Author: Frieman, Matthew B.; Chen, Jun; Morrison, Thomas E.; Whitmore, Alan; Funkhouser, William; Ward, Jerrold M.; Lamirande, Elaine W.; Roberts, Anjeanette; Heise, Mark; Subbarao, Kanta; Baric, Ralph S.
Title: SARS-CoV Pathogenesis Is Regulated by a STAT1 Dependent but a Type I, II and III Interferon Receptor Independent Mechanism Document date: 2010_4_8
ID: 15rtwl26_49
Snippet: We propose a new potential pathway by which STAT1 regulates end stage lung disease following viral infection. We hypothesize that the increased susceptibility of STAT12/2 mice results from different roles of STAT1 in the cell. First, loss of STAT1 results in a deficient IFN response that results in higher titers of virus in the lungs. Secondly, loss of STAT1 allows for unregulated cell proliferation in response to the innate immune response, caus.....
Document: We propose a new potential pathway by which STAT1 regulates end stage lung disease following viral infection. We hypothesize that the increased susceptibility of STAT12/2 mice results from different roles of STAT1 in the cell. First, loss of STAT1 results in a deficient IFN response that results in higher titers of virus in the lungs. Secondly, loss of STAT1 allows for unregulated cell proliferation in response to the innate immune response, causing enhanced damage to the lungs and death of the animals. Our findings also point to an increasing role of the cell damage response to viral infection that can be potential targets for therapy in highly pathogenic respiratory infections.
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