The mechanisms by which pulmonary lesions and fibrosis are generated during SARS-CoV infection are not known. Using high-throughput mRNA profiling, we examined the transcriptional response of wild-type (WT), type I interferon receptor knockout (IFNAR1−/−), and STAT1 knockout (STAT1−/−) mice infected with a recombinant mouse-adapted SARS-CoV (rMA15) to better understand the contribution of specific gene expression changes to disease progression.
Overall design
Ten week old 129S6/SvEv wild-type, STAT1−/− (Taconic Farms, Germantown, NY), and IFNAR1−/− mice bred on a 129SvEv background were anesthetized with a ketamine and infected intranasally with either phosphate-buffered saline (PBS) alone (Invitrogen, Carlsbad, CA) or 1 × 10^5 PFU rMA15-PBS. Mice were euthanized and left lungs were harvested from individual mice (a total of 3 infected mice from each strain) at days 2, 5, and 9 postinfection (dpi) for microarray analyses. Lung samples were taken from mock-infected animals from each of the strains at 5 dpi.
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