Ultra-deep sequencing of HIV populations
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR1051010.fastq.gz | Fastqsanger.gz | |||
| SRR1051011.fastq.gz | Fastqsanger.gz | |||
| SRR1051012.fastq.gz | Fastqsanger.gz | |||
| SRR1051013.fastq.gz | Fastqsanger.gz |
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2011-03-25 | E-GEOD-28177 | biostudies-arrayexpress
Project description:This study examines the gene expression profiles of resident lymph node B cell populations in HIV-infected and uninfected controls.
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Project description:We evaluated longitudinal changes in viral replication and emergence of viral variants in the context of T cell homeostasis and gene expression in GALT of three HIV-positive patients who initiated HAART during primary HIV infection but opted to interrupt therapy thereafter. Longitudinal viral sequence analysis revealed that a stable proviral reservoir was established in GALT during primary HIV infection that persisted through early HAART and post-therapy interruption. Proviral variants in GALT and peripheral blood mononuclear cells (PBMCs) displayed low levels of genomic diversity at all times. A rapid increase in viral loads with a modest decline of CD4 T cells in peripheral blood was observed, while gut mucosal CD4 T cell loss was severe following HAART interruption. This was accompanied by increased mucosal gene expression regulating interferon (IFN)-mediated antiviral responses and immune activation, a profile similar to those found in HAART-naive HIV-infected patients.
2011-03-26 | GSE28177 | GEO
Project description:Gene copy-number variation, which provides the raw material for the evolution of novel genes, is surprisingly widespread in natural populations. Experimental evolution studies have demonstrated an extremely high spontaneous rate of origin of gene duplications. When organisms are suboptimally adapted to their environment, gene duplication may compensate for reduced fitness by amplifying promiscuous activity of a gene, or increasing dosage of a suboptimal gene. The overarching goal of this study is to inverstigate whether CNVs constitute a common mechanism of adaptive genetic change during compensatory evolution and to further characterize the role of natural selection in dictating their evolutionary spread at a population-genomic level. Outcrossing populations of C. elegans with low fitness were evolved for >200 generations and the frequencies of CNVs in these populations were analyzed by oligonucleotide array comparative genome hybridization, quantitative PCR, and single-worm PCR. Multiple duplications and deletions were detected in intermediate to high frequencies and several lines of evidence suggest that the changes in frequency were adaptive. 1) Many copy-number changes reached high frequency, were near fixation, or were fixed in a short time. 2) Many independent duplications and deletions in high frequency harbor overlapping regions which likely include genes that are under selection for either higher or lower rates of expression. 3) The size spectrum of deuplications and deletions in the adaptive recovery populations is significantly larger than that of spontaneous copy-number variants in mutation accumulation experiments. This is expected if larger CNVs are more likely to encompass genes that are being selected for altered gene dosage. Out results validate the great potential borne by gene copy-number changes for compensatory evolution and adaptation. Experimental genome evolution of copy-number variants in 25 experimental lines compared to 5 ancestral control lines.
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Project description:The development of combined chromatin immunoprecipitation and next generation sequencing (ChIP-seq) technologies has enabled genome-wide epigenetic profiling of numerous cell lines and tissue types. A major limitation of ChIP-seq, however, is the large number of cells required to generate high quality datasets, precluding the study of rare cell populations. Here, we present an ultra-low-input micrococcal nuclease-based native ChIP (ULI-NChIP) and sequencing method, to generate genome-wide histone mark profiles with high resolution and reproducibility from as few as one thousand cells. Using ULI-NChIP, we generated high quality maps of several covalent histone marks from 10^3-10^6 embryonic stem cells. To further validate our procedure we demonstrate that genome-wide H3K27me3 profiles generated from 10^3 E13.5 primordial germ cells (PGCs) using ULI-NChIP-seq show high similarity to recently generated datasets using 50-180× more material, illustrating the utility of this method for generating high quality libraries with improved complexity from rare cell populations.
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Project description:The response of human immunodeficiency virus type 1 (HIV-1) quasispecies to antiretroviral therapy is influenced by the ensemble of mutants that composes the evolving population. Low-abundance subpopulations within HIV-1 quasispecies may determine the viral response to the administered drug combinations. However, routine sequencing assays available to clinical laboratories do not recognize HIV-1 minority variants representing less than 25% of the population. Although several alternative and more sensitive genotyping techniques have been developed, including next-generation sequencing (NGS) methods, they are usually very time consuming, expensive and require highly trained personnel, thus becoming unrealistic approaches in daily clinical practice. Here we describe the development and testing of a HIV-1 genotyping DNA microarray that detects and quantifies, in majority and minority viral subpopulations, relevant mutations and amino acid insertions in 42 codons of the pol gene associated with resistance and multidrug resistance to protease (PR) and reverse transcriptase (RT) inhibitors. A customized bioinformatics protocol has been implemented to analyze the microarray hybridization data by including a new normalization procedure and a stepwise filtering algorithm which resulted in the highly accurate (96.33%) detection of positive/negative signals. This microarray has been tested with 57 subtype B HIV-1 clinical samples extracted from multi-treated patients, showing an overall identification of 95.53% and 89.24% of the queried PR and RT codons, respectively, and enough sensitivity to detect minority subpopulations representing as low as 5-10% of the total quasispecies. Such a genotyping platform represents an efficient diagnostic and prognostic tool useful to personalize antiviral treatments in clinical practice.
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Project description:Cell activation is a vital step for T cell memory/effector differentiation as well as for productive HIV infection. To identify novel regulators of this process, we used next generation sequencing to profile changes in microRNA expression occurring in purified human naive CD4 T cells in response to TCR stimulation and HIV infection. HIV infection had no significant impact on global miR expression in quiescent nave CD4 T cells. We identified miR-34c-5p as a novel miR strongly induced by TCR stimulation of nave CD4 T cells, and found that it was consistently down-regulated in response to viral infection. Over-expression of miR-34c-5p had a positive effect on HIV-1 replication. Finally, we demonstrated that miR-34c-5p alters the expression of several genes involved in TCR signaling and cell activation, identifying it as a novel regulator of nave CD4 T cell activation potentially targeted by HIV infection.
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