Spatial transcriptomics of the Rhesus Macaque Hippocampus during homeostasis and chronic SIV CL757 infection
Ontology highlight
ABSTRACT:
ORGANISM(S): Macaca mulatta
PROVIDER: GSE261969 | GEO | 2024/03/26
REPOSITORIES: GEO
Similar Datasets
Project description:Question Addressed: Does gene expression change in the buccal mucosa of Lymphocryptovirus (LCV) infected animals when they are chronically infected with Simian immunodeficiency virus (SIV)? Oropharyngeal mucosal tissue samples were collected from rhesus macaques. A pooled common reference was used for all hybridizations. This reference was composed of RNA harvested from rhesus macaques not infected with either LCV or SIV. Infection: Animals were infected with SIV and/or LCV
2024-05-24 | GSE38918 | GEO
Project description:Question Addressed: How does Simian immunodeficiency virus (SIV) infection alter gene expression in memory CD4 T cell subsets very early during the 1st 10 days after infection? Memory CD4 T cells were sorted from rhesus macaque peripheral blood samples before infection and then at 4 and 10 days post SIV infection. RNA was recovered from the sorted memory CD4 T cells samples. RNA from the time point prior to SIV infection from each individual animal was used as the reference for the post SIV infection time points for that same animal. Thus, for each data set, the 4 and 10 day time points are being directly compared to the pre-infection data from the same animal. RNA samples as indicated above were used for reverse transcription reactions that directly incorporate Cy5 and Cy3 labeled nucleotides into the cDNA. Time: Time after infection with SIV
2019-09-23 | GSE38917 | GEO
Project description:Natural SIV infection of sooty mangabeys (SMs) does not progress to disease despite chronic virus replication. In contrast to pathogenic SIV infection of rhesus macaques (RMs), chronic SIV infection of SMs is characterized by low immune activation. To elucidate the mechanisms underlying this phenotype, we longitudinally assessed host gene expression in SIV-infected SMs and RMs. We found that acute SIV infection of SMs is consistently associated with a robust innate immune response, including widespread up-regulation of interferon-stimulated genes (ISGs). Our findings indicate that active immune regulatory mechanisms, rather than intrinsically attenuated innate immune responses, underlie the low immuneactivation of chronically SIV-infected SMs. We infected 5 SMs with SIVsmm and assessed their gene expression in RNA derived from whole blood at 3,7,10,14,30 and 180 days post-infection using Rhesus Affymetrix GeneChips. As a comparison, we also analyzed gene expression in 4 RMs infected with SIVsmm, and 8 RMs infected with SIVmac239, a classical pathogenic SIV.
2010-03-08 | E-GEOD-16147 | biostudies-arrayexpress
Project description:Cannabinoid administration before and after simian immunodeficiency virus (SIV)-inoculation ameliorated disease progression and decreased inflammation in male rhesus macaques. Δ9-tetrahydrocannabinol (Δ9-THC) did not increase viral load in brain tissue or produce additive neuropsychological impairment in SIV-infected macaques. To determine if the neuroimmunomodulation of Δ9-THC involved differential microRNA (miR) expression, miR expression in the striatum of uninfected macaques receiving vehicle (VEH) or Δ9-THC (THC) and SIV-infected macaques administered either vehicle (VEH/SIV) or Δ9-THC (THC/SIV) was profiled using next generation deep sequencing.
2016-01-22 | GSE72766 | GEO
Project description:In SIV/HIV infection, the gastrointestinal tissue dominates as an important site due to the impact of massive mucosal CD4 depletion and immune activation-induced tissue pathology. Unlike AIDS-susceptible rhesus macaques, natural hosts do not progress to AIDS and resolve immune activation earlier. Here, we examine the role of dendritic cells in mediating immune activation and disease progression. We demonstrate that plasmacytoid dendritic cells (pDC) in the blood upregulate ?7-integrin and are rapidly recruited to the colorectum following a pathogenic SIV infection in rhesus macaques. These pDC were capable of producing proinflammatory cytokines and primed a Tc1 response in vitro. Consistent with the upregulation of ?7-integrin on pDC, in vivo blockade of ?4?7-integrin dampened pDC recruitment to the colorectum and resulted in reduced immune activation. The upregulation of ?7-integrin expression on pDC in the blood was also observed in HIV-infected humans but not in chronically SIV-infected sooty mangabeys that show low levels of immune activation. Our results uncover a new mechanism by which pDC influence immune activation in colorectal tissue following pathogenic immunodeficiency virus infections. SIV negative controls (n=4) and week 12 post SIV infected (n=4) groups of Rhesus macaques and SIV negative controls (n=4) and week 55 post SIV infected (n=4) groups of Sooty mangabeys colorectal tissue biopsies were collected in to RNA later reagent (Qiagen) and were homogenized with syringe and needle method. RNA was extracted with Rneasy mini kit (Qiagen) and was used for microarray experiments. Rhesus GeneChip assays were performed in the Yerkes Microarray Core Facility (www.microarray.emory.edu) , one of the Affymetrix Microarray Core Labs.The 0.5µg of total RNA sample was analyzed on Rhesus Macaque Genome GeneChip that consists of over 52,000 probe sets (Affymetrix, Santa Clara, CA). Target RNA labeling, hybridization and post-hybridization processing were performed following the Affymetrix GeneChip Expression Analysis standard protocols. In brief, The 5 ?g of RNA sample was first reverse-transcribed using T7-Oligo(dT) Promoter Primer and SuperScript II in the first-strand cDNAs synthesis reaction. Following RNase H-mediated second-stranded cDNA synthesis, the double-stranded cDNAs were purified by use of a GeneChip sample clean-up module and served as templates in the generation of biotinylated complementary RNAs (cRNAs) in the presence of T7 RNA Polymerase and a biotinylated nucleotide analog/ribonucleotide mix by in vitro transcription (IVT) reaction. The biotinylated cRNAs were cleaned up, fragmented, and hybridized to the rhesus macaque expression arrays at 45°C for 16 h with constant rotation at 60 rpm. The gene chips were then washed and stained with Affymetrix fluidics stations 450 and scanned on Affymetrix scanner 3000. The images are processed to collect raw data with GeneChip Operating Software (GCOS) 1.4. Tissue: Colorectal tissue Time after SIV infection: 12 weeks for SIV infected Rhesus macaques, 55 weeks for Sooty mangabeys Infection: SIVmac251 infection for Rhesus macaques, SIVsm infection for Sooty mangabeys
2011-09-05 | E-GEOD-29980 | biostudies-arrayexpress
Project description:Salmonella enterica serotype Typhimurium cause a localized enteric infection in immunocompetent patients while human immunodeficiency virus (HIV)-infected patients develop a life threatening bacteremia. We used a rhesus macaque ileal loop model to study how simian immunodeficiency virus (SIV) infection triggers defects in mucosal barrier function that enhance S. Typhimurium dissemination. SIV infection resulted in significant depletion of CD4+ T cells in the intestinal mucosa. Gene expression profiling revealed a defective TH17 response (with suppression of IL-17 and IL-22 expression) and impaired homeostasis of the intestinal epithelium in SIV-infected animals during NTS infection. These findings correlated with an impaired ability of lamina propria CD4+ T cells from SIV-infected macaques to produce IL-17 upon ex vivo stimulation, while production of IFNï§ was not affected. This cytokine imbalance in SIV-infected animals was associated with reduced expression of genes required for intestinal epithelial maintenance and repair, increased fluid secretion during NTS infection, epithelial damage and translocation of a non-invasive S. Typhimurium mutant. Although no defects in neutrophil recruitment were noted, the ileum of SIV-infected animals contained lower levels of the enzyme myeloperoxidase, which may indicate defects in neutrophil killing capacity. S. Typhimurium was recovered in markedly increased numbers from the mesenteric lymph nodes of SIV-infected macaques, illustrating the increased potential for systemic dissemination during co-infection. Our data suggest that SIV-infection causes a multi-factorial defect in mucosal barrier function that promotes bacterial dissemination. Keywords: Disease state analysis Comparison of ileal gene expression profiles in SIV infected rhesus macaques in response to Salmonella challange.
2010-05-26 | E-GEOD-10567 | biostudies-arrayexpress
Project description:Microbial Dysbiosis in gut of Acutely and Chronically SIV Infected macaques
| PRJEB11999 | ENA
Project description:Spatial transcriptomics of the Rhesus Macaque Hippocampus during homeostasis and chronic SIV CL757 infection
| PRJNA1089649 | ENA
Project description:Rhesus macaque acute SIV infection and SIV LCV co-infection studies
| PRJNA169327 | ENA
Project description:Human immunodeficiency virus (HIV) is widely recognized for its striking impact on the immune system. Even though HIV is primarily known for the impairment of the peripheral CD4 T cells, its influence on the central nervous system (CNS) also cannot be neglected. The main immune constituents in the brain, microglia and macrophages, are the target for HIV in the brain, as well as for the simian immunodeficiency virus (SIV) in nonhuman primates. This infection can lead to neurological effects as well as the establishment of a virus reservoir. Given the gaps in our knowledge on how these cells respond in vivo to CNS infection, we performed single-cell RNA sequencing (scRNA-seq) on myeloid cells from the brains of 3 rhesus macaque with 12-day SIV infection as well as 3 uninfected controls. We identified six microglial clusters and two macrophage clusters by transcriptomic profiling. Intriguingly, there were two microglial clusters populated with the cells from infected animals. These two infection-specific clusters had significantly higher expression (p < 0.05) of MHC class I molecules, interferon-induced proteins, chemokines, and cytokines than did the other clusters. Although only a low proportion of SIV-infected cells were detected in microglia and macrophages (~0.14%), almost all the microglia and macrophages in infected animals were activated to certain extents. In addition, the clusters with higher expression of cytotoxic molecules increased their populations during the infection, suggesting their potential to cause HIV-associated neurological disorders.
2024-05-01 | GSE253835 | GEO