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Role of Top1 and Genome structure in SARS-CoV-2 infection [RNA-Seq hamster]

ABSTRACT: Role of Top1 and Genome structure in SARS-CoV-2 infection [RNA-Seq hamster]

PROVIDER: PRJNA682410 | ENA |

REPOSITORIES: ENA

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Role of Top1 and Genome structure in SARS-CoV-2 infection [RNA-Seq hamster]

Project description:The ongoing pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level of inflammatory cytokines and pro-inflammatory factors are associated with both increased disease severity and mortality. Targeting these pathways might therefore be a viable therapeutic strategy. Previously, we have reported that chromatin factors such as Topoisomerase I (Top1) play key roles in controlling the induction of inflammatory gene expression programs. Here, by using multidimensional epigenetic, transcriptional, in vitro and in vivo analyses, we show that Topoisomerase 1 (Top1) inhibition in infected cells and animals suppresses lethal inflammation induced by SARS-CoV-2.

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Role of Top1 and Genome structure in SARS-CoV-2 infection [RNA-Seq human]

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Role of Top1 and Genome structure in SARS-CoV-2 infection

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Project description:Despite being largely confined to the airways, SARS-CoV-2 infection has been associated with sensory abnormalities that manifest in both acute and long-lasting phenotypes. To gain insight on the molecular basis of these sensory abnormalities, we used the golden hamster infection model to characterize the effects of SARS-CoV-2 versus Influenza A virus (IAV) infection on the sensory nervous system. SARS-CoV-2-infected hamsters demonstrated mechanical hypersensitivity during acute infection; intriguingly, this hypersensitivity was milder, but prolonged when compared to IAV-infected hamsters. RNA sequencing (RNA-seq) of thoracic DRGs from acute infection revealed predominantly neuron-biased signaling perturbations in SARS-CoV-2-infected animals as opposed to type I interferon signaling in tissue derived from IAV-infected animals. RNA-seq of 31dpi thoracic DRGs from SARS-CoV-2-infected animals highlighted a uniquely neuropathic transcriptomic landscape, which was consistent with substantial SARS-CoV-2-specific mechanical hypersensitivity at 28dpi. Overall, this work elucidates novel transcriptomic signatures triggered by SARS-CoV-2 that may underlie both short- and long-term sensory abnormalities while also highlighting several therapeutic targets for alleviation of infection-induced hypersensitivity.

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Non-productive infection of glial cells with SARS-CoV-2 in hamster organotypic cerebellar slice cultures

Project description:The numerous neurological syndromes associated with COVID-19 implicate an effect of viral pathogenesis on neuronal function, yet reports of direct SARS-CoV-2 infection in the brain are conflicting. We used a well-established organotypic brain slice culture to determine the permissivity of hamster brain tissues to SARS-CoV-2 infection. We found levels of live virus waned after inoculation and observed no evidence of cell-to-cell spread, indicating that SARS-CoV-2 infection was non-productive. Nonetheless, we identified a small number of infected cells with glial phenotypes; yet no evidence of viral infection or replication was observed in neurons. Our data corroborates several clinical studies that have assessed patients with COVID-19 and their association with neurological involvement.

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Role of Top1 and 3D Genome structure in SARS-CoV-2 infection [Hi-C]

Project description:Role of Top1 and 3D Genome structure in SARS-CoV-2 infection [Hi-C]

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RNA-seq of Golden Hamster lung tissues according to sex, SARS-CoV-2 infection and treatment

Project description:Evaluating the effect of SARS-CoV-2 on the transcriptional landscape in lung tissues, assess differences relative to sex and to candidate treatment.

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