Simian-Human immunodeficiency virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA355237 | ENA |
REPOSITORIES: ENA
Similar Datasets
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.
2016-11-30 | GSE90621 | GEO
Project description:Genetic evolution of non-human primate (NHP) lentiviruses towards HIV in humanized mice
| PRJNA640803 | ENA
Project description:HIV low frequency drug resistance mutations on naive patients
| PRJNA209812 | ENA
Project description:Finding the differences in gene expression in three regions of the brai, basal ganglia, white matter, and frontal cortex, in normal, HIV infected, HIV inefected with neurocognitive impairment, and HIV infected with both neurocognitive impairment and encephalitis patients. We used microarrays to identify differentially expressed genes in normal, HIV infected, HIV inefected with neurocognitive impairment, and HIV infected with both neurocognitive impairment and encephalitis patients. Samples from three different brain regions from normal, HIV infected, HIV infected with neurocognitive impairment (HAD: HIV-associated dementia), and HIV infected with both neurocognitive impairment and encephalitis (HIVE: HIV encephalitis) patients were collected for RNA isolation and supsequent Affymetrix microarray analysis. We sought to obtain gene expression levels in different brain regions to find implication of HIV and the neurological impairment and inflammation associated with HIV infection.
2012-07-31 | E-GEOD-35864 | biostudies-arrayexpress
Project description:The goal of this study was to determine how an HIV quasispecies is maintained in the face of selection. We deep sequenced the HIV provirus from cell populations as well as single cells at different time points from in vitro evolution experiments and found that when a less fit and more fit infect the same cell, they share components (complmentation) and therefore allow the less fit to perpetuate. We reproduced a quasispecies to an HIV reverse transcriptase inhibitor. The drug resistant genotype never completely supplanted the drug sensitive genotype, which stabilized at about 20% of viral sequences. Single-cell sequencing showed that resistant genotype frequency plateaued when cells were co-infected with sensitive and resistant genotypes, suggesting a sharing of viral proteins in co-infected cells (complementation), masking genotypic differences. To test if complementation can confer phenotypic drug resistance, we co-transfected fluorescently labelled molecular clones of sensitive and resistant HIV and observed drug resistance in genotypically sensitive virus from co-transfected cells. Resistant virus preferentially co-infected cells with drug sensitive HIV, explaining initiation of co-infections. Modelling showed that a stable quasispecies could form at the experimental multiplicities of infection. Conclusions: Complementation can lead to a quasispecies in infection environments where multiple infections per cell are common
2020-05-13 | GSE150390 | GEO
Project description:The goal of this project is todetermine if natural killer (NK) cells could be able to control HIV replication and reduce or eliminate viral reservoirs leading to HIV cure or a functional cure. Despite thirty years of work and significant progress, HIV infection continues to be an incurable disease. Antiretroviral therapy (ART) has significantly decreased the morbidity and mortality, but lifelong treatment is merely suppressive and does not cure HIV/AIDS. This is because of the existence of a reservoir of viral DNA+ (vDNA+) in cells of the lymphoid tissues with an intact provirus that is thought capable of initiating new rounds of HIV replication (i.e. latency). In addition to this inducible reservoir data suggest ongoing low-level virus replication and persistence in lymphatic tissues of some patients that is related to suboptimal drug levels in these tissues. Strategies are needed that can address both issues. NK cells are innate immune effectors that recognize virally infected targets through a cadre of activating and inhibitory receptors but become dysfunctional in HIV infected people. Strikingly, African green monkeys (AGM) and sooty mangabeys mount a strong control of viral replication in lymph node follicles shortly after the viremia peak that lasts throughout infection. Several mechanisms have been proposed to be implicated in the strong control of viral replication in natural host’s lymph nodes, such as NK cell-mediated control. Indeed, we have recently shown that NK cells could migrate into the b cells follicles in a CXCR5 dependent manner and thus participate to the elimination of viral replication. Thus the purpose of this study is too compare at the transcriptomic level different subset of NK cell isolated from blood and peripheral lymph node of chronically infected AGM to identify a transcriptomic signature which could be linked to an efficient control of SIV replication. This results could then provide a new aproche which could be exploited to generate functional NK cells against HIV in infected patients.
2020-12-21 | GSE140600 | GEO
Project description:Simian immunodeficiency virus overview
| PRJNA69627 | ENA
Project description:Simian immunodeficiency virus Variation
| PRJNA176620 | ENA
Project description:Simian immunodeficiency virus Genome sequencing and assembly
| PRJNA317777 | ENA