SrasV1, PascalFrancis, Corpus, bibRecord, 000479

Nasopharyngeal shedding of severe acute respiratory syndrome-associated coronavirus is associated with genetic polymorphisms

Identifieur interne : 000479 ( PascalFrancis/Corpus ); précédent : 000478; suivant : 000480

Nasopharyngeal shedding of severe acute respiratory syndrome-associated coronavirus is associated with genetic polymorphisms

Auteurs : Wei-Ju Chen ; Jyh-Yuan Yang ; Jih-Hui Lin ; Cathy S. J. Fann ; Valeriy Osyetrov ; Chwan-Chuen King ; Yi-Ming Arthur Chen ; Hsiao-Ling Chang ; Hung-Wei Kuo ; FONG LIAO ; Mei-Shang Ho

Source :

Clinical infectious diseases [ 1058-4838 ] ; 2006.

RBID : Pascal:06-0348647

Descripteurs français

Pascal (Inist)
- Syndrome respiratoire aigu sévère, Nasopharynx, Polymorphisme, Coronavirus.

English descriptors

KwdEn :
- Coronavirus, Nasopharynx, Polymorphism, Severe acute respiratory syndrome.

Abstract

Background. A high initial or peak severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) load in nasopharyngeal specimens was shown to be associated with a high mortality rate. Because all infected individuals were devoid of preeexisting protective immunity against SARS-CoV, the biological basis for the variable virus burdens in different patients remains elusive. Methods. The nationwide SARS database in Taiwan was analyzed, and genotyping of 281 single-nucleotide polymorphisms (SNPs) of 65 genes was performed for 94 patients with SARS, to identify SNPs for which distribution between patients with or without detectable nasopharyngeal shedding of SARS-CoV was biased. Results. Titers of SARS-CoV shed in nasopharyngeal specimens varied widely, ranging from nondetectable to 10⁸ SARS-CoV RNA copies/mL, and they were correlated positively with a high mortality rate (P<.0001, by trend test) and with early death (i.e., death occurring within 2 weeks of the onset of illness) (P =.0015, by trend test). Virus shedding was found to be higher among male patients (P =.0014, by multivariate logistic regression) and among older patients (P =.015, by multivariate logistic regression). Detectable nasopharyngeal shedding of SARS-CoV was associated with polymorphic alleles of interleukins 18 (P =.014) and 1A (P =.031) and a member of NFκB complex (reticuloendotheliosis viral oncogene homolog B [RelB]) (P =.034), all of which are proinflammatory in nature, as well as the procoagulation molecule fibrinogen-like protein 2 (P =.008). Conclusion. The SARS-CoV load is a determinant of clinical outcomes of SARS, and it is associated with polymorphisms of genes involved in innate immunity, which might be regulated in an age- and sex-dependent manner. The findings of the present study provided leads to genes involved in the host response to SARS-CoV infection; if substantiated with functional studies, these findings may be applicable to other newly emerged respiratory viruses (e.g., the influenza pandemic strain).

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 1058-4838`
A02	`01`			`@0 CIDIEL`
A03		`1`		`@0 Clin. infect. dis.`
A05				`@2 42`
A06				`@2 11`
A08	`01`	`1`	`ENG`	`@1 Nasopharyngeal shedding of severe acute respiratory syndrome-associated coronavirus is associated with genetic polymorphisms`
A11	`01`	`1`		`@1 CHEN (Wei-Ju)`
A11	`02`	`1`		`@1 YANG (Jyh-Yuan)`
A11	`03`	`1`		`@1 LIN (Jih-Hui)`
A11	`04`	`1`		`@1 FANN (Cathy S. J.)`
A11	`05`	`1`		`@1 OSYETROV (Valeriy)`
A11	`06`	`1`		`@1 KING (Chwan-Chuen)`
A11	`07`	`1`		`@1 CHEN (Yi-Ming Arthur)`
A11	`08`	`1`		`@1 CHANG (Hsiao-Ling)`
A11	`09`	`1`		`@1 KUO (Hung-Wei)`
A11	`10`	`1`		`@1 FONG LIAO`
A11	`11`	`1`		`@1 HO (Mei-Shang)`
A14	`01`			`@1 Institute of Biomedical Science, Academia Sinica, National Taiwan University @3 TWN @Z 1 aut. @Z 4 aut. @Z 5 aut. @Z 10 aut. @Z 11 aut.`
A14	`02`			`@1 Center for Disease Control, National Taiwan University @3 TWN @Z 2 aut. @Z 3 aut. @Z 8 aut. @Z 9 aut.`
A14	`03`			`@1 Graduate Institute of Epidemiology, National Taiwan University @3 TWN @Z 6 aut. @Z 11 aut.`
A14	`04`			`@1 Institute of Public Health, National Yang-Ming University @2 Taipei @3 TWN @Z 7 aut. @Z 11 aut.`
A20				`@1 1561-1569`
A21				`@1 2006`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 18407 @5 354000142370600070`
A44				`@0 0000 @1 © 2006 INIST-CNRS. All rights reserved.`
A45				`@0 46 ref.`
A47	`01`	`1`		`@0 06-0348647`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Clinical infectious diseases`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 Background. A high initial or peak severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) load in nasopharyngeal specimens was shown to be associated with a high mortality rate. Because all infected individuals were devoid of preeexisting protective immunity against SARS-CoV, the biological basis for the variable virus burdens in different patients remains elusive. Methods. The nationwide SARS database in Taiwan was analyzed, and genotyping of 281 single-nucleotide polymorphisms (SNPs) of 65 genes was performed for 94 patients with SARS, to identify SNPs for which distribution between patients with or without detectable nasopharyngeal shedding of SARS-CoV was biased. Results. Titers of SARS-CoV shed in nasopharyngeal specimens varied widely, ranging from nondetectable to 10⁸ SARS-CoV RNA copies/mL, and they were correlated positively with a high mortality rate (P<.0001, by trend test) and with early death (i.e., death occurring within 2 weeks of the onset of illness) (P =.0015, by trend test). Virus shedding was found to be higher among male patients (P =.0014, by multivariate logistic regression) and among older patients (P =.015, by multivariate logistic regression). Detectable nasopharyngeal shedding of SARS-CoV was associated with polymorphic alleles of interleukins 18 (P =.014) and 1A (P =.031) and a member of NFκB complex (reticuloendotheliosis viral oncogene homolog B [RelB]) (P =.034), all of which are proinflammatory in nature, as well as the procoagulation molecule fibrinogen-like protein 2 (P =.008). Conclusion. The SARS-CoV load is a determinant of clinical outcomes of SARS, and it is associated with polymorphisms of genes involved in innate immunity, which might be regulated in an age- and sex-dependent manner. The findings of the present study provided leads to genes involved in the host response to SARS-CoV infection; if substantiated with functional studies, these findings may be applicable to other newly emerged respiratory viruses (e.g., the influenza pandemic strain).
C02	`01`	`X`		`@0 002B05C02C`
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C03	`01`	`X`	`ENG`	`@0 Severe acute respiratory syndrome @2 NM @5 01`
C03	`01`	`X`	`SPA`	`@0 Síndrome respiratorio agudo severo @2 NM @5 01`
C03	`02`	`X`	`FRE`	`@0 Nasopharynx @5 07`
C03	`02`	`X`	`ENG`	`@0 Nasopharynx @5 07`
C03	`02`	`X`	`SPA`	`@0 Nasofaringe @5 07`
C03	`03`	`X`	`FRE`	`@0 Polymorphisme @5 08`
C03	`03`	`X`	`ENG`	`@0 Polymorphism @5 08`
C03	`03`	`X`	`SPA`	`@0 Polimorfismo @5 08`
C03	`04`	`X`	`FRE`	`@0 Coronavirus @2 NW @5 10`
C03	`04`	`X`	`ENG`	`@0 Coronavirus @2 NW @5 10`
C03	`04`	`X`	`SPA`	`@0 Coronavirus @2 NW @5 10`
C07	`01`	`X`	`FRE`	`@0 Virose`
C07	`01`	`X`	`ENG`	`@0 Viral disease`
C07	`01`	`X`	`SPA`	`@0 Virosis`
C07	`02`	`X`	`FRE`	`@0 Infection`
C07	`02`	`X`	`ENG`	`@0 Infection`
C07	`02`	`X`	`SPA`	`@0 Infección`
C07	`03`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`03`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
C07	`03`	`X`	`SPA`	`@0 Coronaviridae @2 NW`
C07	`04`	`X`	`FRE`	`@0 Nidovirales @2 NW`
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C07	`06`	`X`	`FRE`	`@0 Appareil respiratoire pathologie @5 37`
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C07	`06`	`X`	`SPA`	`@0 Aparato respiratorio patología @5 37`
C07	`07`	`X`	`FRE`	`@0 Poumon pathologie @5 38`
C07	`07`	`X`	`ENG`	`@0 Lung disease @5 38`
C07	`07`	`X`	`SPA`	`@0 Pulmón patología @5 38`
N21				`@1 227`
N44	`01`			`@1 OTO`
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Format Inist (serveur)

NO :	PASCAL 06-0348647 INIST
ET :	Nasopharyngeal shedding of severe acute respiratory syndrome-associated coronavirus is associated with genetic polymorphisms
AU :	CHEN (Wei-Ju); YANG (Jyh-Yuan); LIN (Jih-Hui); FANN (Cathy S. J.); OSYETROV (Valeriy); KING (Chwan-Chuen); CHEN (Yi-Ming Arthur); CHANG (Hsiao-Ling); KUO (Hung-Wei); FONG LIAO; HO (Mei-Shang)
AF :	Institute of Biomedical Science, Academia Sinica, National Taiwan University/Taïwan (1 aut., 4 aut., 5 aut., 10 aut., 11 aut.); Center for Disease Control, National Taiwan University/Taïwan (2 aut., 3 aut., 8 aut., 9 aut.); Graduate Institute of Epidemiology, National Taiwan University/Taïwan (6 aut., 11 aut.); Institute of Public Health, National Yang-Ming University/Taipei/Taïwan (7 aut., 11 aut.)
DT :	Publication en série; Niveau analytique
SO :	Clinical infectious diseases; ISSN 1058-4838; Coden CIDIEL; Etats-Unis; Da. 2006; Vol. 42; No. 11; Pp. 1561-1569; Bibl. 46 ref.
LA :	Anglais
EA :	Background. A high initial or peak severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) load in nasopharyngeal specimens was shown to be associated with a high mortality rate. Because all infected individuals were devoid of preeexisting protective immunity against SARS-CoV, the biological basis for the variable virus burdens in different patients remains elusive. Methods. The nationwide SARS database in Taiwan was analyzed, and genotyping of 281 single-nucleotide polymorphisms (SNPs) of 65 genes was performed for 94 patients with SARS, to identify SNPs for which distribution between patients with or without detectable nasopharyngeal shedding of SARS-CoV was biased. Results. Titers of SARS-CoV shed in nasopharyngeal specimens varied widely, ranging from nondetectable to 10⁸ SARS-CoV RNA copies/mL, and they were correlated positively with a high mortality rate (P<.0001, by trend test) and with early death (i.e., death occurring within 2 weeks of the onset of illness) (P =.0015, by trend test). Virus shedding was found to be higher among male patients (P =.0014, by multivariate logistic regression) and among older patients (P =.015, by multivariate logistic regression). Detectable nasopharyngeal shedding of SARS-CoV was associated with polymorphic alleles of interleukins 18 (P =.014) and 1A (P =.031) and a member of NFκB complex (reticuloendotheliosis viral oncogene homolog B [RelB]) (P =.034), all of which are proinflammatory in nature, as well as the procoagulation molecule fibrinogen-like protein 2 (P =.008). Conclusion. The SARS-CoV load is a determinant of clinical outcomes of SARS, and it is associated with polymorphisms of genes involved in innate immunity, which might be regulated in an age- and sex-dependent manner. The findings of the present study provided leads to genes involved in the host response to SARS-CoV infection; if substantiated with functional studies, these findings may be applicable to other newly emerged respiratory viruses (e.g., the influenza pandemic strain).
CC :	002B05C02C
FD :	Syndrome respiratoire aigu sévère; Nasopharynx; Polymorphisme; Coronavirus
FG :	Virose; Infection; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Poumon pathologie
ED :	Severe acute respiratory syndrome; Nasopharynx; Polymorphism; Coronavirus
EG :	Viral disease; Infection; Coronaviridae; Nidovirales; Virus; Respiratory disease; Lung disease
SD :	Síndrome respiratorio agudo severo; Nasofaringe; Polimorfismo; Coronavirus
LO :	INIST-18407.354000142370600070
ID :	06-0348647

Links to Exploration step

Pascal:06-0348647

Le document en format XML

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<affiliation><inist:fA14 i1="03"><s1>Graduate Institute of Epidemiology, National Taiwan University</s1>
<s3>TWN</s3>
<sZ>6 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="04"><s1>Institute of Public Health, National Yang-Ming University</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>7 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Clinical infectious diseases</title>
<title level="j" type="abbreviated">Clin. infect. dis.</title>
<idno type="ISSN">1058-4838</idno>
<imprint><date when="2006">2006</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Clinical infectious diseases</title>
<title level="j" type="abbreviated">Clin. infect. dis.</title>
<idno type="ISSN">1058-4838</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Coronavirus</term>
<term>Nasopharynx</term>
<term>Polymorphism</term>
<term>Severe acute respiratory syndrome</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
<term>Nasopharynx</term>
<term>Polymorphisme</term>
<term>Coronavirus</term>
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<front><div type="abstract" xml:lang="en">Background. A high initial or peak severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) load in nasopharyngeal specimens was shown to be associated with a high mortality rate. Because all infected individuals were devoid of preeexisting protective immunity against SARS-CoV, the biological basis for the variable virus burdens in different patients remains elusive. Methods. The nationwide SARS database in Taiwan was analyzed, and genotyping of 281 single-nucleotide polymorphisms (SNPs) of 65 genes was performed for 94 patients with SARS, to identify SNPs for which distribution between patients with or without detectable nasopharyngeal shedding of SARS-CoV was biased. Results. Titers of SARS-CoV shed in nasopharyngeal specimens varied widely, ranging from nondetectable to 10<sup>8</sup>
 SARS-CoV RNA copies/mL, and they were correlated positively with a high mortality rate (P<.0001, by trend test) and with early death (i.e., death occurring within 2 weeks of the onset of illness) (P =.0015, by trend test). Virus shedding was found to be higher among male patients (P =.0014, by multivariate logistic regression) and among older patients (P =.015, by multivariate logistic regression). Detectable nasopharyngeal shedding of SARS-CoV was associated with polymorphic alleles of interleukins 18 (P =.014) and 1A (P =.031) and a member of NFκB complex (reticuloendotheliosis viral oncogene homolog B [RelB]) (P =.034), all of which are proinflammatory in nature, as well as the procoagulation molecule fibrinogen-like protein 2 (P =.008). Conclusion. The SARS-CoV load is a determinant of clinical outcomes of SARS, and it is associated with polymorphisms of genes involved in innate immunity, which might be regulated in an age- and sex-dependent manner. The findings of the present study provided leads to genes involved in the host response to SARS-CoV infection; if substantiated with functional studies, these findings may be applicable to other newly emerged respiratory viruses (e.g., the influenza pandemic strain).</div>
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<fA11 i1="01" i2="1"><s1>CHEN (Wei-Ju)</s1>
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<fA11 i1="02" i2="1"><s1>YANG (Jyh-Yuan)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>LIN (Jih-Hui)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>FANN (Cathy S. J.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>OSYETROV (Valeriy)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>KING (Chwan-Chuen)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>CHEN (Yi-Ming Arthur)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>CHANG (Hsiao-Ling)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>KUO (Hung-Wei)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>FONG LIAO</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>HO (Mei-Shang)</s1>
</fA11>
<fA14 i1="01"><s1>Institute of Biomedical Science, Academia Sinica, National Taiwan University</s1>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Center for Disease Control, National Taiwan University</s1>
<s3>TWN</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Graduate Institute of Epidemiology, National Taiwan University</s1>
<s3>TWN</s3>
<sZ>6 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Institute of Public Health, National Yang-Ming University</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>7 aut.</sZ>
<sZ>11 aut.</sZ>
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</fA20>
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<s1>© 2006 INIST-CNRS. All rights reserved.</s1>
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<fC01 i1="01" l="ENG"><s0>Background. A high initial or peak severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) load in nasopharyngeal specimens was shown to be associated with a high mortality rate. Because all infected individuals were devoid of preeexisting protective immunity against SARS-CoV, the biological basis for the variable virus burdens in different patients remains elusive. Methods. The nationwide SARS database in Taiwan was analyzed, and genotyping of 281 single-nucleotide polymorphisms (SNPs) of 65 genes was performed for 94 patients with SARS, to identify SNPs for which distribution between patients with or without detectable nasopharyngeal shedding of SARS-CoV was biased. Results. Titers of SARS-CoV shed in nasopharyngeal specimens varied widely, ranging from nondetectable to 10<sup>8</sup>
 SARS-CoV RNA copies/mL, and they were correlated positively with a high mortality rate (P<.0001, by trend test) and with early death (i.e., death occurring within 2 weeks of the onset of illness) (P =.0015, by trend test). Virus shedding was found to be higher among male patients (P =.0014, by multivariate logistic regression) and among older patients (P =.015, by multivariate logistic regression). Detectable nasopharyngeal shedding of SARS-CoV was associated with polymorphic alleles of interleukins 18 (P =.014) and 1A (P =.031) and a member of NFκB complex (reticuloendotheliosis viral oncogene homolog B [RelB]) (P =.034), all of which are proinflammatory in nature, as well as the procoagulation molecule fibrinogen-like protein 2 (P =.008). Conclusion. The SARS-CoV load is a determinant of clinical outcomes of SARS, and it is associated with polymorphisms of genes involved in innate immunity, which might be regulated in an age- and sex-dependent manner. The findings of the present study provided leads to genes involved in the host response to SARS-CoV infection; if substantiated with functional studies, these findings may be applicable to other newly emerged respiratory viruses (e.g., the influenza pandemic strain).</s0>
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<s5>01</s5>
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<fC03 i1="01" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>01</s5>
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<s5>07</s5>
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<s5>08</s5>
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<s5>08</s5>
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<s2>NW</s2>
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<fC07 i1="04" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
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<s2>NW</s2>
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<s5>37</s5>
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<fC07 i1="07" i2="X" l="FRE"><s0>Poumon pathologie</s0>
<s5>38</s5>
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<fC07 i1="07" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>38</s5>
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<fC07 i1="07" i2="X" l="SPA"><s0>Pulmón patología</s0>
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<fN21><s1>227</s1>
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<server><NO>PASCAL 06-0348647 INIST</NO>
<ET>Nasopharyngeal shedding of severe acute respiratory syndrome-associated coronavirus is associated with genetic polymorphisms</ET>
<AU>CHEN (Wei-Ju); YANG (Jyh-Yuan); LIN (Jih-Hui); FANN (Cathy S. J.); OSYETROV (Valeriy); KING (Chwan-Chuen); CHEN (Yi-Ming Arthur); CHANG (Hsiao-Ling); KUO (Hung-Wei); FONG LIAO; HO (Mei-Shang)</AU>
<AF>Institute of Biomedical Science, Academia Sinica, National Taiwan University/Taïwan (1 aut., 4 aut., 5 aut., 10 aut., 11 aut.); Center for Disease Control, National Taiwan University/Taïwan (2 aut., 3 aut., 8 aut., 9 aut.); Graduate Institute of Epidemiology, National Taiwan University/Taïwan (6 aut., 11 aut.); Institute of Public Health, National Yang-Ming University/Taipei/Taïwan (7 aut., 11 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Clinical infectious diseases; ISSN 1058-4838; Coden CIDIEL; Etats-Unis; Da. 2006; Vol. 42; No. 11; Pp. 1561-1569; Bibl. 46 ref.</SO>
<LA>Anglais</LA>
<EA>Background. A high initial or peak severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) load in nasopharyngeal specimens was shown to be associated with a high mortality rate. Because all infected individuals were devoid of preeexisting protective immunity against SARS-CoV, the biological basis for the variable virus burdens in different patients remains elusive. Methods. The nationwide SARS database in Taiwan was analyzed, and genotyping of 281 single-nucleotide polymorphisms (SNPs) of 65 genes was performed for 94 patients with SARS, to identify SNPs for which distribution between patients with or without detectable nasopharyngeal shedding of SARS-CoV was biased. Results. Titers of SARS-CoV shed in nasopharyngeal specimens varied widely, ranging from nondetectable to 10<sup>8</sup>
 SARS-CoV RNA copies/mL, and they were correlated positively with a high mortality rate (P<.0001, by trend test) and with early death (i.e., death occurring within 2 weeks of the onset of illness) (P =.0015, by trend test). Virus shedding was found to be higher among male patients (P =.0014, by multivariate logistic regression) and among older patients (P =.015, by multivariate logistic regression). Detectable nasopharyngeal shedding of SARS-CoV was associated with polymorphic alleles of interleukins 18 (P =.014) and 1A (P =.031) and a member of NFκB complex (reticuloendotheliosis viral oncogene homolog B [RelB]) (P =.034), all of which are proinflammatory in nature, as well as the procoagulation molecule fibrinogen-like protein 2 (P =.008). Conclusion. The SARS-CoV load is a determinant of clinical outcomes of SARS, and it is associated with polymorphisms of genes involved in innate immunity, which might be regulated in an age- and sex-dependent manner. The findings of the present study provided leads to genes involved in the host response to SARS-CoV infection; if substantiated with functional studies, these findings may be applicable to other newly emerged respiratory viruses (e.g., the influenza pandemic strain).</EA>
<CC>002B05C02C</CC>
<FD>Syndrome respiratoire aigu sévère; Nasopharynx; Polymorphisme; Coronavirus</FD>
<FG>Virose; Infection; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Poumon pathologie</FG>
<ED>Severe acute respiratory syndrome; Nasopharynx; Polymorphism; Coronavirus</ED>
<EG>Viral disease; Infection; Coronaviridae; Nidovirales; Virus; Respiratory disease; Lung disease</EG>
<SD>Síndrome respiratorio agudo severo; Nasofaringe; Polimorfismo; Coronavirus</SD>
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<ID>06-0348647</ID>
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Nasopharyngeal shedding of severe acute respiratory syndrome-associated coronavirus is associated with genetic polymorphisms

Nasopharyngeal shedding of severe acute respiratory syndrome-associated coronavirus is associated with genetic polymorphisms

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