Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SARS-CoV-2 variants divergently infect and damage cardiomyocytes in vitro and in vivo

ABSTRACT: SARS-CoV-2 variants are known to exhibit different tropism and pathogenicity in respiratory cells, but their effect on cardiomyocytes (CMs) is unclear. Cardiac infection and damage induced by SARS-CoV-2 variants were examined using human induced pluripotent stem cell-derived (hiPSC-) CMs. Different variants exhibited distinct tropism, mechanism of viral entry and pathology in the heart. Omicron BA.2 efficiently infected CMs in vitro and in vivo, induced the most severe phenotype, and exhibited transcriptomic changes indicative of increased cardiac dysfunction, compared to other variants tested. Bioinformatics analysis identified transcription factors predicted to regulate the unique transcriptome induced by Omicron BA.2. Increased infectivity of Omicron BA.2 is attributed to its ability to infect independently of TMPRSS2, which is absent in CMs. Here we reveal previously unknown differences in how different SARS-CoV-2 variants infect and damage CMs. Omicron BA.2, which is generally considered mild, is capable of inducing severe CM damage in vitro and in vivo. Our study highlights the need for further investigations to define the pathogenesis of cardiac complications arising from different SARS-CoV-2 variants.

ORGANISM(S): Homo sapiens

PROVIDER: GSE250333 | GEO | 2026/07/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Differential pathogenic and molecular features in neurological infection of SARS-CoV-2 Omicron BA.5.2 and BA.2.75 and Delta

Project description:The Coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains a global threat, exacerbated by the emergence of viral variants. Two variants of SARS-CoV-2, Omicron BA.2.75 and BA.5, led to global infection peaks between May 2022 and May 2023, yet their precise characteristics in pathogenesis are not well understood. In this study, we compared these two Omicron sublineages with the previously dominant Delta variant using a human angiotensin-converting enzyme 2 knock-in mouse model. As expected, Delta exhibited higher viral replication in the lung and brain than both Omicron sublineages which induced less severe lung damage and immune activation. In contrast, the Omicron variants especially BA.5.2 showed a propensity for cellular proliferation and developmental pathways. Both Delta and BA.5.2 variants, but not BA.2.75, led to decreased pulmonary lymphocytes, indicating differential adaptive immune response. Neuroinvasiveness was shared with all strains, accompanied by vascular abnormalities, synaptic injury, and loss of astrocytes. However, Immunostaining assays and transcriptomic analysis showed that BA.5.2 displayed stronger immune suppression and neurodegeneration, while BA.2.75 exhibited more similar characteristics to Delta in the cortex. Such differentially infectious features could be partially attributed to the weakened interaction between Omicron Spike protein and host proteomes decoded via co-immunoprecipitation followed by mass spectrometry in neuronal cells. Our present study supports attenuated replication and pathogenicity of Omicron variants but also highlights their newly infectious characteristics in the lung and brain, especially with BA.5.2 demonstrating enhanced immune evasion and neural damage that could exacerbate neurological sequelae.

2025-04-17 | GSE234799 | GEO

Total Proteomics of SARS-CoV-2 variants

Project description:The ancestral SARS-CoV-2 strain that initiated the Covid-19 pandemic at the end of 2019 has rapidly mutated into multiple variants of concern with variable pathogenicity and increasing immune escape strategies. However, differences in host cellular antiviral responses upon infection with SARS-CoV-2 variants remains elusive. Leveraging whole cell proteomics, we determined host signalling pathways that are differentially modulated upon infection with the clinical isolates of the ancestral SARS-CoV-2 B.1 and the variants of concern Delta and Omicron BA.1. Our findings illustrate alterations in the global host proteome landscape upon infection with SARS-CoV-2 variants and the resulting host immune responses. Additionally, viral proteome kinetics reveal declining levels of viral protein expression during Omicron BA.1 infection when compared to ancestral B.1 and Delta variants, consistent with its reduced replication rates. Moreover, molecular assays reveal deferral activation of specific host antiviral signalling upon Omicron BA.1 and BA.2 infection. Our study provides an overview of host proteome profile of multiple SARS-CoV-2 variants and brings forth a better understanding of the instigation of key immune signalling pathways causative for the differential pathogenicity of SARS-CoV-2 variants.

2023-05-10 | PXD037265 | Pride

HTGTS-Rep-Seq for Humanized Antibodies that Broadly Neutralize Omicron Sub-variants

Project description:During V(D)J recombination antibody diversity is enhanced by non-templated junctional modifications that generate immensely diverse heavy chain (HC) and light chain (LC) complementarity-determining 3 antigen-contact regions (CDR3s). We previously developed a mouse model that generates diverse antibody repertoires by rearranging a single human VH1-2 and Vk1-33, associated with highly diverse CDR3s generated by V(D)J recombination with mouse Ds and/or Js. Immunization of this model with SARS-CoV-2 D614G spike elicited an antibody that potently neutralized SARS-CoV-2 variants through Omicron BA.2.754. Here, we report a next generation mouse model in which a single VH1-2 rearranges to human D3-3 and JH6, generating diverse HC-CDR3s much longer on average than those of our prior model. Omicron BA.4/.5 spike ferritin nanoparticle-immunization of the new model elicited four highly-related humanized antibodies that potently neutralize downstream Omicron sub-variants. All four antibodies had 12 AA HC-CDR3s with two aromatic amino acids that engage an epitope comprising a hydrophobic patch opened-up by early omicron lineage mutations and conserved in subsequent variants. Immunization of our prior, shorter CDR3-based model, elicited slightly less potent neutralizing antibodies that bound the same Omicron epitope, and were similar in all other aspects to those from the long, fully-human CDR3 model. One tested antibody from each set reduced lung viral titers in a mouse-adapted BQ1.1 challenge. The antibodies we describe are highly related to, but more potent than, recently described antibodies from omicron-infected humans. These studies validate the utility of single human VH- and Vk-rearranging mice for discovering humanized antibodies that neutralize emerging pathogens.

2026-02-23 | E-MTAB-16106 | biostudies-arrayexpress

Limited cross-variant immune response from SARS-CoV-2 Omicron BA.2 in naïve but not previously infected outpatients

Project description:Omicron is currently the dominant SARS-CoV-2 variant and several sublineages have emerged. Questions remain about the impact of previous SARS-CoV-2 exposure on cross-variant immune responses elicited by the SARS-CoV-2 Omicron sublineage BA.2 compared to BA.1. Here we show that without previous history of COVID-19, BA.2 infection induces a reduced immune response against all variants of concern (VOC) compared to BA.1 infection. The absence of ACE2 binding in sera of previously naïve BA.1 and BA.2 patients indicates a lack of meaningful neutralization. In contrast, anti-spike antibody levels and neutralizing activity greatly increased in the BA.1 and BA.2 patients with a previous history of COVID-19. Transcriptome analyses of peripheral immune cells showed significant differences in immune response and specific antibody generation between BA.1 and BA.2 patients as well as significant differences in the expression of specific immune genes. In summary, prior infection status significantly impacts the innate and adaptive immune response against VOC following BA.2 infection.

2022-12-20 | GSE205244 | GEO

Exploring host cellular responses to SARS-CoV-2 variants using RNA sequencing of infected human airway epithelial cells

Project description:This study explores the interaction between various SARS-CoV-2 variants and host cells by using RNA sequencing (RNA-seq) of human airway epithelial cells. The primary objective was to elucidate the host cellular responses, including metabolic and immune pathways, to different SARS-CoV-2 variants. Human airway epithelial cells were infected with SARS-CoV-2 variants (IC19, Alpha, Beta, Delta, Omicron BA.1, and BA.5) and compared with mock samples at time 0. Samples were collected at 24 and 72 hours post-infection for RNA isolation and subsequent bulk RNA-sequencing. The RNA-seq data processing involved quality checks, mapping reads to a reference genome, and identifying differentially expressed genes to determine changes in gene expression in response to viral infection. This analysis aims to provide a deeper understanding of the molecular interactions between SARS-CoV-2 variants and host cells, contributing to the broader knowledge of viral pathogenicity and host-pathogen interactions.

2025-07-01 | GSE271378 | GEO

Merkt2024 - SEIR based model of SARS-CoV-2 variant spread and cross-immunity in Ethiopia

Project description:Spanning August 2020 to July 2022, this model reconstructs SARS-CoV-2 infection and reinfection dynamics across multiple variants — mainly wildtype, Alpha, Delta, and Omicron BA.4/5. It describes how each variant spread through the population, incorporating cross-immunity between variants. The model is calibrated using seroprevalence data, PCR positivity rates, and variant sequencing, providing insights into how prior infections shaped susceptibility to future waves.

2025-04-12 | MODEL2504120001 | BioModels

Host Saliva RNA Responses to COVID-19 Infection

Project description:RNA-Seq was used to study changes in gene expression in saliva samples from 266 human subjects after SARS-COV-2 infection, vaccination, or combined infection and vaccination (breakthrough). Approximately equal numbers of males and females, matched for age, were profiled after subjects tested positive for COVID-19 by PCR and sequencing of the variant. In addition to samples from uninfected controls with and without vaccination, samples from infected subjects with and without vaccination that represent eight major SARS-COV-2 lineages are included: epsilon, iota, alpha, delta, omicron BA.1, omicron BA.2, omicron BA.4, and omicron BA.5. Stranded single-end sequencing was performed using standard Illumina protocols. Reads were quantified to hg38 human transcriptome using Salmon after adapter trimming. Quantified reads were filtered to remove features with fewer than one count in 80% of the samples, and normalized using TPM, followed by quantile and log2 transformation.

2023-09-19 | GSE212191 | GEO

Attenuated pathogenicity coupled with novel features of SARS-CoV-2 Omicron BA.2.75 and BA.5 variants

Project description:The Coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains a global threat, exacerbated by the emergence of viral variants. Two recent variants of SARS-CoV-2, Omicron BA.2.75 and BA.5, have been reported globally, yet their precise characteristics are not well understood. In this study, we compared these two Omicron sub-lineages with the previously dominant Delta variant using a hACE2 knock-in mouse model. As expected, Delta exhibited higher viral replication in the lung and brain than both Omicron sub-lineages that induced less severe lung damage and immune activation. In contrast, the Omicron variants especially BA.5 showed a propensity for cellular proliferation and developmental pathways. Both Delta and BA.5 variants, but not BA.2.75, led to decreased pulmonary lymphocytes, indicating differential adaptive immune response. Neuroinvasiveness was shared with all strains, accompanied by vascular abnormalities, synaptic injury, and loss of astrocytes. However, Immunostaining assays and transcriptomic analysis showed that BA.5 displayed stronger immune suppression and neurodegeneration, while BA.2.75 exhibited more similar characteristics to Delta in the cortex. Such differentially infectious features could be partially attributed to the weakened interaction between Omicron Spike protein and host proteomes decoded via co-immunoprecipitation followed by mass spectrometry in neuronal cells. Our present study supports attenuated replication and pathogenicity of Omicron variants but also highlights their newly infectious characteristics in the lung and brain, especially with BA.5 demonstrating enhanced immune evasion and neural damage that could exacerbate neurological sequelae.

2023-06-09 | PXD042841 |

Preparation of the working viruses of B.1.1, Delta and Omicron SARS-CoV-2

Project description:To investigate the virological properties of SARS-CoV-2 variants, we amplified the clinical isolates of an early pandemic D614G-bearing isolate (B.1.1 lineage, strain TKYE610670; GISAID ID: EPI_ISL_479681), a Delta isolate (B.1.617.2 lineage, strain TKYTK1734; GISAID ID: EPI_ISL_2378732) and an Omicron isolate (BA.1 lineage, strain TY38-873; GISAID ID: EPI_ISL_7418017) and prepared the working viruses.

2022-01-07 | GSE192472 | GEO

Mutation T9I in Envelope conveys autophagy resistance of SARS-CoV-2 Omicron

Project description:To date five variants of concern (VOC) of SARS-CoV-2 have emerged that show increased immune evasion. While their evolving escape from humoral immune responses has been analyzed in detail, adaptation of SARS-CoV-2 to human innate immune processes like autophagy are less understood. Here we demonstrate that currently predominant mutation T9I in the structural envelope (E) protein conveys increased resistance against autophagy of recent Omicron VOCs (BA.1, BA5 and XBB.5) compared to earlier SARS-CoV-2 variants. Rare omicron isolates that do not carry E T9I are sensitive towards autophagy. Mechanistic analyses revealed that E I9 inhibits autophagic turnover more efficiently than E T9 due to increased recruitment to autophagosomes and enhanced interaction with early autophagosome markers. Using pseudotyping assays we revealed that mutation T9I in E reduces release efficiency, but protects incoming virion from autophagy. In line, introduction of E T9I into recombinant 2020 SARS-CoV-2 increases its resistance against autophagy, but also attenuates replication. Our data thus reveal autophagy as a fundamental driver of SARS-CoV-2 evolution and improved autophagy escape may have contributed to the success of the Omicron variant.

2025-06-06 | PXD048080 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data