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 | 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 | 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 | 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: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
Project description:The purpose of this experiment was to evaluate how wild-type Human coronavirus strain 229E (HCoV-229E) infection alters chromatin accessiblity in infected but not mock-infected samples.
2025-12-23 | GSE280627 | GEO
Project description:Understanding how human coronavirus dysregulate host proteome during infection in human cells will identify general pathways that are common to coronavirus infection. NMS-873 is an allosteric p97/VCP ATPase inhibitor and was show to have antiviral effect in multiple viruses including SARS-CoV2. We first demonstrated that genetic knock down of p97 reduced HCoV-229E, HCoV-OC43 infection and secretion. To investigate how p97/VCP assists virus infection, we used unbiased quantitative proteomics to compare dysregulated proteomes caused by HCoV-229E, HCoV-OC43 and SARS-CoV2 infection. We then compared dysregulated proteomes after HCoV-229E and HCoV-OC43 infection with and without p97 knockdown. Moreover, we elucidated the impact of p97 on different stages of viral life cycle using two potent p97 inhibitors, CB-5083 and NMS-873 and demonstrate their can block HCoV replication. Together, our data provide insights to repurpose potential cancer drugs that target the essential host protein p97/VCP.
2021-11-03 | PXD026216 | Pride
Project description:The emergence of novel betacoronaviruses has posed significant financial and human health burdens, necessitating the development of appropriate tools to combat future outbreaks. In this study, we have characterized a human cell line, IGROV-1, as a robust tool to detect, propagate, and titrate betacoronavirus SARS-CoV-2 and HCoV-OC43. IGROV-1 cells can be used for serological assays, antiviral drug testing, and isolating SARS-CoV-2 variants from patient samples. Using time-course transcriptomics, we confirmed that IGROV-1 cells exhibit a robust innate immune response upon SARS-CoV-2 infection, recapitulating the response previously observed in primary human nasal epithelial cells. We performed genome-wide CRISPR knockout genetic screens in IGROV-1 cells and identified Aryl hydrocarbon receptor (AHR) as a critical host dependency factor for both SARS-CoV-2 and HCoV-OC43. Using DiMNF, a small molecule inhibitor of AHR, we observed that the drug selectively inhibits HCoV-OC43 infection but not SARS-CoV-2. Transcriptomic analysis in primary normal human bronchial epithelial cells revealed that DiMNF blocks HCoV-OC43 infection via basal activation of innate immune responses. Our findings highlight the potential of IGROV-1 cells as a valuable diagnostic and research tool to combat betacoronavirus diseases.
2023-09-19 | GSE237131 | GEO