Detection of DENV infected cells following natural dengue infection
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA613039 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11321526_1.fastq.gz | Fastqsanger.gz | |||
| SRR11321526_2.fastq.gz | Fastqsanger.gz | |||
| SRR11321527_1.fastq.gz | Fastqsanger.gz | |||
| SRR11321527_2.fastq.gz | Fastqsanger.gz | |||
| SRR11321528.fastq.gz | Fastqsanger.gz |
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Project description:Controlled dengue human challenge studies present a unique opportunity to address many longstanding questions in the field of flavivirus biology. These fundamental questions include defining the early immunological signatures of infection, the host/environmental factors that impact disease severity, and the role of preexisting immunity on the development of symptomatic viral infection. However, while several controlled dengue human challenge studies have been performed and appear to clinically recapitulate may features of mild natural DENV infection, limited data are available on how the immunological and transcriptional response elicited by these attenuated challenge viruses compares to the profile associated with a natural, unattenuated DENV infection. To bridge this knowledge gap, we performed scRNAseq analysis on longitudinally collected PBMC samples obtained from 3 individuals (8 time points per subject) enrolled in the SUNY/WRAIR DENV-1 controlled human challenge study. In addition, 3 time points (two acute infection time points, one control time point) from two individuals experiencing a natural DENV-1 infection were analyzed and computationally integrated with the challenge model dataset. This temporally integrated dataset contains a total of 171,208 cells and 22 statistically distinct populations corresponding to all major anticipated leukocyte subsets. While all identified cell populations demonstrated significant and consistant perturbations in their transcriptional profile in response to either natural or experimental DENV infection, conventional monocytes respond most robustly to infection across all subjects and study groups from an unbiased transcriptional perspective. Using these data, core sets of genes that were consistently induced by either natural or experimental DENV were identified, and the overlap between the two arms of the study assessed.
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Project description:Dengue virus (DENV) is the causative agent of dengue, a mosquito-borne disease that represents a significant and growing public health burden around the world. A unique pathophysiological feature of dengue is immune-mediated enhancement, wherein preexisting immunity elicited by a primary infection can enhance the severity of a subsequent infection by a heterologous DENV serotype. A leading mechanistic explanation for this phenomenon is antibody dependent enhancement (ADE), where sub-neutralizing concentrations of DENV-specific IgG antibodies facilitate entry of DENV into FcR expressing cells such as monocytes, macrophages, and dendritic cells. Accordingly, this model posits that phagocytic mononuclear cells are the primary reservoir of DENV. However, analysis of samples from individuals experiencing acute DENV infection reveals that B cells are the largest reservoir of infected circulating cells, representing a disconnect in our understanding of immune-mediated DENV tropism. In this study, we demonstrate that the expression of a DENV-specific B cell receptor (BCR) renders cells highly susceptible to DENV infection, with the infection-enhancing activity of the membrane-restricted BCR correlating with the ADE potential of the IgG version of the antibody. In addition, we observed that the frequency of DENV-infectable B cells increases in previously flavivirus-naïve volunteers after a primary DENV infection. These findings suggest that BCR-dependent infection of B cells is a novel mechanism immune-mediated enhancement of DENV-infection.
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Project description:Dengue virus can infect and cause systemic damage in many organs, resulting in organ failure. Here, we present a novel report showing a tailored stem cell-based therapy which can aid in viral clearance and rescue liver and blood vessels cells from further damage during dengue infection by administering combination of hematopoietic stem cells, endothelial progenitor cells and dental pulp stem cells in a dengue virus-infected BALB/c mouse model. To analyze the molecular level changes induced by DENV infection and stem cell treatment in dengue-infected mice, RNA sequencing (RNA-seq) using MiSeq next-generation sequencing was employed in this study. Transcriptomics analysis was performed comparing gene expression patterns in different experimental groups. Methods: Liver mRNA profiles of 21-day-old healthy, Dengue virus infected, and dengue infected plus stem cells treated BALB/C mice were generated by sequencing, in triplicate, using Illumina Miseq V3 150. The sequence reads that passed quality filters were assembled and analyzed using Tuxedo software. The results were analyzed using Cuffdiff to identify differentially expressed genes and transcripts. The relative expression of genes was determined based on FPKM (total fragments per kilobase of exon per million mapped reads) values Results: After analysis, it was found that 59 genes were significantly up-regulated in the DVI group, and in the DVI-SCT group, 47 of the genes were successfully corrected to the level similar to that of control group, while the remaining genes showed down-regulation Conclusion: In the recent years, the incidence of dengue has continued to increase, but there is currently no rapid and effective treatment available. This study demonstrates stem cell therapy as a promising management to reduce the global burden of dengue.
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