Human coronavirus OC43
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1183988 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31296519.fastq.gz | Fastqsanger.gz |
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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.
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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.
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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.
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Project description:The human coronavirus OC43 is responsible for 15-30% of seasonal “common cold” infections with typically mild respiratory symptoms. We demonstrated that the coronavirus OC43 derived small peptide encoded by the viral p65 proteins may exhibit molecular mimicry with the pro-algesic fragment of Myelin Basic Protein (MBP). After intrasciatic injection, the p65-derived peptide induced robust pain hypersensitivity in rats lasting for up to 21 days. Transcriptomic analysis at day 21 revealed extensive spinal up-regulation of pro-nociceptive genes. Strikingly, genome-wide isoform switching due to activation of transcriptional start sites and alternative splicing events has occurred. We hypothesized that the coronavirus-derived peptides can dysregulate MBP function in the PNS/CNS and promote neuropathic chronic pain. Our findings offer paradigm-shifting mechanistic understanding of the viral origin of idiopathic neurological effects including chronic neuropathic pain, a condition currently refractory to therapeutic treatment. This new knowledge will lead to new diagnostic, prognostic, and therapeutic approaches to benefit patients with chronic pain.
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Project description:Human coronavirus OC43 genome sequencing and assembly in clinical context with amplicon-seq data
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