Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA110347 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional profiling of N-Tera2 differentiated human neuronal cells, comparing control uninfected cells to HCoV-OC43 infected cells at 24, 48 and 72 hour post-infection Keywords: Cell response to viral infection Two-condition experiment, N-Tera2 differentiated human neuronal cell mock infected vs. N-Tera2 differentiated human neuronal cell HCoV-OC43 infected at 24, 48 and 72 hours. Biological replicates: 2 at each time-course point. Technical replicate: 2 dye-swap at each time-point. 2 arrays hybridized with mock(cy3) vs infected(cy5) and 2 array with infected(cy3) vs mock(cy5).
2008-12-10 | E-GEOD-13879 | biostudies-arrayexpress
Project description:Transcriptional profiling of N-Tera2 differentiated human neuronal cells, comparing control uninfected cells to HCoV-OC43 infected cells at 24, 48 and 72 hour post-infection Keywords: Cell response to viral infection
2008-12-11 | GSE13879 | GEO
Project description:Seasonal coronaviruses, similar to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), only cause severe respiratory symptoms in a small fraction of infected individuals. However, the host factors that determine the variable responses to coronavirus infection remain unclear. Here, we use seasonal human coronavirus OC43 (HCoV-OC43) infection as an asymptomatic model that triggers both innate and adaptive immune responses in mice. Interestingly, innate sensing pathways as well as adaptive immune cells are not essential in protection against HCoV-OC43. Instead, alveolar macrophage (AMΦ) deficiency in mice results in COVID-19-like severe pneumonia post HCoV-OC43 infection, with abundant neutrophil infiltration, neutrophil extracellular trap (NET) release, and exaggerated pro-inflammatory cytokine production. Mechanistically, AMΦ efficiently phagocytose HCoV-OC43, effectively blocking virus spread, whereas, in their absence, HCoV-OC43 triggers Toll-like receptor (TLR)-dependent chemokine production to cause pneumonia. These findings reveal the central role of AMΦ in defending against seasonal HCoV-OC43 with clinical implications for human immunopathology associated with coronavirus infection.
2025-10-21 | GSE289734 | GEO
Project description:Seasonal coronaviruses, similar to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), only cause severe respiratory symptoms in a small fraction of infected individuals. However, the host factors that determine the variable responses to coronavirus infection remain unclear. Here, we use seasonal human coronavirus OC43 (HCoV-OC43) infection as an asymptomatic model that triggers both innate and adaptive immune responses in mice. Interestingly, innate sensing pathways as well as adaptive immune cells are not essential in protection against HCoV-OC43. Instead, alveolar macrophage (AMΦ) deficiency in mice results in COVID-19-like severe pneumonia post HCoV-OC43 infection, with abundant neutrophil infiltration, neutrophil extracellular trap (NET) release, and exaggerated pro-inflammatory cytokine production. Mechanistically, AMΦ efficiently phagocytose HCoV-OC43, effectively blocking virus spread, whereas, in their absence, HCoV-OC43 triggers Toll-like receptor (TLR)-dependent chemokine production to cause pneumonia. These findings reveal the central role of AMΦ in defending against seasonal HCoV-OC43 with clinical implications for human immunopathology associated with coronavirus infection.
2025-10-21 | GSE288214 | GEO
Project description:Seasonal coronaviruses, similar to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), only cause severe respiratory symptoms in a small fraction of infected individuals. However, the host factors that determine the variable responses to coronavirus infection remain unclear. Here, we use seasonal human coronavirus OC43 (HCoV-OC43) infection as an asymptomatic model that triggers both innate and adaptive immune responses in mice. Interestingly, innate sensing pathways as well as adaptive immune cells are not essential in protection against HCoV-OC43. Instead, alveolar macrophage (AMΦ) deficiency in mice results in COVID-19-like severe pneumonia post HCoV-OC43 infection, with abundant neutrophil infiltration, neutrophil extracellular trap (NET) release, and exaggerated pro-inflammatory cytokine production. Mechanistically, AMΦ efficiently phagocytose HCoV-OC43, effectively blocking virus spread, whereas, in their absence, HCoV-OC43 triggers Toll-like receptor (TLR)-dependent chemokine production to cause pneumonia. These findings reveal the central role of AMΦ in defending against seasonal HCoV-OC43 with clinical implications for human immunopathology associated with coronavirus infection.
2025-10-21 | GSE288215 | GEO
Project description:Coronaviruses express a repertoire of accessory proteins for evading host immune responses. A small internal (I) accessory gene overlaps with the nucleocapsid (N) gene in an alternative reading frame of viruses that belong to the genus Betacoronavirus. Previous studies reported that I proteins of SARS-CoV (9b), MERS-CoV (8b) and SARS-CoV-2 (9b) inhibit type I interferon (IFN-I) expression through distinct mechanisms and have different roles in pathogenesis. In contrast, the functions of the I proteins of human coronaviruses HCoV-HKU1 (7b) and HCoV-OC43 (8b) have not been previously reported. Although HCoV-HKU1 and HCoV-OC43 predominantly cause common cold in healthy adults (common cold CoVs, CCCoVs), susceptible individuals infected with these viruses can develop severe disease. The lack of robust reverse genetic systems, tissue culture and animal models limit the study of HCoV-HKU1 and HCoV-OC43 pathogenesis. Here, we examined how the heterologous expression of the HCoV-HKU1 and HCoV-OC43 I proteins impact pathogenesis in a mouse model of infection using a prototypic betacoronavirus. We inserted the I gene of HCoV-HKU1 (ORF 7b) and HCoV-OC43 (ORF 8b) independently into the genome of a neurotropic strain of mouse hepatitis virus (J2.2). J2.2 infection is well characterized with clearly defined immune responses which allows the study of these genes in the context of authentic coronavirus infection. We showed that ORF 7b of HCoV-HKU1, but not ORF 8b of HCoV-OC43, ameliorated MHV-J2.2 pathogenesis while ORF 8b of MERS-CoV exacerbated disease. The presence of HCoV-HKU1 ORF 7b decreased virus titers and cytokine expression while ORF 8b of MERS-CoV led to increased immune cell infiltration and virus titers in mice after J2.2 infection. Moreover, proteins expressed by ORF 7b of HCoV-HKU1 and ORF 8b of HCoV-OC43 showed different patterns of subcellular localization. Overall, our findings suggest that the I genes of different betacoronaviruses play unique roles in pathogenesis.
2025-04-23 | GSE291309 | GEO
Project description:To explore host factors and pathways modulated by coronavirus infections, we performed global quantitative proteomics profiling. Huh7 cells were infected with SARS-CoV-2 (MOI=1.0), HCoV-229E (MOI=0.1), or HCoV-OC43 (MOI=1.0) for 24 hours, compared with MOCK infection. Protein samples were digested and analyzed using mass spectrometry with a data-independent acquisition (DIA) approach to measure changes in global protein abundance. This study complements the phosphoproteomics dataset (PXD057224) from the same study
2026-04-01 | PXD057194 | Pride
Project description:Insertion of fluorescent reporter genes into viral genomes is a powerful tool for monitoring infection. In coronaviruses, this is commonly achieved by replacing accessory open reading frames, thereby deleting endogenous gene functions. An alternative strategy is to manipulate viral transcription by inserting copies of the viral transcription regulatory sequence (TRS) which drive viral subgenomic RNA transcription. However, coronavirus transcription is tightly regulated, and these modifications frequently disrupt native subgenomic RNA synthesis and attenuate viral growth. Here, we report a reporter coronavirus that overcomes these limitations. Using human coronavirus (HCoV)-OC43 as a model system, we inserted an mNeonGreen reporter between the Spike and ORF5 coding regions, engineering the TRS and surrounding sequence to minimise off-target effects to transcription. This virus is genetically stable, with wildtype growth kinetics and unaltered subgenomic RNA transcriptional ratios. We developed a flexible reverse genetics system, which allows rapid cloning and virus recover, supported by optimised HCoV-OC43 culture conditions, which support high titre stock growth, and validated analytical reagents. Our reporter virus enabled sensitive detection and isolation of infected cells, facilitating transcriptomic analyses that distinguish host responses in infected and bystander populations. Together, these tools expand the experimental utility of HCoV-OC43, an important seasonal respiratory pathogen and low containment model for betacoronavirus biology.
2026-05-19 | GSE324533 | GEO
Project description:To identify potential cellular RNA-binding proteins (RBPs) that interact with the FSE RNA of SARS-CoV-2, biotinylated in vitro transcription (IVT) FSE RNA from the SARS-CoV-2 genome was incubated with lysates of H460 cells infected with human coronavirus OC43 (HCoV-OC43) and Huh7 cells infected with human coronavirus 229E (HCoV-229E). To exclude non-specific binders, a non-related RNA was used as a control.
| PXD076663 |
Project description:Seasonal coronaviruses, including HCoV-229E, -NL63, -OC43, and -HKU1, are prevalent worldwide, predominantly causing mild, self-limiting upper respiratory (re-)infections in adults, often presenting as the common cold. However, in individuals with compromised immune systems, these viruses may lead to more severe illness and even fatalities. Recently, there has been a renewed interest in studying HCoVs due to their amenability to handling in reduced biosafety containment, offering valuable alternatives to SARS-CoV-2 for preclinical screening and the development of antiviral treatments. Despite their significance, research on HCoVs has been hindered by limited host-genomic data. To address this, we performed RNA-sequencing on 3D air-liquid interface human nasal airway epithelial cells (hNECs) infected with the alphacoronavirus HCoV-229E and the betacoronavirus HCoV-OC43. These hNECs were derived from pooled adult donors and exhibited pseudostratified mucociliated differentiation, faithfully replicating the complexities of normal airway biology. Our study aimed to identify specific immune signatures associated with HCoV infections in a physiologically relevant model. By elucidating the host responses induced by different seasonal coronaviruses, we can gain valuable insights into their pathogenesis and interactions with the respiratory epithelium. This knowledge may pave the way for the development of targeted therapeutics and prophylactics to combat HCoV infections effectively.
2025-07-01 | GSE238079 | GEO