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Heterogeneous ribonucleoprotein interactions and impeded translational elongation in the respiratory tissue of SARS-CoV-2 pathology

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE222252 | GEO | 2023/12/01

REPOSITORIES: GEO

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Heterogeneous ribonucleoprotein interactions and impeded translational elongation in the respiratory tissue of SARS-CoV-2 pathology (RNA-Seq)

Project description:Translational regulation in in vivo tissue environments during viral pathogenesis has hardly been scrutinized due to the lack of tissue translatomes upon viral infection despite a number of the translatome studies on virus-infected cells cultured in vitro. We constructed the first temporal profile of lung translatomes during SARS-CoV-2 pathogenesis by applying ribosome profiling (Ribo-seq) to a severe COVID-19 mouse model. Unexpectedly, we observed gradual accumulations of non-canonical Ribo-seq reads representing hitherto-unidentified ribonucleoproteins (RNPs) that are likely involved in impeded translational elongation in the infected tissues. Contemporarily developing ribosome heterogeneity with prominently deviated 5S rRNP association supported the malfunction of elongating ribosomes. The analyses of canonical Riboseq reads (ribosome footprints) highlighted two obstructive characteristics to host gene expression: attenuated translation for transcriptionally up-regulated genes including immune response genes and ribosome stalling on codons within transmembrane domain-coding regions. Our study elucidates hidden molecular features of gene regulation in vivo underlying SARS-CoV-2 pathogenesis.

2023-12-01 | GSE222251 | GEO

Heterogeneous ribonucleoprotein interactions and impeded translational elongation in the respiratory tissue of SARS-CoV-2 pathology (Ribo-Seq)

2023-12-01 | GSE222249 | GEO

Heterogeneous ribonucleoprotein interactions and impeded translational elongation in the respiratory tissue of SARS-CoV-2 pathology

Project description:Heterogeneous ribonucleoprotein interactions and impeded translational elongation in the respiratory tissue of SARS-CoV-2 pathology

| PRJNA918676 | ENA

Heterogeneous ribonucleoprotein interactions and impeded translational elongation in the respiratory tissue of SARS-CoV-2 pathology (Ribo-Seq)

Project description:Heterogeneous ribonucleoprotein interactions and impeded translational elongation in the respiratory tissue of SARS-CoV-2 pathology (Ribo-Seq)

| PRJNA918681 | ENA

Heterogeneous ribonucleoprotein interactions and impeded translational elongation in the respiratory tissue of SARS-CoV-2 pathology (RNA-Seq)

Project description:Heterogeneous ribonucleoprotein interactions and impeded translational elongation in the respiratory tissue of SARS-CoV-2 pathology (RNA-Seq)

| PRJNA918680 | ENA

COVID-19 tissue atlases reveal SARS-COV-2 pathology and cellular targets

Project description:COVID-19, caused by SARS-CoV-2, can result in acute respiratory distress syndrome and multiple-organ failure, but little is known about its pathophysiology. Here, we generated single-cell atlases of 23 lung, 16 kidney, 15 liver and 18 heart COVID-19 autopsy donor tissue samples, and spatial atlases of 14 lung donors. Integrated computational analysis uncovered substantial remodeling in the lung epithelial, immune and stromal compartments, with evidence of multiple paths of failed tissue regeneration, including defective alveolar type 2 differentiation and expansion of myofibroblasts and putative TP63+ intrapulmonary basal-like progenitor cells. Viral RNAs were enriched in mononuclear phagocytic and endothelial lung cells which induced specific host programs. Spatial analysis in lung distinguished inflammatory host responses in lung regions with and without viral RNA. Analysis of the other tissue atlases showed transcriptional alterations in multiple cell types in COVID-19 donor heart tissue, and mapped cell types and genes implicated with disease severity based on COVID-19 GWAS. Our foundational dataset elucidates the biological impact of severe SARS-CoV-2 infection across the body a key step towards new treatments.

2021-04-09 | GSE171668 | GEO

Viral anti-inflammatory serpin reduces immuno-coagulopathic pathology in SARS-CoV-2 infection

Project description:Abstract: SARS-CoV-2 acute respiratory distress syndrome (ARDS) induces uncontrolled lung inflammation and coagulopathy with high mortality. Anti-viral drugs and monoclonal antibodies reduce early COVID-19 severity, but treatments for late-stage immuno-thrombotic syndromes and long COVID are limited. Serine protease inhibitors (SERPINS) regulate activated proteases. The myxoma virus-derived Serp-1 protein is a secreted immunomodulatory serpin that targets activated thrombotic, thrombolytic and complement proteases as a self-defense strategy to combat clearance. Serp-1 is effective in multiple animal models of inflammatory lung disease and vasculitis. Here, we describe systemic treatment with purified PEGylated Serp-1 as a therapy for immune-coagulopathic complications during ARDS. Treatment with PEGSerp-1 in two mouse-adapted SARS-CoV-2 models in C57Bl/6 and BALB/c mice reduced lung and heart inflammation, with improved outcomes. PEGSerp-1 significantly reduced M1 macrophages in the lung and heart by modifying urokinase-type plasminogen activator receptor (uPAR), thrombotic proteases and complement membrane attack complex (MAC). Sequential changes in gene expression for uPAR and serpins (complement and plasminogen inhibitors) were observed. PEGSerp-1 is a highly effective immune-modulator with therapeutic potential for severe viral ARDS, immune-coagulopathic responses and Long COVID.

| S-SCDT-10_15252-EMMM_202317376 | biostudies-other

SARS-CoV-2 and immune-microbiome interactions: Lessons from respiratory viral infections.

Project description:By the beginning of 2020, infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) had rapidly evolved into an emergent worldwide pandemic, an outbreak whose unprecedented consequences highlighted many existing flaws within public healthcare systems across the world. While coronavirus disease 2019 (COVID-19) is bestowed with a broad spectrum of clinical manifestations, involving the vital organs, the respiratory system transpires as the main route of entry for SARS-CoV-2, with the lungs being its primary target. Of those infected, up to 20% require hospitalization on account of severity, while the majority of patients are either asymptomatic or exhibit mild symptoms. Exacerbation in the disease severity and complications of COVID-19 infection have been associated with multiple comorbidities, including hypertension, diabetes mellitus, cardiovascular disorders, cancer, and chronic lung disease. Interestingly, a recent body of evidence indicated the pulmonary and gut microbiomes as potential modulators for altering the course of COVID-19, potentially via the microbiome-immune system axis. While the relative concordance between microbes and immunity has yet to be fully elucidated with regards to COVID-19, we present an overview of our current understanding of COVID-19-microbiome-immune cross talk and discuss the potential contributions of microbiome-related immunity to SARS-CoV-2 pathogenesis and COVID-19 disease progression.

| S-EPMC7891052 | biostudies-literature

Structures from "Engineering Neutralizing SARS-CoV Antibodies to Bind SARS-CoV-2"

Project description: Not available

| S-BSST379 | biostudies-other

Liver Pathology and SARS-CoV-2 Detection in Formalin-Fixed Tissue of Patients With COVID-19.

Project description:ObjectivesThe novel coronavirus, severe acute respiratory syndrome coronavirus 2, causing coronavirus disease 2019 (COVID-19) remains a global health threat and a significant source of human morbidity and mortality. While the virus primarily induces lung injury, it also has been reported to cause hepatic sequelae.MethodsWe aimed to detect the virus in formalin-fixed tissue blocks and document the liver injury patterns in patients with COVID-19 compared with a control group.ResultsWe were able to detect viral RNA in the bronchioalveolar cell blocks (12/12, 100%) and formalin-fixed, paraffin-embedded tissue of the lung (8/8, 100%) and liver (4/9, 44%) of patients with COVID-19. Although the peak values of the main liver enzymes and bilirubin were higher in the patients with COVID-19 compared with the control group, the differences were not significant. The main histologic findings were minimal to focal mild portal tract chronic inflammation (7/8, 88%, P < .05) and mild focal lobular activity (6/8, 75%, P = .06).ConclusionsWe found that most patients who died of COVID-19 had evidence of mild focal hepatitis clinically and histologically; however, the virus was detected in less than half of the cases.

| S-EPMC8135761 | biostudies-literature

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