https://www.socictopen.socict.org/files/original/8202dbbdb163012bcab784a0659d595d.pdf f3cb24ecb5e7eb0b9ac8d40da7c11b94 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Coronavirus Description An account of the resource Dominio científico: Coronavirus Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Allelic Variation in the Toll-Like Receptor Adaptor Protein Ticam2 Contributes to SARS-Coronavirus Pathogenesis in Mice Creator An entity primarily responsible for making the resource Lisa E Gralinski, Vineet D. Menachery, Andrew P. Morgan, Allison L. Totura, Anne Beall, Jacob Kocher, Jessica Plante, D. Corinne Harrison-Shostak, Alexandra Schäfer, Fernando Pardo-Manuel de Villena, Martin T. Ferris, Ralph S. Baric Description An account of the resource Host genetic variation is known to contribute to differential pathogenesis following infection. Mouse models allow direct assessment of host genetic factors responsible for susceptibility to Severe Acute Respiratory Syndrome coronavirus (SARS-CoV). Based on an assessment of early stage lines from the Collaborative Cross mouse multi-parent population, we identified two lines showing highly divergent susceptibilities to SARS-CoV: the resistant CC003/Unc and the susceptible CC053/Unc. We generated 264 F2 mice between these strains, and infected them with SARS-CoV. Weight loss, pulmonary hemorrhage, and viral load were all highly correlated disease phenotypes. We identified a quantitative trait locus of major effect on chromosome 18 (27.1–58.6 Mb) which affected weight loss, viral titer and hemorrhage. Additionally, each of these three phenotypes had distinct quantitative trait loci [Chr 9 (weight loss), Chrs 7 and 12 (virus titer), and Chr 15 (hemorrhage)]. We identified Ticam2, an adaptor protein in the TLR signaling pathways, as a candidate driving differential disease at the Chr 18 locus. Ticam2−/− mice were highly susceptible to SARS-CoV infection, exhibiting increased weight loss and more pulmonary hemorrhage than control mice. These results indicate a critical role for Ticam2 in SARS-CoV disease, and highlight the importance of host genetic variation in disease responses. Date A point or period of time associated with an event in the lifecycle of the resource 2017 Subject The topic of the resource SARS-CoV, Collaborative Cross, F2, Ticam2, host susceptibility genes, Multiparent Advanced Generation Inter-Cross (MAGIC), multiparental populations, MPP Identifier An unambiguous reference to the resource within a given context DOI: 10.1534/g3.117.041434 Source A related resource from which the described resource is derived G3: Genes, Genomes, Genetics Publisher An entity responsible for making the resource available Genetics Society of America Coverage The spatial or temporal topic of the resource, the spatial applicability of the resource, or the jurisdiction under which the resource is relevant Genetics Language A language of the resource EN