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Primary Human Airway Epithelial Cultures infected with SARS-CoV-2
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Transcriptome analysis of Severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)-infected and Influenza A/H1N1-infected nasal turbinate and lung tissues
Transcriptional response to SARS-CoV-2 infection
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SARS-CoV-2 infection in the lungs of human ACE2 transgenic mice causes severe inflammation and immune cell infiltration, and compromised respiratory function
CCR2-dependent monocyte-derived cells restrict SARS-CoV-2 infection
Characterization of the SARS-CoV-2 Host Response in Primary Human Airway Epithelial Cells from Aged Individuals
In vivo antiviral host response to SARS-CoV-2 by viral load, sex, and age
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In vivo antiviral host response to SARS-CoV-2 by viral load, sex, and age [dataset III]
In vivo antiviral host response to SARS-CoV-2 by viral load, sex, and age [dataset II]
In vivo antiviral host response to SARS-CoV-2 by viral load, sex, and age [dataset I]
Differential interferon-α immune signatures prevent SARS-CoV-2 infection
SARS-CoV-2 infection is effectively treated and prevented by EIDD-2801
Single-cell RNA-seq of air-liquid interface bronchioalveolar cells
Bulk RNA sequencing of SARS-CoV-2 infected alveolar type I- and type II like cells
Expression of SARS-CoV-2 receptor ACE2 and coincident host response signature varies by asthma inflammatory phenotype
Gene expression of wild-type C57BL/6 mouse lungs infected with C2-202 human metapneumovirus (HMPV)
Pharmacological Activation of STING blocks SARS-CoV-2 infection
Upper airway gene expression differentiates COVID-19 from other acute respiratory illnesses and reveals suppression of innate immune responses by SARS-CoV-2
Ebolavirus species associated with differential pathogenicity induce distinct host responses in human macrophages
Early differentially expressed immunological genes in mild and severe COVID-19
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