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Conference Paper: Integrating genetic linkage analysis and computational prioritzation in identifying host genetic factors response to influenza A virus infection
Title | Integrating genetic linkage analysis and computational prioritzation in identifying host genetic factors response to influenza A virus infection |
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Authors | |
Issue Date | 2012 |
Publisher | The American Society of Human Genetics (ASHG). The Poster Abstracts' website is located at http://www.ashg.org/2012meeting/pdf/38731_poster_complete.pdf |
Citation | The 62nd Annual Meeting of the American Society of Human Genetics (ASHG 2012), San Francisco, CA., 6-10 November 2012. In Poster Abstracts, 2012, p. 544, abstract no. 2254T How to Cite? |
Abstract | The genetic background of the host has a major ole on its resistance to
pathogens infection. Several independent studies acumulatively aded to
the evidence that host genetic make-up may be a key factor in the epidemiology
of avian influenza A (H5N1) virus infection in humans. Recently, studies
based on mouse models, e.g. quantiative trait loci (QTL) analysis on inbred
mouse strains, have shed lights on deciphering the molecular basis of host
choice behavior. However, few in silco platforms have ben developed to
systematicaly identify genetic factors before they were further experimentaly
verifed. Here, we tried to identify the host factors for influenza virus
resistance by integrating genetic linkage analysis and gene prioritzation
algorithms. We colected al genes within mouse QTLs linked to host
response to influenza virus by several independent studies as candidate
genes. The genetic polymorphism of the two mouse strains (C57BL/6J, DBA/
2J), which exhibited diferent kinetics after they were infected by influenza A
virus, help us filter out candidates which were unlikely to be genetic factors.
Totaly, we identifed 20 genes as candidates by integrating the results
from thre frely available prioritzation tols (Endeavour, TopGene and
SUSPECT). After anotated by the Database for Anotation, Visualization
and Integrated Discovery (DAVID), most of them functioned as protein binding
genes and participated in the biological proceses related to stimulus
response, immunity and defense. Interestingly, among the genes expresing
non-synonymous coding SNPs on DBA genome, Enp2 and Tnfrsf1b were
both maped to Bhr2 MGI QTL, which is related to influenza infection consequence.
The results indicate that genes identifed by our model have great
potential as genetic factors in causing host specifc response to influenza
infection and ned to be further studied. |
Description | Session: Complex Traits and Polygenic Disorders |
Persistent Identifier | http://hdl.handle.net/10722/189728 |
DC Field | Value | Language |
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dc.contributor.author | Bao, S | en_US |
dc.contributor.author | Zhou, X | en_US |
dc.contributor.author | Zhang, X | en_US |
dc.contributor.author | Tang, P | - |
dc.contributor.author | Zhou, J | - |
dc.contributor.author | Li, Y | - |
dc.contributor.author | To, K | - |
dc.contributor.author | Song, Y | - |
dc.date.accessioned | 2013-09-17T14:55:56Z | - |
dc.date.available | 2013-09-17T14:55:56Z | - |
dc.date.issued | 2012 | en_US |
dc.identifier.citation | The 62nd Annual Meeting of the American Society of Human Genetics (ASHG 2012), San Francisco, CA., 6-10 November 2012. In Poster Abstracts, 2012, p. 544, abstract no. 2254T | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/189728 | - |
dc.description | Session: Complex Traits and Polygenic Disorders | - |
dc.description.abstract | The genetic background of the host has a major ole on its resistance to pathogens infection. Several independent studies acumulatively aded to the evidence that host genetic make-up may be a key factor in the epidemiology of avian influenza A (H5N1) virus infection in humans. Recently, studies based on mouse models, e.g. quantiative trait loci (QTL) analysis on inbred mouse strains, have shed lights on deciphering the molecular basis of host choice behavior. However, few in silco platforms have ben developed to systematicaly identify genetic factors before they were further experimentaly verifed. Here, we tried to identify the host factors for influenza virus resistance by integrating genetic linkage analysis and gene prioritzation algorithms. We colected al genes within mouse QTLs linked to host response to influenza virus by several independent studies as candidate genes. The genetic polymorphism of the two mouse strains (C57BL/6J, DBA/ 2J), which exhibited diferent kinetics after they were infected by influenza A virus, help us filter out candidates which were unlikely to be genetic factors. Totaly, we identifed 20 genes as candidates by integrating the results from thre frely available prioritzation tols (Endeavour, TopGene and SUSPECT). After anotated by the Database for Anotation, Visualization and Integrated Discovery (DAVID), most of them functioned as protein binding genes and participated in the biological proceses related to stimulus response, immunity and defense. Interestingly, among the genes expresing non-synonymous coding SNPs on DBA genome, Enp2 and Tnfrsf1b were both maped to Bhr2 MGI QTL, which is related to influenza infection consequence. The results indicate that genes identifed by our model have great potential as genetic factors in causing host specifc response to influenza infection and ned to be further studied. | - |
dc.language | eng | en_US |
dc.publisher | The American Society of Human Genetics (ASHG). The Poster Abstracts' website is located at http://www.ashg.org/2012meeting/pdf/38731_poster_complete.pdf | - |
dc.relation.ispartof | Annual Meeting of the American Society of Human Genetics, ASHG 2012 | en_US |
dc.title | Integrating genetic linkage analysis and computational prioritzation in identifying host genetic factors response to influenza A virus infection | en_US |
dc.type | Conference_Paper | en_US |
dc.identifier.email | Song, Y: songy@hku.hk | en_US |
dc.identifier.authority | Song, Y=rp00488 | en_US |
dc.identifier.hkuros | 222302 | en_US |
dc.identifier.spage | 544, abstract no. 2254T | - |
dc.identifier.epage | 544, abstract no. 2254T | - |
dc.publisher.place | United States | - |