Homo sapiens PBMCs: pre-vaccination (stimulation vs. no stimulation with EV71 antigen) vs. post-vaccination (stimulation vs. no stimulation with EV71 antigen)
ABSTRACT: To characterize the primary and recall responses to EV71 vaccines, PBMC from 19 recipients before and after vaccination with EV71 vaccine are collected and their gene expression signatures after stimulation with EV71 antigen were compared. Four-condition experiment,pre-vaccination PBMCs (stimulation vs. no stimulation with EV71 antigen) vs. post-vaccination PBMCs (stimulation vs. no stimulation with EV71 antigen)
Project description:HT29 cells was infected with EV71 at MOI 1 or nil respectively and harvested at 36hpi We use miRNA microarray to profile and identify miRNA which are up or down regulated due to EV71 infection 3 biological replicate (6 samples)
Project description:We attempted to identify potential miRNAs that can regulate viral replication by screening host miRNAs in EV71-infected RD cells. To compare the differential expression of miRNAs in EV71-infected cells at different time points, miRNA expression profiles were analyzed using Agilent Human MicroRNA Array chips. At 5 h p.i., the expression levels of most miRNAs in EV71-infected cells were not different from those of mock-infected cells. However, five miRNAs (miR-574-3p, miR-574-5p, miR-181d, miR-197, and miR-939) showed a miRNAs (miR-193a-3p and miR-324-5p) exhibited a increase in expression level in response to EV71 infection at 10 h p.i. RD cells were seeded (2*106 cells) in 10 cm dishes and incubated overnight. The cells were infected with EV71 (strain 2231) on ice at an M.O.I. of 10. After adsorption for 1 h, the virus suspension was replaced with DMEM containing 2% FBS, and the cells were harvested at the indicated times. Total cellular RNA extraction and miRNA microarray analyses were performed using the Agilent Human MicroRNA Array V2 chip, which contains 723 human and 76 viral miRNAs, each with 16 duplicates. Total gene signals were detected and analyzed using the GeneSpring 7.3.1 software and were normalized to the 75th percentile.
Project description:Enterovirus 71 (EV71), a member of Picornaviridae, causes severe neurological and systemic illness in children. To better understand the virus-host cell interactions, we performed a triple-SILAC-based quantitative proteomics study monitoring host cell proteome changes after EV71 infection. Based on the quantitative data for more than 4100 proteins, ~17% of the proteins were found as significantly changed (p<0.01) at either 8 or 20 hours post infection (h.p.i.). Five biological processes and seven protein classes showed significant differences. Functional screening of 9 regulated proteins discovered the regulatory role of CHCH2, a mitochondrial protein known as a transcriptional activator for cytochrome c oxidase (COX), in EV71 replication. Further studies showed that CHCH2 served as a negative regulator of innate immune responses.
Project description:To explore the molecular mechanisms of obesity and insulin resistance in the patients with polycystic ovary syndrome (PCOS) at the level of human embryonic stem cells (hESCs).Three PCOS-derived and one non-PCOS-derived hESC lines were induced into adipocytes, and then total mRNA was extracted from these adipocytes. The differential genes between PCOS-derived and non-PCOS-derived adipocytes were identified with GeneChip, and then were validated with real-time PCR.There were 153 differential genes. Of the 153 genes, 91 genes were up-regulated and 62 down-regulated. Nuclear receptor subfamily 0, group B, member 2 (NR0B2) was an up-regulated gene, and GeneChip software system indicated that it was associated with obesity and diabetes. Three PCOS-derived and one non-PCOS-derived hESC lines were induced into adipocytes, and then total mRNA was extracted from these adipocytes. The differential genes between PCOS-derived and non-PCOS-derived adipocytes were identified with GeneChip, and then were validated with real-time PCR.
Project description:Restif2007 - Vaccination invasion
This model is described in the article:
Vaccination and the dynamics
of immune evasion.
Restif O, Grenfell BT.
J R Soc Interface 2007 Feb; 4(12):
Vaccines exert strong selective pressures on pathogens,
favouring the spread of antigenic variants. We propose a simple
mathematical model to investigate the dynamics of a novel
pathogenic strain that emerges in a population where a previous
strain is maintained at low endemic level by a vaccine. We
compare three methods to assess the ability of the novel strain
to invade and persist: algebraic rate of invasion;
deterministic dynamics; and stochastic dynamics. These three
techniques provide complementary predictions on the fate of the
system. In particular, we emphasize the importance of
stochastic simulations, which account for the possibility of
extinctions of either strain. More specifically, our model
suggests that the probability of persistence of an invasive
strain (i) can be minimized for intermediate levels of vaccine
cross-protection (i.e. immune protection against the novel
strain) and (ii) is lower if cross-immunity acts through a
reduced infectious period rather than through reduced
version of the model can be used for both the stochastic and the
deterministic simulations described in the article. For
deterministic interpretations with infinite population sizes, set
the population size
N = 1. The model does reproduces the deterministic
time course. The initial values are set to the steady state
values for a latent infection with strain 1 with an invading
infection of strain 2 (I2=1e-06), 100 percent vaccination with a
susceptibility reduction τ=0.7 at birth (p=1), and all other
parameters as in figure 3 of the publication.
be compatible with older software tools, the english letter names
instead of the greek symbols were used for parameter names:
rate of loss of natural immunity
rate of loss of vaccine immunity
reduction of susceptibility by primary infection
reduction of infection period by primary infection
reduction of susceptibility by vaccination
reduction of infection period by vaccination
created by libAntimony v1.4 (using libSBML 3.4.1)
This model is hosted on
and identified by:
To cite BioModels Database, please use:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
Public Domain Dedication for more information.
Project description:We found PML was responsible for ATO resistance in HCC cells, PML knockdown cells show better sensitivity to ATO treatment. To further explore the mechanism of PML-induced ATO resistance, we performed a microarray assay to compare the differential gene expression profiles of PML-siRNA-treated (PML knockdown) and negative control siRNA-treated cells. Two-condition experiment, PML-siRNA vs. control cells. Biological replicates: two cell lines and each cell line has 1 control, 1 transfected, independently grown and harvested. One replicate per array. Comparisons were made between PML siRNA group and control group for each cell line
Project description:We performed comprehensive miRNA proﬁling in EV71- and CA16-infected human umbilical vein endothelial cells (HUVECs) at multiple time points using high-throughput sequencing. The results showed that 135 known miRNAs exhibited remarkable differences in expression. Of these, 30differentially expressed miRNAs presented opposite trends in EV71- and CA16-infected samples. Subsequently, we mainly focused on the 30 key differentially expressed miRNAs through further screening to predict targets.Gene ontology (GO) and pathway analysis of the predicted targets showed the enrichment of 14 biological processes, 9 molecular functions, 8 cellular components, and 85 pathways. The regulatory networks of these miRNAs with predicted targets, GOs, pathways, and coexpression genes were determined, suggesting that miRNAs display intricate regulatory mechanisms during the infection phase. Consequently, we specifically analyzed the hierarchical GO categories of the predicted targets involved in biological adhesion. The results indicated that the distinct changes induced by EV71 and CA16 infection may be partly linked to the function of the blood-brain barrier. Taken together, this is the first report describing miRNA expression profiles in HUVECs with EV71 and CA16 infections using high-throughput sequencing. Our data provide useful insights that may help to elucidate the different host-pathogen interactions following EV71 and CA16 infection and offer novel therapeutic targets for these infections. Overall design: There are 6 samples, including EV71-0h, EV71-72h, EV71-96h,CA16-0h CA16-72h, CA16-96h.
Project description:Enterovirus 71 (EV71) and Coxsackievirus A16 (CA16) are the predominant etiological agents of hand, foot, and mouth disease (HFMD) and both belong to the human enterovirus A species of the Picornaviridae family. These viruses share similar genetic homology, although the clinical manifestations of HFMD caused by the two viruses have some discrepancies. Furthermore, the underlying mechanisms leading to these differences remain unclear. microRNAs (miRNAs) participate in numerous biological or pathological processes, including host responses to viral infections, by targeting messenger RNAs (mRNAs) for translational repression or degradation. Here, we focused on differences in miRNA expression patterns in peripheral blood mononuclear cells (PBMCs) of rhesus monkeys infected with EV71 or CA16 at different time points using high-throughput sequencing technology. For the first time, this study demonstrated that EV71 and CA16 infection result in specific miRNA expression patterns in PBMCs. Overall design: The EV71 virus strain (sub-genotype C4, GenBank: EU812515.1) that originated from an epidemic in Fuyang, China in 2008 and the CA16 virus G20 strain (sub-genotype B, GenBank: JN590244.1), which originated from an HFMD patient in Guangxi in 2010, were propagated in PBMCs at a multiplicity of infection (MOI) of 1 the following day. Cells were infected in triplicate and collected at 0, 24 and 48 hours post infection (hpi). Cells infected with EV71 and CA16 for 0 hpi were used as controls. We defined the different experimental groups as EV71-0h, EV71-24h, EV71-48h, CA16-0h, CA16-24h and CA16-48h.