Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparative plasma proteomics of COVID-19 and Dengue patients with relevance to cardiovascular-associated pathways

ABSTRACT: The COVID-19 pandemic has highlighted the association between SARS-CoV-2 infection and a range of systemic complications, including cardiovascular abnormalities. Increasing clinical evidence indicates that COVID-19 patients are at an elevated risk of myocardial injury, arrhythmias, myocarditis, and thromboembolic events. To better characterize molecular alterations associated with infection-related cardiovascular risk, we performed a comparative proteomic analysis of human plasma samples obtained from healthy controls, COVID-19 patients, and Dengue patients. High-resolution liquid chromatography–tandem mass spectrometry (LC–MS/MS) was used to identify and quantify circulating proteins, followed by bioinformatic analyses to evaluate functional enrichment and pathway associations. The dataset reveals infection-associated alterations in proteins linked to inflammatory signaling, coagulation cascades, immune activation, and vascular homeostasis. Comparative analyses highlight both shared and infection-specific proteomic signatures between COVID-19 and Dengue plasma samples. This proteomic dataset provides a resource for exploring circulating molecular changes associated with viral infections and their potential links to cardiovascular complications, and is intended to support further mechanistic and translational investigations.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Plasma

DISEASE(S): Covid-19,Dengue Disease,Disease Free

SUBMITTER: Trina Roy

LAB HEAD: Dr. Subhajit Biswas

PROVIDER: PXD072757 | Pride | 2026-05-20

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	107ZD-03.msf	Msf
	107ZD-03.xlsx	Xlsx
	107ZD.mgf	Mgf
	107ZD.mzML	Mzml
	107ZD.mzid	Mzid

Items per page:

1 - 5 of 85

Similar Datasets

Human cardiac pericytes are susceptible to SARS-CoV-2 infection

Project description:Coronavirus disease 2019 (COVID-19) is associated with serious cardiovascular complications, including myocarditis, thrombosis, and dysregulated hemodynamic responses. The mechanism(s) underlying these disease manifestations are incompletely understood. Given a critical role for pericytes in supporting endothelial cell health and maintaining vascular integrity, we hypothesized that infection of pericytes could explain some of the cardiovascular complications of COVID-19. Here, we present evidence of SARS-CoV-2 infection in cardiac pericytes in patients with COVID-19 myocarditis. We show that cardiac pericytes are permissive to SARS-CoV-2 infection in organotypic slice and primary cell cultures. SARS-CoV-2 enters cardiac pericytes through an ACE2 and endosomal-dependent mechanism. Consequences of cardiac pericyte infection include upregulation of inflammatory chemokine and cytokine expression, type I interferon signaling, mediators of endothelial constriction, and cell death. Collectively, these data demonstrate that human cardiac pericytes are susceptible to SARS-CoV-2 infection and suggest a possible role for pericyte infection in the pathogenesis of COVID-19.

2022-08-31 | GSE183850 | GEO

RNA-Seq of Human iPSC-cardiomyocytes infected with SARS-CoV-2

Project description:Coronavirus disease 2019 (COVID-19) is a viral pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is predominantly defined by respiratory symptoms, but cardiac complications including arrhythmias, heart failure, and viral myocarditis are also prevalent. Although the systemic ischemic and inflammatory responses caused by COVID-19 can detrimentally affect cardiac function, the direct impact of SARS-CoV-2 infection on human cardiomyocytes is not well understood.

2020-06-19 | GSE150392 | GEO

Extracellular vesicles alter trophoblast function in pregnancies complicated by COVID-19

Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and resulting coronavirus disease (COVID-19) causes placental dysfunction, which increases the risk of adverse pregnancy outcomes. While abnormal placental pathology resulting from COVID-19 is common, direct infection of the placenta is rare. This suggests that pathophysiology associated with maternal COVID-19, rather than direct placental infection, is responsible for placental dysfunction and alteration of the placental transcriptome. We hypothesized that maternal circulating extracellular vesicles (EVs), altered by COVID-19 during pregnancy, contribute to placental dysfunction. To examine this hypothesis, we characterized maternal circulating EVs from pregnancies complicated by COVID-19 and tested their effects on trophoblast cell physiology in vitro. We found that the gestational timing of COVID-19 is a major determinant of circulating EV function and cargo. In vitro trophoblast exposure to EVs isolated from patients with an active infection at the time of delivery, but not EVs isolated from Controls, altered key trophoblast functions including hormone production and invasion. Thus, circulating EVs from participants with an active infection, both symptomatic and asymptomatic cases, can disrupt vital trophoblast functions. EV cargo differed between participants with COVID-19 and Controls, which may contribute to the disruption of the placental transcriptome and morphology. Our findings show that COVID-19 can have effects throughout pregnancy on circulating EVs and circulating EVs are likely to participate in placental dysfunction induced by COVID-19.

2025-04-17 | GSE268230 | GEO

SARS-CoV-2 Nsp6 damages Drosophila heart and mouse cardiomyocytes through MGA/MAX complex-mediated increased glycolysis

Project description:SARS-CoV-2 infection causes COVID-19, a severe acute respiratory disease associated with cardiovascular complications including long-term outcomes. The presence of virus in cardiac tissue of patients with COVID-19 suggests this is a direct, rather than secondary, effect of infection.Here, by expressing individual SARS-CoV-2 proteins in the Drosophila heart, we demonstrate interaction of virus Nsp6 with host proteins of the MGA/MAX complex (MGA, PCGF6 and TFDP1).

2022-10-04 | PXD036447 | Pride

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [scRNA-seq]

Project description:COVID-19 patients present higher risk for myocardial infarction (MI), acute coronary syndrome, and stroke for up to 1 year after SARS-CoV-2 infection. While the systemic inflammatory response to SARS-CoV-2 infection likely contributes to this increased cardiovascular risk, whether SARS35 CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques to locally promote inflammation remains unknown. Here, we report that SARS-CoV-2 viral RNA (vRNA) is detectable and the virus replicates in coronary atherosclerotic lesions taken at autopsy from patients with severe COVID-19.

2023-08-18 | GSE235436 | GEO

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [plaque]

2023-08-18 | GSE235435 | GEO

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary [MAC_FOAM-RNAseq]

2023-08-18 | GSE235433 | GEO

Severe COVID-19 is Characterized by an Impaired Type I Interferon Response and Elevated Levels of Arginase Producing Granulocytic Myeloid Derived Suppressor Cells

Project description:COVID-19 ranges from asymptomatic in 35% of cases to severe in 20% of patients. Differences in the type and degree of inflammation appear to determine the severity of the disease. Recent reports show an increase in circulating monocytic-myeloid-derived suppressor cells (M-MDSC) in severe COVID 19 that deplete arginine but are not associated with respiratory complications. Our data shows that differences in the type, function and transcriptome of granulocytic-MDSC (G-MDSC) may in part explain the severity COVID-19, in particular the association with pulmonary complications. Large infiltrates by Arginase 1+ G-MDSC (Arg+G-MDSC), expressing NOX-1 and NOX-2 (important for production of reactive oxygen species) were found in the lungs of patients who died from COVID-19 complications. Increased circulating Arg+G-MDSC depleted arginine, which impaired T cell receptor and endothelial cell function. Transcriptomic signatures of G-MDSC from patients with different stages of COVID-19, revealed that asymptomatic patients had increased expression of pathways and genes associated with type I interferon (IFN), while patients with severe COVID-19 had increased expression of genes associated with arginase production, and granulocyte degranulation and function. These results suggest that asymptomatic patients develop a protective type I IFN response, while patients with severe COVID-19 have an increased inflammatory response that depletes arginine, impairs T cell and endothelial cell function, and causes extensive pulmonary damage. Therefore, inhibition of arginase-1 and/or replenishment of arginine may be important in preventing/treating severe COVID-19.

2021-06-25 | GSE178824 | GEO

CXCL10 and IFN-γ Mediate Myocarditis Post-COVID19 mRNA Vaccination [mouse]

Project description:The mRNA vaccines against COVID-19 are highly effective yet associated with rare myocarditis cases, particularly in young males post-second dose. Here we explore the mediators of this adverse effect and its potential solutions, aiming to enhance the safety of future mRNA vaccines. Analysis of post-vaccination plasma highlighted a substantial increase in CXCL10 and IFN-γ levels in patients. Correspondingly, human iPSC-derived macrophages exposed to COVID-19 mRNA vaccines exhibited increased production of these two cytokines. iPSC-derived cardiomyocytes subjected to these cytokines exhibited impaired contractility, arrhythmogenicity, and myocarditis-like gene expression patterns. Genistein, an anti-inflammatory phytoestrogen, notably mitigated these effects, reducing cytokine-induced proteasomal degradation of cardiac proteins and preserving contractile function. In vivo, genistein significantly decreased cardiac injury markers and immune cell infiltration in a mouse model of cytokine-induced myocarditis. These findings underscore CXCL10 and IFN-γ as key mediators of myocarditis post-mRNA vaccination and propose genistein as a potential therapeutic to mitigate associated cardiovascular risks.

2025-10-20 | GSE254538 | GEO

Inhibition of CXCL10 and IFN-γ ameliorates myocarditis in preclinical models of SARS-CoV- 2 mRNA vaccination

2025-10-20 | GSE254537 | GEO