The effect of inhibition of PP1 and TNFα signaling on pathogenesis of SARS coronavirus.
Identifieur interne : 000F26 ( Main/Curation ); précédent : 000F25; suivant : 000F27The effect of inhibition of PP1 and TNFα signaling on pathogenesis of SARS coronavirus.
Auteurs : Jason E. Mcdermott [États-Unis] ; Hugh D. Mitchell [États-Unis] ; Lisa E. Gralinski [États-Unis] ; Amie J. Eisfeld [États-Unis] ; Laurence Josset [États-Unis] ; Armand Bankhead [États-Unis] ; Gabriele Neumann [États-Unis] ; Susan C. Tilton [États-Unis] ; Alexandra Sch Fer [États-Unis] ; Chengjun Li [États-Unis] ; Shufang Fan [États-Unis] ; Shannon Mcweeney [États-Unis] ; Ralph S. Baric [États-Unis] ; Michael G. Katze [États-Unis] ; Katrina M. Waters [États-Unis]Source :
- BMC systems biology [ 1752-0509 ] ; 2016.
Abstract
The complex interplay between viral replication and host immune response during infection remains poorly understood. While many viruses are known to employ anti-immune strategies to facilitate their replication, highly pathogenic virus infections can also cause an excessive immune response that exacerbates, rather than reduces pathogenicity. To investigate this dichotomy in severe acute respiratory syndrome coronavirus (SARS-CoV), we developed a transcriptional network model of SARS-CoV infection in mice and used the model to prioritize candidate regulatory targets for further investigation.
DOI: 10.1186/s12918-016-0336-6
PubMed: 27663205
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<author><name sortKey="Li, Chengjun" sort="Li, Chengjun" uniqKey="Li C" first="Chengjun" last="Li">Chengjun Li</name>
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<author><name sortKey="Li, Chengjun" sort="Li, Chengjun" uniqKey="Li C" first="Chengjun" last="Li">Chengjun Li</name>
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<author><name sortKey="Fan, Shufang" sort="Fan, Shufang" uniqKey="Fan S" first="Shufang" last="Fan">Shufang Fan</name>
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<front><div type="abstract" xml:lang="en">The complex interplay between viral replication and host immune response during infection remains poorly understood. While many viruses are known to employ anti-immune strategies to facilitate their replication, highly pathogenic virus infections can also cause an excessive immune response that exacerbates, rather than reduces pathogenicity. To investigate this dichotomy in severe acute respiratory syndrome coronavirus (SARS-CoV), we developed a transcriptional network model of SARS-CoV infection in mice and used the model to prioritize candidate regulatory targets for further investigation.</div>
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