About: Modeling Host Genetic Regulation of Influenza Pathogenesis in the Collaborative Cross

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About: Modeling Host Genetic Regulation of Influenza Pathogenesis in the Collaborative Cross Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Modeling Host Genetic Regulation of Influenza Pathogenesis in the Collaborative Cross
Creator	Baric, Ralph Gralinski, Lisa Valdar, William Whitmore, Alan Heise, Mark Threadgill, David Wang, Jeremy Bottomly, Daniel Bradel-Tretheway, Birgit Rosenzweig, Elizabeth Aicher, Lauri Haagmans, Bart Ferris, Martin Aylor, David Bell, Timothy Bryan, Janine Buus, Ryan Churchill, Gary Katze, Michael Mcmillan, Leonard Mcweeney, Shannon Miller, Darla Pardo-Manuel De Villena, Fernando
Source	PMC
abstract	Genetic variation contributes to host responses and outcomes following infection by influenza A virus or other viral infections. Yet narrow windows of disease symptoms and confounding environmental factors have made it difficult to identify polymorphic genes that contribute to differential disease outcomes in human populations. Therefore, to control for these confounding environmental variables in a system that models the levels of genetic diversity found in outbred populations such as humans, we used incipient lines of the highly genetically diverse Collaborative Cross (CC) recombinant inbred (RI) panel (the pre-CC population) to study how genetic variation impacts influenza associated disease across a genetically diverse population. A wide range of variation in influenza disease related phenotypes including virus replication, virus-induced inflammation, and weight loss was observed. Many of the disease associated phenotypes were correlated, with viral replication and virus-induced inflammation being predictors of virus-induced weight loss. Despite these correlations, pre-CC mice with unique and novel disease phenotype combinations were observed. We also identified sets of transcripts (modules) that were correlated with aspects of disease. In order to identify how host genetic polymorphisms contribute to the observed variation in disease, we conducted quantitative trait loci (QTL) mapping. We identified several QTL contributing to specific aspects of the host response including virus-induced weight loss, titer, pulmonary edema, neutrophil recruitment to the airways, and transcriptional expression. Existing whole-genome sequence data was applied to identify high priority candidate genes within QTL regions. A key host response QTL was located at the site of the known anti-influenza Mx1 gene. We sequenced the coding regions of Mx1 in the eight CC founder strains, and identified a novel Mx1 allele that showed reduced ability to inhibit viral replication, while maintaining protection from weight loss.
has issue date	2013-02-28(xsd:dateTime)
bibo:doi	10.1371/journal.ppat.1003196
bibo:pmid	23468633
has license	cc-by
sha1sum (hex)	df4824b457c47934bafd828367bb0377132a903c
schema:url	https://doi.org/10.1371/journal.ppat.1003196
resource representing a document's title	Modeling Host Genetic Regulation of Influenza Pathogenesis in the Collaborative Cross
has PubMed Central identifier	PMC3585141
has PubMed identifier	23468633
schema:publication	PLoS Pathog
resource representing a document's body	covid:df4824b457c47934bafd828367bb0377132a903c#body_text
is schema:about of	named entity 'MODELING' named entity 'modules' named entity 'disease' named entity 'inbred' named entity 'located' named entity 'QTL' named entity 'reduced' named entity 'PHENOTYPES' named entity 'GENES' named entity 'INFLAMMATION' named entity 'GENETIC DIVERSITY' named entity 'DIVERSE POPULATION' named entity 'WEIGHT LOSS' named entity 'APPLIED' named entity 'FOUND' named entity 'PRE' named entity 'GENOME SEQUENCE' named entity 'CROSS' named entity 'POPULATION' named entity 'WIDE' named entity 'CORRELATIONS' named entity 'VIRUS REPLICATION' named entity 'MICE' named entity 'DIFFERENTIAL' named entity 'SPECIFIC' named entity 'RANGE' named entity 'DISEASE ASSOCIATED' named entity 'HUMANS' named entity 'QUANTITATIVE TRAIT LOCI' named entity 'HOST RESPONSE' named entity 'VARIATION' named entity 'TRANSCRIPTIONAL' named entity 'ASSOCIATED' named entity 'INFLUENZA' named entity 'TO IDENTIFY' named entity 'DISEASE PHENOTYPE' named entity 'INDUCED' named entity 'MX1' named entity 'THESE' named entity 'VIRAL REPLICATION' named entity 'LEVELS' named entity 'EXPRESSION' named entity 'CONTRIBUTE ' named entity 'HAVE' named entity 'COMBINATIONS' named entity 'DIVERSE' named entity 'TRANSCRIPTS' named entity 'HIGH PRIORITY' named entity 'GENETIC' named entity 'CONTRIBUTING' named entity 'WINDOWS' named entity 'POLYMORPHIC' named entity 'SYMPTOMS' named entity 'DISEASE RELATED' named entity 'CODING' named entity 'OUTCOMES' named entity 'GENETIC REGULATION' named entity 'INBRED' named entity 'REGIONS'

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