Genetic variation of the human α-2-Heremans-Schmid glycoprotein (AHSG) gene associated with the risk of SARS-CoV infection.
Identifieur interne : 001476 ( PubMed/Corpus ); précédent : 001475; suivant : 001477Genetic variation of the human α-2-Heremans-Schmid glycoprotein (AHSG) gene associated with the risk of SARS-CoV infection.
Auteurs : Xiaohui Zhu ; Yan Wang ; Hongxing Zhang ; Xuan Liu ; Ting Chen ; Ruifu Yang ; Yuling Shi ; Wuchun Cao ; Ping Li ; Qingjun Ma ; Yun Zhai ; Fuchu He ; Gangqiao Zhou ; Cheng CaoSource :
- PloS one [ 1932-6203 ] ; 2011.
English descriptors
- KwdEn :
- Adolescent, Adult, Cell Line, Female, Genetic Variation (genetics), Genotype, Hep G2 Cells, Humans, Linkage Disequilibrium (genetics), Male, Polymorphism, Single Nucleotide (genetics), Promoter Regions, Genetic, SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (blood), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (virology), Young Adult, alpha-2-HS-Glycoprotein (genetics), alpha-2-HS-Glycoprotein (metabolism).
- MESH :
- chemical , genetics : alpha-2-HS-Glycoprotein.
- blood : Severe Acute Respiratory Syndrome.
- genetics : Genetic Variation, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Severe Acute Respiratory Syndrome.
- chemical , metabolism : alpha-2-HS-Glycoprotein.
- pathogenicity : SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Adolescent, Adult, Cell Line, Female, Genotype, Hep G2 Cells, Humans, Male, Promoter Regions, Genetic, Young Adult.
Abstract
Genetic background may play an important role in the process of SARS-CoV infection and SARS development. We found several proteins that could interact with the nucleocapsid protein of the SARS coronavirus (SARS-CoV). α-2-Heremans-Schmid Glycoprotein (AHSG), which is required for macrophage deactivation by endogenous cations, is associated with inflammatory regulation. Cytochrome P450 Family 3A (CYP4F3A) is an ω-oxidase that inactivates Leukotriene B4 (LTB4) in human neutrophils and the liver. We investigated the association between the polymorphisms of these two inflammation-associated genes and SARS development. The linkage disequilibrium (LD) maps of these two genes were built with Haploview using data on CHB+JPT (version 2) from the HapMap. A total of ten tag SNPs were selected and genotyped. In the Guangzhou cohort study, after adjusting for age and sex, two AHSG SNPs and one CYP4F3 SNP were found to be associated with SARS susceptibility: rs2248690 (adjusted odds ratio [AOR] 2.42; 95% confidence interval [CI] 1.30-4.51); rs4917 (AOR 1.84; 95% CI 1.02-3.34); and rs3794987 (AOR 2.01; 95% CI 1.10-3.68). To further validate the association, the ten tag SNPs were genotyped in the Beijing cohort. After adjusting for age and sex, only rs2248690 (AOR, 1.63; 95% CI, 1.30-2.04) was found to be associated with SARS susceptibility. The combined analysis of the two studies confirmed tag SNP rs2248690 in AHSG as a susceptibility variant (AOR 1.70; 95% CI 1.37-2.09). The statistical analysis of the rs2248690 genotype data among the patients and healthy controls in the HCW cohort, who were all similarly exposed to the SARS virus, also supported the findings. Further, the SNP rs2248690 affected the transcriptional activity of the AHSG promoter and thus regulated the AHSG serum level. Therefore, our study has demonstrated that the AA genotype of rs2268690, which leads to a higher AHSG serum concentration, was significantly associated with protection against SARS development.
DOI: 10.1371/journal.pone.0023730
PubMed: 21904596
Links to Exploration step
pubmed:21904596Le document en format XML
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uniqKey="Wang Y" first="Yan" last="Wang">Yan Wang</name></author><author><name sortKey="Zhang, Hongxing" sort="Zhang, Hongxing" uniqKey="Zhang H" first="Hongxing" last="Zhang">Hongxing Zhang</name></author><author><name sortKey="Liu, Xuan" sort="Liu, Xuan" uniqKey="Liu X" first="Xuan" last="Liu">Xuan Liu</name></author><author><name sortKey="Chen, Ting" sort="Chen, Ting" uniqKey="Chen T" first="Ting" last="Chen">Ting Chen</name></author><author><name sortKey="Yang, Ruifu" sort="Yang, Ruifu" uniqKey="Yang R" first="Ruifu" last="Yang">Ruifu Yang</name></author><author><name sortKey="Shi, Yuling" sort="Shi, Yuling" uniqKey="Shi Y" first="Yuling" last="Shi">Yuling Shi</name></author><author><name sortKey="Cao, Wuchun" sort="Cao, Wuchun" uniqKey="Cao W" first="Wuchun" last="Cao">Wuchun Cao</name></author><author><name sortKey="Li, Ping" sort="Li, Ping" uniqKey="Li P" first="Ping" last="Li">Ping Li</name></author><author><name sortKey="Ma, Qingjun" sort="Ma, Qingjun" uniqKey="Ma Q" first="Qingjun" last="Ma">Qingjun Ma</name></author><author><name sortKey="Zhai, Yun" sort="Zhai, Yun" uniqKey="Zhai Y" first="Yun" last="Zhai">Yun Zhai</name></author><author><name sortKey="He, Fuchu" sort="He, Fuchu" uniqKey="He F" first="Fuchu" last="He">Fuchu He</name></author><author><name sortKey="Zhou, Gangqiao" sort="Zhou, Gangqiao" uniqKey="Zhou G" first="Gangqiao" last="Zhou">Gangqiao Zhou</name></author><author><name sortKey="Cao, Cheng" sort="Cao, Cheng" uniqKey="Cao C" first="Cheng" last="Cao">Cheng Cao</name></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Cell Line</term><term>Female</term><term>Genetic Variation (genetics)</term><term>Genotype</term><term>Hep G2 Cells</term><term>Humans</term><term>Linkage 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qualifier="metabolism" xml:lang="en"><term>alpha-2-HS-Glycoprotein</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Cell Line</term><term>Female</term><term>Genotype</term><term>Hep G2 Cells</term><term>Humans</term><term>Male</term><term>Promoter Regions, Genetic</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Genetic background may play an important role in the process of SARS-CoV infection and SARS development. We found several proteins that could interact with the nucleocapsid protein of the SARS coronavirus (SARS-CoV). α-2-Heremans-Schmid Glycoprotein (AHSG), which is required for macrophage deactivation by endogenous cations, is associated with inflammatory regulation. Cytochrome P450 Family 3A (CYP4F3A) is an ω-oxidase that inactivates Leukotriene B4 (LTB4) in human neutrophils and the liver. We investigated the association between the polymorphisms of these two inflammation-associated genes and SARS development. The linkage disequilibrium (LD) maps of these two genes were built with Haploview using data on CHB+JPT (version 2) from the HapMap. A total of ten tag SNPs were selected and genotyped. In the Guangzhou cohort study, after adjusting for age and sex, two AHSG SNPs and one CYP4F3 SNP were found to be associated with SARS susceptibility: rs2248690 (adjusted odds ratio [AOR] 2.42; 95% confidence interval [CI] 1.30-4.51); rs4917 (AOR 1.84; 95% CI 1.02-3.34); and rs3794987 (AOR 2.01; 95% CI 1.10-3.68). To further validate the association, the ten tag SNPs were genotyped in the Beijing cohort. After adjusting for age and sex, only rs2248690 (AOR, 1.63; 95% CI, 1.30-2.04) was found to be associated with SARS susceptibility. The combined analysis of the two studies confirmed tag SNP rs2248690 in AHSG as a susceptibility variant (AOR 1.70; 95% CI 1.37-2.09). The statistical analysis of the rs2248690 genotype data among the patients and healthy controls in the HCW cohort, who were all similarly exposed to the SARS virus, also supported the findings. Further, the SNP rs2248690 affected the transcriptional activity of the AHSG promoter and thus regulated the AHSG serum level. Therefore, our study has demonstrated that the AA genotype of rs2268690, which leads to a higher AHSG serum concentration, was significantly associated with protection against SARS development.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21904596</PMID><DateCompleted><Year>2012</Year><Month>04</Month><Day>25</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>6</Volume><Issue>8</Issue><PubDate><Year>2011</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Genetic variation of the human α-2-Heremans-Schmid glycoprotein (AHSG) gene associated with the risk of SARS-CoV infection.</ArticleTitle><Pagination><MedlinePgn>e23730</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0023730</ELocationID><Abstract><AbstractText>Genetic background may play an important role in the process of SARS-CoV infection and SARS development. We found several proteins that could interact with the nucleocapsid protein of the SARS coronavirus (SARS-CoV). α-2-Heremans-Schmid Glycoprotein (AHSG), which is required for macrophage deactivation by endogenous cations, is associated with inflammatory regulation. Cytochrome P450 Family 3A (CYP4F3A) is an ω-oxidase that inactivates Leukotriene B4 (LTB4) in human neutrophils and the liver. We investigated the association between the polymorphisms of these two inflammation-associated genes and SARS development. The linkage disequilibrium (LD) maps of these two genes were built with Haploview using data on CHB+JPT (version 2) from the HapMap. A total of ten tag SNPs were selected and genotyped. In the Guangzhou cohort study, after adjusting for age and sex, two AHSG SNPs and one CYP4F3 SNP were found to be associated with SARS susceptibility: rs2248690 (adjusted odds ratio [AOR] 2.42; 95% confidence interval [CI] 1.30-4.51); rs4917 (AOR 1.84; 95% CI 1.02-3.34); and rs3794987 (AOR 2.01; 95% CI 1.10-3.68). To further validate the association, the ten tag SNPs were genotyped in the Beijing cohort. After adjusting for age and sex, only rs2248690 (AOR, 1.63; 95% CI, 1.30-2.04) was found to be associated with SARS susceptibility. The combined analysis of the two studies confirmed tag SNP rs2248690 in AHSG as a susceptibility variant (AOR 1.70; 95% CI 1.37-2.09). The statistical analysis of the rs2248690 genotype data among the patients and healthy controls in the HCW cohort, who were all similarly exposed to the SARS virus, also supported the findings. Further, the SNP rs2248690 affected the transcriptional activity of the AHSG promoter and thus regulated the AHSG serum level. Therefore, our study has demonstrated that the AA genotype of rs2268690, which leads to a higher AHSG serum concentration, was significantly associated with protection against SARS development.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Xiaohui</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Pathogen and Bio-Security, Beijing Institute of Biotechnology, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Yan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Hongxing</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xuan</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Ting</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Ruifu</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Shi</LastName><ForeName>Yuling</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>Wuchun</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Ping</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Qingjun</ForeName><Initials>Q</Initials></Author><Author ValidYN="Y"><LastName>Zhai</LastName><ForeName>Yun</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>Fuchu</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Gangqiao</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>Cheng</ForeName><Initials>C</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>08</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C556354">AHSG protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D060749">alpha-2-HS-Glycoprotein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014644" MajorTopicYN="N">Genetic Variation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056945" MajorTopicYN="N">Hep G2 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015810" MajorTopicYN="N">Linkage Disequilibrium</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020641" MajorTopicYN="N">Polymorphism, Single Nucleotide</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011401" MajorTopicYN="N">Promoter Regions, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D060749" MajorTopicYN="N">alpha-2-HS-Glycoprotein</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" 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IdType="pmc">PMC3163911</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Shock. 2001 Mar;15(3):181-5</Citation><ArticleIdList><ArticleId IdType="pubmed">11236900</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2011;6(2):e16945</Citation><ArticleIdList><ArticleId IdType="pubmed">21347455</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet. 2003 Apr 19;361(9366):1319-25</Citation><ArticleIdList><ArticleId IdType="pubmed">12711465</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1967-76</Citation><ArticleIdList><ArticleId IdType="pubmed">12690091</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1953-66</Citation><ArticleIdList><ArticleId IdType="pubmed">12690092</ArticleId></ArticleIdList></Reference><Reference><Citation>Emerg Infect Dis. 2003 Sep;9(9):1182-3</Citation><ArticleIdList><ArticleId IdType="pubmed">14531381</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Microbiol. 2003 Dec;41(12):5781-2</Citation><ArticleIdList><ArticleId IdType="pubmed">14662982</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Diagn Lab Immunol. 2004 Jan;11(1):227-8</Citation><ArticleIdList><ArticleId IdType="pubmed">14715574</ArticleId></ArticleIdList></Reference><Reference><Citation>J Infect Dis. 2004 Feb 15;189(4):642-7</Citation><ArticleIdList><ArticleId IdType="pubmed">14767817</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet. 2004 Mar 13;363(9412):841-5</Citation><ArticleIdList><ArticleId IdType="pubmed">15031027</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunol Lett. 2004 Apr 15;92(3):237-43</Citation><ArticleIdList><ArticleId IdType="pubmed">15081618</ArticleId></ArticleIdList></Reference><Reference><Citation>BMC Med Genet. 2003 Sep 12;4:9</Citation><ArticleIdList><ArticleId IdType="pubmed">12969506</ArticleId></ArticleIdList></Reference><Reference><Citation>Emerg Infect Dis. 2004 Jun;10(6):1117-9</Citation><ArticleIdList><ArticleId IdType="pubmed">15207066</ArticleId></ArticleIdList></Reference><Reference><Citation>J Infect Dis. 2004 Aug 1;190(3):515-8</Citation><ArticleIdList><ArticleId IdType="pubmed">15243926</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Invest. 1979 Oct;64(4):1118-29</Citation><ArticleIdList><ArticleId IdType="pubmed">90057</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Chim Acta. 1988 Aug 15;176(1):49-57</Citation><ArticleIdList><ArticleId IdType="pubmed">3168293</ArticleId></ArticleIdList></Reference><Reference><Citation>Ann Hematol. 1991 Nov;63(5):264-9</Citation><ArticleIdList><ArticleId IdType="pubmed">1958751</ArticleId></ArticleIdList></Reference><Reference><Citation>Orv Hetil. 1992 Jun 21;133(25):1553-4; 1559-60</Citation><ArticleIdList><ArticleId IdType="pubmed">1408055</ArticleId></ArticleIdList></Reference><Reference><Citation>Oncogene. 1995 Apr 6;10(7):1361-70</Citation><ArticleIdList><ArticleId IdType="pubmed">7731687</ArticleId></ArticleIdList></Reference><Reference><Citation>Hum Genet. 1997 Jan;99(1):18-21</Citation><ArticleIdList><ArticleId IdType="pubmed">9003486</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1998 Nov 24;95(24):14429-34</Citation><ArticleIdList><ArticleId IdType="pubmed">9826717</ArticleId></ArticleIdList></Reference><Reference><Citation>Genes Dev. 1999 Mar 1;13(5):607-19</Citation><ArticleIdList><ArticleId IdType="pubmed">10072388</ArticleId></ArticleIdList></Reference><Reference><Citation>Emerg Infect Dis. 2004 Nov;10(11):1947-9</Citation><ArticleIdList><ArticleId IdType="pubmed">15550204</ArticleId></ArticleIdList></Reference><Reference><Citation>Hum Genet. 2005 Feb;116(3):146-51</Citation><ArticleIdList><ArticleId IdType="pubmed">15592877</ArticleId></ArticleIdList></Reference><Reference><Citation>J Infect Dis. 2005 May 15;191(10):1697-704</Citation><ArticleIdList><ArticleId IdType="pubmed">15838797</ArticleId></ArticleIdList></Reference><Reference><Citation>Emerg Infect Dis. 2005 Jul;11(7):1142-5</Citation><ArticleIdList><ArticleId IdType="pubmed">16022801</ArticleId></ArticleIdList></Reference><Reference><Citation>J Infect Dis. 2005 Oct 15;192(8):1355-61</Citation><ArticleIdList><ArticleId IdType="pubmed">16170752</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Genet. 2006 Jan;38(1):38-46</Citation><ArticleIdList><ArticleId IdType="pubmed">16369534</ArticleId></ArticleIdList></Reference><Reference><Citation>BMC Infect Dis. 2006;6:82</Citation><ArticleIdList><ArticleId IdType="pubmed">16672072</ArticleId></ArticleIdList></Reference><Reference><Citation>BMC Infect Dis. 2006;6:106</Citation><ArticleIdList><ArticleId IdType="pubmed">16824203</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2007 Jun;81(11):6079-88</Citation><ArticleIdList><ArticleId IdType="pubmed">17392374</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Genet. 2007 Jun;39(6):691-2; author reply 694-6</Citation><ArticleIdList><ArticleId IdType="pubmed">17534354</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Genet. 2007 Jun;39(6):692-4; author reply 694-6</Citation><ArticleIdList><ArticleId IdType="pubmed">17534355</ArticleId></ArticleIdList></Reference><Reference><Citation>BMC Infect Dis. 2007;7:50</Citation><ArticleIdList><ArticleId IdType="pubmed">17540042</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochem J. 2007 Aug 1;405(3):379-95</Citation><ArticleIdList><ArticleId IdType="pubmed">17623009</ArticleId></ArticleIdList></Reference><Reference><Citation>Intern Med. 2007;46(20):1685-91</Citation><ArticleIdList><ArticleId IdType="pubmed">17938521</ArticleId></ArticleIdList></Reference><Reference><Citation>Diabetes Res Clin Pract. 2008 Jan;79(1):164-70</Citation><ArticleIdList><ArticleId IdType="pubmed">17889958</ArticleId></ArticleIdList></Reference><Reference><Citation>Int J Immunogenet. 2008 Feb;35(1):69-74</Citation><ArticleIdList><ArticleId IdType="pubmed">18186801</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2008 Jul;82(14):6962-71</Citation><ArticleIdList><ArticleId IdType="pubmed">18448518</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2008 Nov 1;181(9):6337-48</Citation><ArticleIdList><ArticleId IdType="pubmed">18941225</ArticleId></ArticleIdList></Reference><Reference><Citation>Med Hypotheses. 2002 Sep;59(3):261-5</Citation><ArticleIdList><ArticleId IdType="pubmed">12208150</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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