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Mouse lung tissue transcriptome response to a mouse-adapted strain of SARS-CoV in wild type C57BL6/NJ mice and TLR3-/- mice

ABSTRACT: The purpose is to determine the role of TLR3-/- on the regulation of the host immune response during lethal SARS-CoV infection

ORGANISM(S): Mus musculus

PROVIDER: GSE68820 | GEO | 2015/05/12

SECONDARY ACCESSION(S): PRJNA283822

REPOSITORIES: GEO

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Mouse lung tissue transcriptome response to a mouse-adapted strain of SARS-CoV in wild type C57BL6/NJ mice and TLR3-/- mice

Project description:The purpose is to determine the role of TLR3-/- on the regulation of the host immune response during lethal SARS-CoV infection Groups of 10 week old C57BL6/NJ or TLR3-/- mice were infected with MA15 virus at a dose of 10^5 PFU or time-matched mock infected. Time points were 2, 4 and 7 days post infection. There were 4 or 5 animals/time point. Lung samples were collected for virus load, lung pathology, and transcriptional analysis. Weight loss and animal survival were also monitored.

2015-05-12 | E-GEOD-68820 | biostudies-arrayexpress

Increased morbidity of obese mice infected with mouse-adapted SARS-CoV-2.

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Mouse Adapted SARS-CoV-2 protects animals from lethal SARS-CoV challenge.

Project description:The emergence of SARS-CoV-2 has resulted in a worldwide pandemic causing significant damage to public health and the economy. Efforts to understand the mechanisms of COVID-19 disease have been hampered by the lack of robust mouse models. To overcome this barrier, we utilized a reverse genetic system to generate a mouse-adapted strain of SARS-CoV-2. Incorporating key mutations found in SARSCoV-2 variants, this model recapitulates critical elements of human infection including viral replication in the lung, immune cell infiltration, and significant in vivo disease. Importantly, mouse-adaptation of SARS-CoV-2 does not impair replication in human airway cells and maintains antigenicity similar to human SARS-CoV-2 strains. Utilizing this model, we demonstrate that SARS-CoV-2 infected mice are protected from lethal challenge with the original SARS-CoV, suggesting immunity from heterologous CoV strains. Together, the results highlight the utility of this mouse model for further study of SARS-CoV-2 infection and disease.

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Mouse-adapted SARS-CoV-2 protects animals from lethal SARS-CoV challenge.

Project description:The emergence of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has resulted in a pandemic causing significant damage to public health and the economy. Efforts to understand the mechanisms of Coronavirus Disease 2019 (COVID-19) have been hampered by the lack of robust mouse models. To overcome this barrier, we used a reverse genetic system to generate a mouse-adapted strain of SARS-CoV-2. Incorporating key mutations found in SARS-CoV-2 variants, this model recapitulates critical elements of human infection including viral replication in the lung, immune cell infiltration, and significant in vivo disease. Importantly, mouse adaptation of SARS-CoV-2 does not impair replication in human airway cells and maintains antigenicity similar to human SARS-CoV-2 strains. Coupled with the incorporation of mutations found in variants of concern, CMA3p20 offers several advantages over other mouse-adapted SARS-CoV-2 strains. Using this model, we demonstrate that SARS-CoV-2-infected mice are protected from lethal challenge with the original Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV), suggesting immunity from heterologous Coronavirus (CoV) strains. Together, the results highlight the use of this mouse model for further study of SARS-CoV-2 infection and disease.

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Mouse Adapted SARS-CoV-2 (MA10) Viral Infection Induces Neuroinflammation in Standard Laboratory Mice.

Project description:Increasing evidence suggests that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection impacts neurological function both acutely and chronically, even in the absence of pronounced respiratory distress. Developing clinically relevant laboratory mouse models of the neuropathogenesis of SARS-CoV-2 infection is an important step toward elucidating the underlying mechanisms of SARS-CoV-2-induced neurological dysfunction. Although various transgenic models and viral delivery methods have been used to study the infection potential of SARS-CoV-2 in mice, the use of commonly available laboratory mice would facilitate the study of SARS-CoV-2 neuropathology. Herein we show neuroinflammatory profiles of immunologically intact mice, C57BL/6J and BALB/c, as well as immunodeficient (Rag2-/-) mice, to a mouse-adapted strain of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2 (MA10)). Our findings indicate that brain IL-6 levels are significantly higher in BALB/c male mice infected with SARS-CoV-2 MA10. Additionally, blood-brain barrier integrity, as measured by the vascular tight junction protein claudin-5, was reduced by SARS-CoV-2 MA10 infection in all three strains. Brain glial fibrillary acidic protein (GFAP) mRNA was also elevated in male C57BL/6J infected mice compared with the mock group. Lastly, immune-vascular effects of SARS-CoV-2 (MA10), as measured by H&E scores, demonstrate an increase in perivascular lymphocyte cuffing (PLC) at 30 days post-infection among infected female BALB/c mice with a significant increase in PLC over time only in SARS-CoV-2 MA10) infected mice. Our study is the first to demonstrate that SARS-CoV-2 (MA10) infection induces neuroinflammation in laboratory mice and could be used as a novel model to study SARS-CoV-2-mediated cerebrovascular pathology.

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microRNA expression profiling of small intestine of Tlr3+/+ and Tlr3-/- mice after total body g-irradiation

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2015-02-01 | E-GEOD-42916 | biostudies-arrayexpress

Mouse-adapted SARS-CoV-2 infected Lungs from wild type or genetically obese mice

Project description:Lung samples were generated from male mice of C57BL/6J(B6), C57BL/6JHamSlc-ob/ob (ob/ob) and C57BLKS/J-db/db on 3 days post infection of mouse-adapted SARS-CoV-2

2023-05-15 | E-MTAB-12617 | biostudies-arrayexpress

Mouse-adapted SARS-CoV-2 infected lungs from lean or obese ob/ob mice

Project description:Lean or obese C57BL/6JHamSlc-ob/ob (ob/ob) were developed continuous leptin (or vehicle) treatment for 6 weeks. Lung samples were generated from male mice of lean or obese ob/ob on 3 days post infection of mouse-adapted SARS-CoV-2.

2023-05-15 | E-MTAB-12623 | biostudies-arrayexpress

Lung samples from obese mice with or without mouse-adapted SARS-CoV-2 infection

Project description:Lung samples were generated from male mice of C57BL/6JHamSlc-ob/ob (ob/ob) and C57BLKS/J-db/db on 3 days post infection of mouse-adapted SARS-CoV-2 or non-infected condition

2023-05-15 | E-MTAB-12618 | biostudies-arrayexpress

Complete TLR3 deficiency

Project description:The objective of this study is to study the Toll-like receptor 3 (TLR3)-dependent gene expression in human fibroblast cells and peripheral blood mononuclear cells (PBMCs) Fibroblast cells and PBMCs from donors with autosomal recessive (AR) complete TLR3 deficiency and autosomal dominant (AD) partial TLR3 deficiency were collected for microarray analysis to measure the transcriptional responsiveness of TLR3 in fibroblast and PBMCs. A total of 3 healthy controls, 1 AD TLR3-deficient patient, 1 AR TLR3-deficient patient, 1 AR UNC-93B-deficient patient, 1 MyD88 deficient patien were used in this study. The fibroblast cells were cultured in DMEM medium supplemented with 10% fetal calf serum (FCS). The PBMCs were cultured in RPMI medium complemented with 10% FCS. Different kinetics (2 hours and 8 hours) of poly(I:C) (25ug/ml, purchased from Amersham) stimulations were performed, aiming to define TLR3-inducible genes in these human cells. A stimulation of IL-1β (20ng/ml, purchased from R&D system Inc.) was used as a positive activation control with same kinetics of stimulations. A total of one million cells per stimulation were used for fibroblasts, and around 1.5 million cells per stimulation for PBMCs.

2011-11-02 | E-GEOD-30951 | biostudies-arrayexpress

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