Host response to respiratory infections
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA732730 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Host response to respiratory infections
| PRJNA732732 | ENA
Project description:Long noncoding RNAs (lncRNAs) are a newer class of noncoding transcripts identified as key regulators of biological processes. Here we aimed to identify novel lncRNA targets that play critical roles in major human respiratory viral infections by systematically mining large-scale transcriptomic datasets. Using bulk RNA-sequencing (RNA-seq) analysis, we identified a previously uncharacterized lncRNA, named virus inducible lncRNA modulator of interferon response (VILMIR), that was consistently upregulated after in vitro influenza infection across multiple human epithelial cell lines and influenza A virus subtypes. VILMIR was also upregulated after SARS-CoV-2 and RSV infections in vitro. We experimentally confirmed the response of VILMIR to influenza infection and interferon-beta (IFN-β) treatment in the A549 human epithelial cell line and found the expression of VILMIR was robustly induced by IFN-β treatment in a dose and time-specific manner. Single cell RNA-seq analysis of bronchoalveolar lavage fluid (BALF) samples from COVID-19 patients uncovered that VILMIR was upregulated across various cell types including at least five immune cells. The upregulation of VILMIR in immune cells was further confirmed in the human T cell and monocyte cell lines, SUP-T1 and THP-1, after IFN-β treatment. Finally, we found that knockdown of VILMIR expression reduced the magnitude of host transcriptional responses to IFN-β treatment in A549 cells. Together, our results show that VILMIR is a novel interferon-stimulated gene (ISG) that regulates the host interferon response and may be a potential therapeutic target for human respiratory viral infections upon further mechanistic investigation.
2024-04-17 | GSE261920 | GEO
Project description:Viral respiratory infections are an important public health concern, due to their prevalence, transmissibility, and potential to cause serious disease. Disease severity is the product of several factors beyond the presence of the infectious agent, including specific host immune responses, host genetic makeup and bacterial co-infections. To understand these interactions within natural infections we designed a longitudinal cohort study actively surveilling 18 different respiratory viruses over the course of 19 months (2016-2018) in Manhattan, New York City. The cohort includes individuals related to daycare facilities, high school students and health care workers. We retrieved weekly epidemiological and clinical data and collected over 4,000 nasal swabs for molecular characterization from 214 participants. Transcriptomic data enabled the characterization of specific markers of immune response, the identification of signatures associated with symptom severity and bacterial co-infections. We created a computational resource to facilitate access to the data and visualization of analytical results.
2023-01-30 | GSE223679 | GEO
Project description:Purpose: The aim of this study is to determine the expression profile in whole blood samples of children infected with respiratory syncytial virus and other respiratory viruses. Method: Host mRNA profiles in whole blood samples of children were generated by next-generation sequencing using Illumina Hiseq. Sequence reads were trimmed for adapter using skewer, mapped to reference human genome using STAR, and quantified using RSEM. Differential expression analysis was performed using DESeq2. Results: Transcriptional module analysis revealed dysregulation of genes related to inflammatory response, neutrophils, monocytes, B-cell and T-cell response. Conclusion: This study showed an imbalance in innate and adaptive immune responses in children with respiratory virus infections. This study also showed that NGS provides a comprehensive assessment of transcripts in whole blood samples.
2021-01-29 | GSE155925 | GEO
Project description:The purpose of the study was to assess the patterns of global gene expression in peripheral blood cells and uncover the complex dynamics of host response to ARIs such as pandemic H1N1. To understand the molecular bases and network orchestration of host responses, we prospectively enrolled 1610 healthy adults in the fall of 2009 and 2010, followed the subjects with influenza-like illness (N=133) for 3 weeks, and examined changes in their peripheral blood gene expression. We discovered distinct phases of the host response spanning 6 days after infection, and identified genes that differentiate influenza from non-influenza virus infection. We examined pre- and post-infection anti-influenza antibody titers defining novel gene expression correlates. Healthy adults were invited to enroll to be followed for acute respiratory illness (ARI) through two consecutive influenza seasons 2009-2010 and 2010-2011. After subjects provided consent, baseline blood specimens were obtained during enrollment. Subjects were given thermometers and instructions to call and report for evaluation within 48 hours of ARI onset. Those persons who had a new ARI were seen within 48 hours of onset (day 0) and 2, 4, and 6 days later for repeat evaluation, blood specimen collections, and medical care (including the antiviral zanamivir if indicated) and 21 days later for collection of convalescent specimens. Nasal wash samples were collected for virus detection by RT-PCR on day 0 and day 2. Surveillance for influenza was terminated after 5.5 months; all subjects were asked to return for specimen collection and to provide a medical and ARI history in spring of next year. Serum specimens obtained at baseline, day 0 and day 21 visits for illnesses, and the terminal visit were tested simultaneously using hemagglutination-inhibition (HAI) antibody assay for Influenza H1N1, H3N2, and Influenza B strains. Peripheral blood RNA (PaxGene) obtained from blood specimens at each visit were analyzed using Illumina Human HT-12 v4. The study was repeated 2010-2011. A total of 880 arrays, corresponding to 133 individuals, passed quality control and are included in this data set.
2015-04-28 | E-GEOD-68310 | biostudies-arrayexpress
Project description:Human long noncoding RNA, VILMIR, is induced by major respiratory viral infections and modulates the host interferon response
| PRJNA1089571 | ENA
Project description:Immune response to Life-Threatening Respiratory Infections in Children and Young Adults
| PRJNA758454 | ENA
Project description:Immune response to Life-Threatening Respiratory Infections in Children and Young Adults
| PRJNA758455 | ENA
Project description:The purpose of the study was to assess the patterns of global gene expression in peripheral blood cells and uncover the complex dynamics of host response to ARIs such as pandemic H1N1. To understand the molecular bases and network orchestration of host responses, we prospectively enrolled 1610 healthy adults in the fall of 2009 and 2010, followed the subjects with influenza-like illness (N=133) for 3 weeks, and examined changes in their peripheral blood gene expression. We discovered distinct phases of the host response spanning 6 days after infection, and identified genes that differentiate influenza from non-influenza virus infection. We examined pre- and post-infection anti-influenza antibody titers defining novel gene expression correlates.
2015-04-28 | GSE68310 | GEO
Project description:MV130 is an inactivated polybacterial mucosal vaccine that confers protection to patients against recurrent respiratory infections, including those of viral etiology. However, its mechanism of action remains poorly understood. Herein, we observe that intranasal prophylaxis with MV130 modulates the lung immune landscape and provides long term heterologous protection against viral respiratory infections in mice. Intranasal administration of MV130 provided protection against systemic candidiasis in wild-type and Rag1-deficient mice lacking functional lymphocytes, indicative of innate immune-mediated protection. Moreover, pharmacological inhibition of trained immunity with metformin abrogated the protection conferred by MV130 against Influenza A virus respiratory infection. MV130 induced reprogramming of mouse bone marrow progenitor cells and human monocytes, promoting an enhanced cytokine production that relied on metabolic and epigenetic shifts. Our results unveil that the mucosal a dministration of a fully inactivated bacterial vaccine provides protection against viral infections by a mechanism associated with the induction of trained immunity. This SuperSeries is composed of the SubSeries listed below.
2021-11-10 | GSE183721 | GEO