Alphavirus chikungunya
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1314437 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A number of inhibitors of chemokine CCL2 and its receptor CCR2 are in development and may find application for treating a range of inflammatory conditions, including autoimmune and viral arthritides. Herein we sought to determine the effect of CCR2 deficiency on arthritis caused by an arthritogenic alphavirus, Chikungunya virus. Chikungunya virus (LR2006-OPY1) was injected subcutaneously into the hind foot of either CCR2 knockout or wild-type control mice (n=4-6). At day 0 and d7 post infection, RNA from the feet was harvested, the RNA was pooled (4-6 feet per time point per mouse strain) and gene expression analysis was performed using Mouse Gene ST arrays (Affymetrix).
2014-04-23 | E-GEOD-56965 | biostudies-arrayexpress
Project description:A number of inhibitors of chemokine CCL2 and its receptor CCR2 are in development and may find application for treating a range of inflammatory conditions, including autoimmune and viral arthritides. Herein we sought to determine the effect of CCR2 deficiency on arthritis caused by an arthritogenic alphavirus, Chikungunya virus.
2014-04-23 | GSE56965 | GEO
Project description:Chikungunya virus strain:06113879 Raw sequence reads
| PRJNA450500 | ENA
Project description:Arthritogenic alphaviruses including chikungunya, Mayaro, and Ross River viruses cause long-lasting musculoskeletal pain and inflammation. However, mechanisms driving chronic disease remain poorly understood. Here, we investigated joint-associated tissues in alphavirus-infected mice at a late stage of infection. Utilizing scRNA-seq, spatial transcriptomics, and flow cytometry we identified an accumulation of inflammatory macrophages in joint-associated tissues with elevated Tnf, Nlrp3, Il1b, and H2-Aa expression, and these cells harbored CHIKV RNA. Moreover, we identified accumulation of CD4+ T cells in joint-associated tissues, which express Ifng. Depletion of CD4+ T cells diminished MHC-II expression on joint macrophages, highlighting their potential role in inflammation. In addition, treatment with a small molecule inhibitor of CHIKV replication during chronic disease reduced viral RNA and joint inflammation, suggesting that viral RNA replication promotes chronic joint disease. Our data suggest that macrophages harbor replicating viral RNA and contribute to the sustained joint inflammation associated with chronic alphavirus disease.
2026-02-05 | GSE300303 | GEO
Project description:Arthritogenic alphaviruses including chikungunya, Mayaro, and Ross River viruses cause long-lasting musculoskeletal pain and inflammation. However, mechanisms driving chronic disease remain poorly understood. Here, we investigated joint-associated tissues in alphavirus-infected mice at a late stage of infection. Utilizing scRNA-seq, spatial transcriptomics, and flow cytometry we identified an accumulation of inflammatory macrophages in joint-associated tissues with elevated Tnf, Nlrp3, Il1b, and H2-Aa expression, and these cells harbored CHIKV RNA. Moreover, we identified accumulation of CD4+ T cells in joint-associated tissues, which express Ifng. Depletion of CD4+ T cells diminished MHC-II expression on joint macrophages, highlighting their potential role in inflammation. In addition, treatment with a small molecule inhibitor of CHIKV replication during chronic disease reduced viral RNA and joint inflammation, suggesting that viral RNA replication promotes chronic joint disease. Our data suggest that macrophages harbor replicating viral RNA and contribute to the sustained joint inflammation associated with chronic alphavirus disease.
2026-02-05 | GSE300299 | GEO
Project description:Although oral antibiotics can predispose to joint inflammation, this phenomenon remains poorly understood. Here, we leverage mouse models of alphavirus arthritis to investigate the gut commensals, metabolites, and host mechanisms that promote musculoskeletal inflammation. Mice treated with a short course of oral antibiotics exhibited worsened arthritis after chikungunya virus (CHIKV) infection. This phenotype was associated with loss of short chain fatty acids (SCFA) and greater intestinal permeability, and required TLR4 signaling, MyD88 expression, monocytes, antigen-specific and bystander CD4+ T cells, and pro-inflammatory cytokines. Administration of exogenous SCFA or colonization of mice with bacterial species that generate SCFA mitigated CHIKV-induced joint inflammation. Single cell RNA sequencing revealed that gut-derived SCFA restrain the inflammatory phenotype of synovial CD4+ T cells and limit activation of monocytes and osteoclast-like cells. Thus, antibiotic-triggered gut dysbiosis exacerbates alphavirus arthritis by shaping the inflammatory profile of both infiltrating and resident immune cells in joint tissues.
2025-02-05 | GSE288863 | GEO
Project description:Morus alba L. Raw protein sequence reads and sequence
2024-02-08 | PXD049451 |
Project description:In this study, we aim to identify common host genes involved in pathogenesis of different Chikungunya virus strains as an attempt to recognize probable antiviral targets. We have compared the host gene regulation after infection of monkey kidney cell line (Vero) with two different wild type CHIKV strains i.e. S 27 (human, ECSA), and DRDE-06 (human, ECSA). Vero cells were mock infected or infected with two Chikungunya virus strains (S 27 and DRDE-06) and harvested at 8hpi and 18hpi. The total RNA was extracted and microarray was done using Agilent protocol.
2021-10-28 | E-MTAB-6645 | biostudies-arrayexpress