB-5418 | biostudies-arrayexpress

DIFFERENTIATION-DEPENDENT SUSCEPTIBILITY OF HUMAN MUSCLE CELLS TO ZIKA VIRUS INFECTION

Project description:Muscle cells are potential targets of many arboviruses, such as Ross River, Dengue, Sindbis, and Chikungunya viruses, that may be involved in the physiopathological course of the infection. During the recent outbreak of Zika virus (ZIKV), myalgia was one of the most frequently reported symptoms. We investigated the susceptibility of human muscle cells to ZIKV infection. Using an in vitro model of human primary myoblasts that can be differentiated into myotubes, we found that myoblasts can be productively infected by ZIKV. In contrast, myotubes were shown to be resistant to ZIKV infection, suggesting a differentiation-dependent susceptibility. Infection was accompanied by a caspase-independent cytopathic effect, associated with paraptosis-like cytoplasmic vacuolization. Proteomic profiling was performed 24h and 48h post-infection in cells infected with two different isolates. Proteome changes indicate that ZIKV infection induces an upregulation of proteins involved in the activation of the Interferon type I pathway, and a downregulation of protein synthesis. This work constitutes the first observation of primary human muscle cells susceptibility to ZIKV infection, and differentiation-dependent restriction of infection from myoblasts to myotubes. Since myoblasts constitute the reservoir of stem cells involved in reparation/regeneration in muscle tissue, the infection of muscle cells and the viral-induced alterations observed here could have consequences in ZIKV infection pathogenesis.

2020-05-11 | PXD017261 | Pride

Using next generation sequencing to study the genetic diversity of candidate live attenuated Zika vaccines

Project description:Zika virus (ZIKV) is a mosquito-transmitted positive-sense RNA virus in the family Flaviviridae. Candidate live-attenuated vaccine (LAV) viruses with engineered deletions in the 3’UTR provide immunity and protection in animal models of ZIKV infection, and phenotypic studies show that LAVs retain protective abilities following in vitro passage. The present study investigates the genetic diversity of wild-type (WT) parent ZIKV and its candidate LAVs using next generation sequencing analysis of five sequential in vitro passages. ZIKV RNA from was transfected into Vero cells, incubated for nine days, harvested, and clarified by centrifugation to generate passage 0 (P0) ZIKV infectious clones. Subsequently, P0 ZIKVs were blind-passaged into fresh cultures to generate P1, then serially through P5. P1-P5 stocks were harvested from cell media at 4-5 days post-infection. ZIKV RNA from 3’UTR deletion mutants were transfected into Vero cells, incubated for nine days, harvested, and clarified by centrifugation to generate passage 0 (P0) ZIKV infectious clones. Subsequently, P0 ZIKVs were blind-passaged into fresh cultures to generate P1, then serially through P5. P1-P5 stocks were harvested from cell media at 4-5 days post-infection. Genetic diversity of the viruses were assessed by evaluating both the variability (or uncertainty) at each nucleotide position was determined using Shannon entropy calculations and identified single nucleotide variants (SNVs). The results showed both the parental WT and LAV derivatives increase in genetic diversity with evidence of adaptation following passage.

2020-04-13 | E-MTAB-8905 | biostudies-arrayexpress

Impact of Zika Virus on the Human Type I Interferon Osteoimmune Response

Project description:Background: The developing field of osteoimmunology supports importance of an interferon(IFN) response pathway in osteoblasts. Clarifying osteoblast-IFN interactions is important because IFN is used as salvage anti-tumor therapy but systemic toxicity is high with variable clinical results. In addition, osteoblast response to systemic bursts and disruptions of IFN pathways induced by viral infection may influence bone remodeling. ZIKA virus(ZIKV) infection impacts bone development in humans and IFN response in vitro. Consistently, initial evidence of permissivity to ZIKV has been reported in human osteoblasts. Hypothesis: Osteoblast-like Saos-2 cells are permissive to ZIKV and responsive to IFN. Methods: Multiple approaches were used to assess whether Saos-2 cells are permissive to ZIKV infection and exhibit IFN-mediated ZIKV suppression. Proteomic methods were used to evaluate impact of ZIKV and IFN on Saos-2 cells. Results: Evidence is presented confirming Saos-2 cells are permissive to ZIKV and support IFN-mediated suppression of ZIKV. ZIKV and IFN differentially impact the Saos-2 proteome. Both ZIKV and IFN suppress proteins associated with microcephaly/pseudo-TORCH syndrome (BI1, KIF20 and UBP18), and ZIKV induces potential entry factor PLVAP. Conclusions: Transient ZIKV infection influences osteoimmune state, and IFN and ZIKV activate distinct proteomes in Saos-2 cells, which could inform therapeutic, engineered, disruptions.

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