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Cell-intrinsic Innate Immune Responses against Chikungunya Virus in a Human Ex Vivo Synovial Fibroblast Model [scRNA-seq]

ABSTRACT: Single-cell RNAseq dataset on CHIKV-infected fibroblasts. Overall conclusions: Strong induction of innate immune responses, depending on the amount of viral RNA in the cells we found an antagonism against transcription factors such as STAT1 and JAK1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE176361 | GEO | 2021/06/09

REPOSITORIES: GEO

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Cell-intrinsic Innate Immune Responses against Chikungunya Virus in a Human Ex Vivo Synovial Fibroblast Model

Project description:Purpose: Human primary synovial fibroblasts extracted from the knee were established as an ex vivo infection model for Chikungunya Virus. The cell-intrinsic immune response was determined using RNA-seq of infected and uninfected fibroblasts from healthy donors and donors with an osteoarthritic background. Methods: Fibroblasts of four osteoarthritic and two healthy donors were infected with CHIKV strain LR2006-OPY at an MOI of 10 in the presence or absence of the CHIKV neutralizing antibody C9 and total RNA was extracted at 24 hours post infection. Deep sequencing with paired-end reads was performed using an Illumina platform and data was analyzed with CLC Genomics Workbench 12 (QIAGEN) by mapping the human reads onto the hg19 reference genome scaffold (GCA_000001405.28). Unmapped reads not matching the human genome were subsequently mapped onto the CHIKV genome LR2006_OPY (DQ443544.2). Results: For osteoartritic fibroblasts ~25-35 Mio reads per sample, for healthy donor fibroblasts ~50-60 Mio reads per sample were achieved. Analysis revealed no major differences in the resting or infection-induced transcriptome (R2 = 0.9085 and 0.9086, respectively), yet some non-inflammation related pathways were significantly different regulated as determined by Gene Ontology analysis. Conclusion: Osteoarthritic fibroblasts were found to be an accessible source of primary cells suitable for studying CHIKV infection and pathophysiology. The cells did not majorly differ from the rarely avaiblabe healthy donor fibroblasts on the transcriptomic level, and did not show signs of pre-activation or inflammation in the absence of infection.

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Project description:HEK293T grown in 6 well plates were infected with CHIKV and total RNA was isolated from cells at 0, 12 and 24 hrs post infection. CHIKV microRNA expression signature was generated. Cells grown on 6-well plates. Three biological replicates of uninfected and two biological replicates of infected samples

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Project description:Human monocyte-derived macrophage cells were infected with Chikungunya virus (CHIKV) to identify and quantify intracellular transcriptional changes that contribute to the host response to infection with CHIKV. RNA was collected from these cells at 8 and 24 hours post-infection (hpi) and were compared to mock-infected cells. The RNAseq data was then analyzed to determine the genes, functions, and signaling pathways that were significantly affected in an effort to predict existing drugs that could be repurposed as potential therapeutics for CHIKV.

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Cell-intrinsic Innate Immune Responses against Chikungunya Virus in a Human Ex Vivo Synovial Fibroblast Model

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Gene expression profile in HEK293T cells infected with Chikungunya virus

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Project description:Chikungunya virus (CHIKV) infection has been associated with severe cardiac manifestations. However, how CHIKV infection leads to heart disease remains unknown. Here, using C57BL/6 mice we show that cardiac fibroblasts are the main target of CHIKV infection in the heart, and that cardiac tissue infection induces activation of the type I interferon (IFN-I) pathway in both infected and non-infected cardiac cells. The loss of IFN-I signaling results in increased CHIKV infection, virus spreading, and apoptosis in cardiac tissue. Importantly, signaling through the mitochondrial antiviral-signaling protein (MAVS) is essential for efficient CHIKV clearance from the heart. Indeed, persistent infection in cardiac tissue of MAVS-deficient mice leads to cardiac damage characterized by focal myocarditis and major vessel vasculitis. This study provides mechanistic insight on how CHIKV can lead to cardiac damage, underscoring the importance of monitoring cardiac function in patients with CHIKV infections.

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Crosstalk between CD64+MHCII+ macrophages and CD4+ T cells mediates joint pathology during chikungunya

Project description:Communications between immune cells are essential to ensure appropriate coordination of their activities. Here, we observed the infiltration of activated macrophages into the joint-footpads of chikungunya virus (CHIKV)-infected animals. Large numbers of CD64+MHCII+ and CD64+MHCII- macrophages were present in the joint-footpad, preceded by the recruitment of their CD11b+Ly6C+ inflammatory monocyte precursors. Regulation of these myeloid subsets was highly dependent on IFNγ and GM-CSF secreted by CHIKV-specific CD4+ T cells. Transcriptomic and gene ontology analyses of CD64+MHCII+ and CD64+MHCII- macrophages revealed 89 differentially expressed genes, including genes involved in T cell proliferation and differentiation pathways. Depletion of CD64+MHCII+ macrophages from CHIKV-infected mice reduced disease pathology, demonstrating that these cells play a pro-inflammatory role in CHIKV infection. Together, these results highlight the synergistic dynamics of immune cell crosstalk in driving CHIKV immunopathogenesis. This study provides new insights in the disease mechanism and offers opportunities for development of novel anti-CHIKV therapeutics.

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