Homo sapiens
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PROVIDER: PRJNA912903 | ENA |
REPOSITORIES: ENA
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Project description:Immune dysfunction in COVID-19 Associated Mucormycosis
| PRJNA941219 | ENA
Project description:The coronavirus pandemic (COVID-19) is associated with secondary bacterial and fungal infections globally. In India, inappropriate use of glucocorticoids, high prevalence of diabetes mellitus and a conducive environment for fungal growth are considered as the main factors for increased incidence of COVID-19 associated mucormycosis (CAM). Few cases of CAM without steroid abuse and normal blood glucose levels were also reported during the pandemic. This study was designed to explore whether altered immune responses due to severe COVID-19 infection predisposes towards development of mucormycosis. The global transcriptome profiling of monocytes and granulocytic cells derived from CAM, Mucormycosis, COVID-19 and healthy control groups were performed to identify the differentially expressed genes (DEGs) involved in dysregulated host immune response towards respective diseased and healthy conditions.
2024-02-09 | GSE226677 | GEO
Project description:Rhizopus arrhizus is the predominant causative agent of mucormycosis worldwide. During COVID-19 pandemic, an upsurge of this disease was noted in many countries including India. Many clinical/epidemiological studies reported that the excessive intake of nutritional supplements, especially that of zinc, owing to self-medication and over-prescription, was one of the risk factors for the emergence of Covid-19 associated mucormycosis. However, the experimental evidence remains limited. This study evaluates the changes in gene expression of Rhizopus arrhizus upon culturing under zinc-enriched conditions.
2025-12-02 | GSE312189 | GEO
Project description:Comprehensive mapping of immune perturbations associated with severe COVID-19
| PRJNA630455 | ENA
Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections cause coronavirus disease 2019 (COVID-19) and are associated with inflammation and coagulopathy and high incidence of thrombosis. Myeloid cells (Mϕ) help coordinate the initial immune response in COVID-19. Although we appreciate that Mϕ lie at the nexus of inflammation and thrombosis, the mechanisms that unite the two in COVID-19 remain largely unknown. In this study, we employed systems biology approaches including proteomics, transcriptomics, and mass cytometry to define the circulating proteome and circulating immune cell phenotypes in subjects with COVID-19. In a cohort of COVID-19 subjects (n=35), circulating markers of inflammation (CCL23, IL-6) and vascular dysfunction (ACE2, tissue factor [TF]) were elevated in subjects with severe compared with mild COVID-19. Additionally, although the total white blood cell (WBC) counts were similar between COVID-19 groups, CD14+ monocytes from severe COVID-19 subjects expressed more TF. At baseline, transcriptomics demonstrated increased IL-6, CCL3, ACOD1, C5AR1, C5AR2, and TF in severe COVID-19 subjects compared with controls. Using “stress” transcriptomics, we found that circulating immune cells from severe COVID-19 subjects had evidence of profound immune paralysis with greatly reduced transcriptional activation and release of inflammatory markers in response to Toll-like receptor (TLR) activation. Finally, sera from severe (but not mild) COVID-19 subjects activated human monocytes and induced TF expression. Taken together, these observations further elucidate the pathological mechanisms that underlie immune dysfunction and coagulation abnormalities in COVID-19, contributing to our growing understanding of SARS-CoV-2 infections that could also be leveraged to develop novel diagnostic and therapeutic strategies.
2024-01-23 | GSE247186 | GEO
Project description:In this prospective observational cohort study, we found transcriptional evidence that persistent immune dysfunction was associated with 28-day mortality in both COVID-19 and non-COVID-19 septic patients. COVID-19 patients had an early antiviral response but became indistinguishable on a gene expression level from non-COVID-19 sepsis patients a week later. Early treatment of COVID-19 and non-COVID-19 sepsis ICU patients should focus on pathogen control, but both patient groups also require novel immunomodulatory treatments, particularly later during ICU hospitalization, independent of admission diagnosis. Some T1 samples were uploaded in GSE185263 and were not re-uploaded in this series.
2023-03-24 | GSE222393 | GEO
Project description:Our understanding of protective vs. pathologic immune responses to SARS-CoV-2, the virus that causes Coronavirus disease 2019 (COVID-19), is limited by inadequate profiling of patients at the extremes of the disease severity spectrum. Here, we performed multi-omic single-cell immune profiling of 64 COVID-19 patients across the full range of disease severity, from outpatients with mild disease to fatal cases. Our transcriptomic, epigenomic, and proteomic analyses reveal widespread dysfunction of peripheral innate immunity in severe and fatal COVID-19, with the most profound disturbances including prominent hyperactivation signatures in neutrophils and monocytes with anti-inflammatory features. We also leverage epigenomic analysis to identify loss of accessibility at NF-kB binding sites within pro-inflammatory cytokine gene loci as a potential mechanism for the striking lack of cytokine production observed in monocytes in severe and fatal COVID-19. We further demonstrate that emergency myelopoiesis is a prominent feature of fatal COVID-19. Collectively, our results reveal disease severity-associated immune phenotypes in COVID-19 and identify pathogenesis-associated pathways that are potential targets for therapeutic intervention.
2021-05-08 | GSE174072 | GEO
Project description:Introduction: SARS-CoV-2 infection during pregnancy has been associated with an increased number or frequency of adverse pregnancy outcomes including preeclampsia (PE). Placental abnormalities that resemble features observed in PE have previously been reported in pregnancies affected by COVID-19 disease. However, the molecular mechanisms linking SARS-CoV-2 infection to placental dysfunction and PE-like presentations remain poorly understood. Methods: We performed bulk RNA sequencing on placental tissues from four groups: uneventful prepandemic pregnancies (preCOVID-19, n=10), prepandemic pregnancies with preeclampsia (PE, n=10), COVID-19 pregnancies without PE (COVID no HDP, n=28), and COVID-19 pregnancies with PE or other hypertensive disorders of pregnancy (HDP) (termed as COVID HDP, n=10). A likelihood ratio (LRT) test was applied to identify genes differentially expressed (DEGs) across groups. Gene set enrichment analysis (GSEA) was conducted to identify enriched pathways in pathological groups compared to preCOVID-19. Expression profiles were aligned with previously defined PE subtypes using a reported PE gene panel. Results: The LRT test identified a set of 16 genes that were differentially expressed (adjusted p-value <0.05) across the four groups, showing stepwise upregulation—lowest in preCOVID-19 uneventful pregnancies, followed by COVID-19 without HDP, then preCOVID-19 PE, and highest in COVID-19 HDP placentas. This cluster included genes linked to placental dysfunction such as LAMA5, BTNL9. COVID HDP and PE groups clustered together, sharing upregulation of FLT1, ENG, and others, while MORN3 and TAP1 were unique to COVID HDP. COVID no HDP formed a distinct cluster, marked by upregulation of SNX10 and MTF1 and downregulation of all the other genes of the panel. Morphogenesis related ontologies were enriched in all pathological groups. However, immune related pathways, such as T cell activation and cytokine signaling, were most strongly overrepresented in the COVID HDP group, followed by moderate enrichment in PE, and were absent in COVID no HDP group. Discussion: Our findings reveal a molecular signature in placenta affected by maternal COVID-19 disease pregnancies that mirrors and amplifies features observed in PE. The progressive expression pattern suggests a continuum of placental stress, with SARS-CoV-2 infection potentially exacerbating underlying dysfunction. These results provide insight into the origin of COVID-19 associated placental dysfunction and its overlap with established PE subtypes.
2026-09-30 | GSE313868 | GEO
Project description:Severe COVID-19 is associated with innate immune dysregulation resembling sepsis-induced immunoparalysis. Epigenetic mechanisms, particularly changes in H3K4me3 enrichment at gene promoters, have been observed in immune tolerance and monocyte dysfunction in sepsis. Whether comparable H3K4me3 alterations occur during acute critical COVID-19 illness has not been investigated. Among 706 differentially bound consensus peaks with promoter association between ICU and non-ICU groups, 704 showed increased H3K4me3 occupancy in ICU patients, predominantly at neutrophil effector gene loci, supported by pathway enrichment of neutrophil degranulation and innate immune activation. Monocyte HLA-DR expression and ex vivo TLR-stimulated IL-6 secretion were persistently reduced throughout the first week of ICU treatment. Longitudinal profiling in the ICU group revealed a shift from an interferon-driven chromatin signature at admission toward sustained innate immune activation and ECM remodelling at day seven. This study provides the first genome-wide H3K4me3 characterization of circulating immune cells during acute critical COVID-19, demonstrating that epigenetic reprogramming is an active and dynamic process that mirrors the functional immune dysregulation observed in these patients.
2026-08-05 | GSE339365 | GEO