SrasV1, PascalFrancis, Corpus, bibRecord, 000879

T-cell epitopes in Severe acute respiratory syndrome (SARS) coronavirus spike protein elicit a specific T-cell immune response in patients who recover from SARS

Identifieur interne : 000879 ( PascalFrancis/Corpus ); précédent : 000878; suivant : 000880

T-cell epitopes in Severe acute respiratory syndrome (SARS) coronavirus spike protein elicit a specific T-cell immune response in patients who recover from SARS

Auteurs : Yue-Dan Wang ; Wan-Yee Fion Sin ; Guo-Bing Xu ; Huang-Hua Yang ; Tin-Yau Wong ; Xue-Wen Pang ; Xiao-Yan He ; Hua-Gang Zhang ; JOICE NA LEE NG ; Chak-Sum Samuel Cheng ; JING JU ; LI MENG ; Rui-Feng Yang ; Sik-To Lai ; Zhi-Hong Guo ; YONG XIE ; Wei-Feng Chen

Source :

Journal of virology [ 0022-538X ] ; 2004.

RBID : Pascal:04-0314703

Descripteurs français

Pascal (Inist)
- Coronavirus, Homme, Lymphocyte T, Déterminant antigénique, Protéine A, Immunité cellulaire, Microbiologie, Virologie, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Antigenic determinant, Cellular immunity, Coronavirus, Human, Microbiology, Protein A, Severe acute respiratory syndrome, T-Lymphocyte, Virology.

Abstract

The immunogenicity of HLA-A2-restricted T-cell epitopes in the S protein of the Severe acute respiratory syndrome coronavirus (SARS-CoV) and of human coronavirus strain 229e (HCoV-229e) was analyzed for the elicitation of a T-cell immune response in donors who had fully recovered from SARS-CoV infection. We employed online database analysis to compare the differences in the amino acid sequences of the homologous T epitopes of HCoV-229e and SARS-CoV. The identified T-cell epitope peptides were synthesized, and their binding affinities for HLA-A2 were validated and compared in the T2 cell system. The immunogenicity of all these peptides was assessed by using T cells obtained from donors who had fully recovered from SARS-CoV infection and from healthy donors with no history of SARS-CoV infection. HLA-A2 typing by indirect immunofluorescent antibody staining showed that 51.6% of SARS-CoV-infected patients were HLA-A2 positive. Online database analysis and the T2 cell binding test disclosed that the number of HLA-A2-restricted immunogenic epitopes of the S protein of SARS-CoV was decreased or even lost in comparison with the homologous sequences of the S protein of HCoV-229e. Among the peptides used in the study, the affinity of peptides from HCoV-229e (H77 and H881) and peptides from SARS-CoV (S978 and S1203) for binding to HLA-A2 was higher than that of other sequences. The gamma interferon (IFN-γ) release Elispot assay revealed that only SARS-CoV-specific peptides S1203 and S978 induced a high frequency of IFN-γ-secreting T-cell response in HLA-A2⁺ donors who had fully recovered from SARS-CoV infection; such a T-cell epitope-specific response was not observed in HLA-A2⁺ healthy donors or in HLA-A2- donors who had been infected with SARS-CoV after full recovery. Thus, T-cell epitopes S1203 and S978 are immunogenic and elicit an overt specific T-cell response in HLA-A2⁺ SARS-CoV-infected patients.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 04-0314703 INIST
ET :	T-cell epitopes in Severe acute respiratory syndrome (SARS) coronavirus spike protein elicit a specific T-cell immune response in patients who recover from SARS
AU :	WANG (Yue-Dan); SIN (Wan-Yee Fion); XU (Guo-Bing); YANG (Huang-Hua); WONG (Tin-Yau); PANG (Xue-Wen); HE (Xiao-Yan); ZHANG (Hua-Gang); JOICE NA LEE NG; CHENG (Chak-Sum Samuel); JING JU; LI MENG; YANG (Rui-Feng); LAI (Sik-To); GUO (Zhi-Hong); YONG XIE; CHEN (Wei-Feng)
AF :	Department of Immunology, Peking University Health Science Centre/Beijing/Chine (1 aut., 6 aut., 7 aut., 8 aut., 17 aut.); Department of Biology, Hong Kong University of Science and Technology, Clear Water Bay/Kowloon/Hong-Kong (1 aut., 2 aut., 10 aut., 11 aut., 12 aut., 16 aut.); First Hospital, Peking University/Beijing/Chine (3 aut., 13 aut.); Department of Chemistry, Hong Kong University of Science and Technology, Clear Water Bay/Kowloon/Danemark (4 aut., 15 aut.); Princess Margaret Hospital/Danemark (5 aut., 9 aut., 14 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2004; Vol. 78; No. 11; Pp. 5612-5618; Bibl. 31 ref.
LA :	Anglais
EA :	The immunogenicity of HLA-A2-restricted T-cell epitopes in the S protein of the Severe acute respiratory syndrome coronavirus (SARS-CoV) and of human coronavirus strain 229e (HCoV-229e) was analyzed for the elicitation of a T-cell immune response in donors who had fully recovered from SARS-CoV infection. We employed online database analysis to compare the differences in the amino acid sequences of the homologous T epitopes of HCoV-229e and SARS-CoV. The identified T-cell epitope peptides were synthesized, and their binding affinities for HLA-A2 were validated and compared in the T2 cell system. The immunogenicity of all these peptides was assessed by using T cells obtained from donors who had fully recovered from SARS-CoV infection and from healthy donors with no history of SARS-CoV infection. HLA-A2 typing by indirect immunofluorescent antibody staining showed that 51.6% of SARS-CoV-infected patients were HLA-A2 positive. Online database analysis and the T2 cell binding test disclosed that the number of HLA-A2-restricted immunogenic epitopes of the S protein of SARS-CoV was decreased or even lost in comparison with the homologous sequences of the S protein of HCoV-229e. Among the peptides used in the study, the affinity of peptides from HCoV-229e (H77 and H881) and peptides from SARS-CoV (S978 and S1203) for binding to HLA-A2 was higher than that of other sequences. The gamma interferon (IFN-γ) release Elispot assay revealed that only SARS-CoV-specific peptides S1203 and S978 induced a high frequency of IFN-γ-secreting T-cell response in HLA-A2⁺ donors who had fully recovered from SARS-CoV infection; such a T-cell epitope-specific response was not observed in HLA-A2⁺ healthy donors or in HLA-A2- donors who had been infected with SARS-CoV after full recovery. Thus, T-cell epitopes S1203 and S978 are immunogenic and elicit an overt specific T-cell response in HLA-A2⁺ SARS-CoV-infected patients.
CC :	002A05C10
FD :	Coronavirus; Homme; Lymphocyte T; Déterminant antigénique; Protéine A; Immunité cellulaire; Microbiologie; Virologie; Syndrome respiratoire aigu sévère
FG :	Coronaviridae; Nidovirales; Virus; Virose; Infection; Appareil respiratoire pathologie; Poumon pathologie
ED :	Coronavirus; Human; T-Lymphocyte; Antigenic determinant; Protein A; Cellular immunity; Microbiology; Virology; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Viral disease; Infection; Respiratory disease; Lung disease
SD :	Coronavirus; Hombre; Linfocito T; Determinante antigénico; Proteína A; Inmunidad celular; Microbiología; Virología; Síndrome respiratorio agudo severo
LO :	INIST-13592.354000111993960090
ID :	04-0314703

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Le document en format XML

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<author><name sortKey="Yong Xie" sort="Yong Xie" uniqKey="Yong Xie" last="Yong Xie">YONG XIE</name>
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<author><name sortKey="Chen, Wei Feng" sort="Chen, Wei Feng" uniqKey="Chen W" first="Wei-Feng" last="Chen">Wei-Feng Chen</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">T-cell epitopes in Severe acute respiratory syndrome (SARS) coronavirus spike protein elicit a specific T-cell immune response in patients who recover from SARS</title>
<author><name sortKey="Wang, Yue Dan" sort="Wang, Yue Dan" uniqKey="Wang Y" first="Yue-Dan" last="Wang">Yue-Dan Wang</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Immunology, Peking University Health Science Centre</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>17 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Department of Biology, Hong Kong University of Science and Technology, Clear Water Bay</s1>
<s2>Kowloon</s2>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>16 aut.</sZ>
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</author>
<author><name sortKey="Sin, Wan Yee Fion" sort="Sin, Wan Yee Fion" uniqKey="Sin W" first="Wan-Yee Fion" last="Sin">Wan-Yee Fion Sin</name>
<affiliation><inist:fA14 i1="02"><s1>Department of Biology, Hong Kong University of Science and Technology, Clear Water Bay</s1>
<s2>Kowloon</s2>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Xu, Guo Bing" sort="Xu, Guo Bing" uniqKey="Xu G" first="Guo-Bing" last="Xu">Guo-Bing Xu</name>
<affiliation><inist:fA14 i1="03"><s1>First Hospital, Peking University</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>3 aut.</sZ>
<sZ>13 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Yang, Huang Hua" sort="Yang, Huang Hua" uniqKey="Yang H" first="Huang-Hua" last="Yang">Huang-Hua Yang</name>
<affiliation><inist:fA14 i1="04"><s1>Department of Chemistry, Hong Kong University of Science and Technology, Clear Water Bay</s1>
<s2>Kowloon</s2>
<s3>DNK</s3>
<sZ>4 aut.</sZ>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Wong, Tin Yau" sort="Wong, Tin Yau" uniqKey="Wong T" first="Tin-Yau" last="Wong">Tin-Yau Wong</name>
<affiliation><inist:fA14 i1="05"><s1>Princess Margaret Hospital</s1>
<s3>DNK</s3>
<sZ>5 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Pang, Xue Wen" sort="Pang, Xue Wen" uniqKey="Pang X" first="Xue-Wen" last="Pang">Xue-Wen Pang</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Immunology, Peking University Health Science Centre</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>17 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="He, Xiao Yan" sort="He, Xiao Yan" uniqKey="He X" first="Xiao-Yan" last="He">Xiao-Yan He</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Immunology, Peking University Health Science Centre</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>17 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Zhang, Hua Gang" sort="Zhang, Hua Gang" uniqKey="Zhang H" first="Hua-Gang" last="Zhang">Hua-Gang Zhang</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Immunology, Peking University Health Science Centre</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
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<author><name sortKey="Joice Na Lee Ng" sort="Joice Na Lee Ng" uniqKey="Joice Na Lee Ng" last="Joice Na Lee Ng">JOICE NA LEE NG</name>
<affiliation><inist:fA14 i1="05"><s1>Princess Margaret Hospital</s1>
<s3>DNK</s3>
<sZ>5 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Cheng, Chak Sum Samuel" sort="Cheng, Chak Sum Samuel" uniqKey="Cheng C" first="Chak-Sum Samuel" last="Cheng">Chak-Sum Samuel Cheng</name>
<affiliation><inist:fA14 i1="02"><s1>Department of Biology, Hong Kong University of Science and Technology, Clear Water Bay</s1>
<s2>Kowloon</s2>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
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</author>
<author><name sortKey="Jing Ju" sort="Jing Ju" uniqKey="Jing Ju" last="Jing Ju">JING JU</name>
<affiliation><inist:fA14 i1="02"><s1>Department of Biology, Hong Kong University of Science and Technology, Clear Water Bay</s1>
<s2>Kowloon</s2>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Li Meng" sort="Li Meng" uniqKey="Li Meng" last="Li Meng">LI MENG</name>
<affiliation><inist:fA14 i1="02"><s1>Department of Biology, Hong Kong University of Science and Technology, Clear Water Bay</s1>
<s2>Kowloon</s2>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Yang, Rui Feng" sort="Yang, Rui Feng" uniqKey="Yang R" first="Rui-Feng" last="Yang">Rui-Feng Yang</name>
<affiliation><inist:fA14 i1="03"><s1>First Hospital, Peking University</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>3 aut.</sZ>
<sZ>13 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Lai, Sik To" sort="Lai, Sik To" uniqKey="Lai S" first="Sik-To" last="Lai">Sik-To Lai</name>
<affiliation><inist:fA14 i1="05"><s1>Princess Margaret Hospital</s1>
<s3>DNK</s3>
<sZ>5 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Guo, Zhi Hong" sort="Guo, Zhi Hong" uniqKey="Guo Z" first="Zhi-Hong" last="Guo">Zhi-Hong Guo</name>
<affiliation><inist:fA14 i1="04"><s1>Department of Chemistry, Hong Kong University of Science and Technology, Clear Water Bay</s1>
<s2>Kowloon</s2>
<s3>DNK</s3>
<sZ>4 aut.</sZ>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Yong Xie" sort="Yong Xie" uniqKey="Yong Xie" last="Yong Xie">YONG XIE</name>
<affiliation><inist:fA14 i1="02"><s1>Department of Biology, Hong Kong University of Science and Technology, Clear Water Bay</s1>
<s2>Kowloon</s2>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chen, Wei Feng" sort="Chen, Wei Feng" uniqKey="Chen W" first="Wei-Feng" last="Chen">Wei-Feng Chen</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Immunology, Peking University Health Science Centre</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>17 aut.</sZ>
</inist:fA14>
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</author>
</analytic>
<series><title level="j" type="main">Journal of virology</title>
<title level="j" type="abbreviated">J. virol.</title>
<idno type="ISSN">0022-538X</idno>
<imprint><date when="2004">2004</date>
</imprint>
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<seriesStmt><title level="j" type="main">Journal of virology</title>
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<idno type="ISSN">0022-538X</idno>
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</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigenic determinant</term>
<term>Cellular immunity</term>
<term>Coronavirus</term>
<term>Human</term>
<term>Microbiology</term>
<term>Protein A</term>
<term>Severe acute respiratory syndrome</term>
<term>T-Lymphocyte</term>
<term>Virology</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Coronavirus</term>
<term>Homme</term>
<term>Lymphocyte T</term>
<term>Déterminant antigénique</term>
<term>Protéine A</term>
<term>Immunité cellulaire</term>
<term>Microbiologie</term>
<term>Virologie</term>
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<front><div type="abstract" xml:lang="en">The immunogenicity of HLA-A2-restricted T-cell epitopes in the S protein of the Severe acute respiratory syndrome coronavirus (SARS-CoV) and of human coronavirus strain 229e (HCoV-229e) was analyzed for the elicitation of a T-cell immune response in donors who had fully recovered from SARS-CoV infection. We employed online database analysis to compare the differences in the amino acid sequences of the homologous T epitopes of HCoV-229e and SARS-CoV. The identified T-cell epitope peptides were synthesized, and their binding affinities for HLA-A2 were validated and compared in the T2 cell system. The immunogenicity of all these peptides was assessed by using T cells obtained from donors who had fully recovered from SARS-CoV infection and from healthy donors with no history of SARS-CoV infection. HLA-A2 typing by indirect immunofluorescent antibody staining showed that 51.6% of SARS-CoV-infected patients were HLA-A2 positive. Online database analysis and the T2 cell binding test disclosed that the number of HLA-A2-restricted immunogenic epitopes of the S protein of SARS-CoV was decreased or even lost in comparison with the homologous sequences of the S protein of HCoV-229e. Among the peptides used in the study, the affinity of peptides from HCoV-229e (H77 and H881) and peptides from SARS-CoV (S978 and S1203) for binding to HLA-A2 was higher than that of other sequences. The gamma interferon (IFN-γ) release Elispot assay revealed that only SARS-CoV-specific peptides S1203 and S978 induced a high frequency of IFN-γ-secreting T-cell response in HLA-A2<sup>+</sup>
 donors who had fully recovered from SARS-CoV infection; such a T-cell epitope-specific response was not observed in HLA-A2<sup>+</sup>
 healthy donors or in HLA-A2- donors who had been infected with SARS-CoV after full recovery. Thus, T-cell epitopes S1203 and S978 are immunogenic and elicit an overt specific T-cell response in HLA-A2<sup>+</sup>
 SARS-CoV-infected patients.</div>
</front>
</TEI>
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<fA06><s2>11</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>T-cell epitopes in Severe acute respiratory syndrome (SARS) coronavirus spike protein elicit a specific T-cell immune response in patients who recover from SARS</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>WANG (Yue-Dan)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>SIN (Wan-Yee Fion)</s1>
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<fA11 i1="03" i2="1"><s1>XU (Guo-Bing)</s1>
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<fA11 i1="04" i2="1"><s1>YANG (Huang-Hua)</s1>
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<fA11 i1="05" i2="1"><s1>WONG (Tin-Yau)</s1>
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<fA11 i1="06" i2="1"><s1>PANG (Xue-Wen)</s1>
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<fA11 i1="09" i2="1"><s1>JOICE NA LEE NG</s1>
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<fA11 i1="10" i2="1"><s1>CHENG (Chak-Sum Samuel)</s1>
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<fA11 i1="11" i2="1"><s1>JING JU</s1>
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<fA11 i1="12" i2="1"><s1>LI MENG</s1>
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<fA11 i1="13" i2="1"><s1>YANG (Rui-Feng)</s1>
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<fA11 i1="14" i2="1"><s1>LAI (Sik-To)</s1>
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<fA11 i1="15" i2="1"><s1>GUO (Zhi-Hong)</s1>
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<fA11 i1="17" i2="1"><s1>CHEN (Wei-Feng)</s1>
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<fA14 i1="01"><s1>Department of Immunology, Peking University Health Science Centre</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>17 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Biology, Hong Kong University of Science and Technology, Clear Water Bay</s1>
<s2>Kowloon</s2>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>16 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>First Hospital, Peking University</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>3 aut.</sZ>
<sZ>13 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Chemistry, Hong Kong University of Science and Technology, Clear Water Bay</s1>
<s2>Kowloon</s2>
<s3>DNK</s3>
<sZ>4 aut.</sZ>
<sZ>15 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Princess Margaret Hospital</s1>
<s3>DNK</s3>
<sZ>5 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>14 aut.</sZ>
</fA14>
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<fA60><s1>P</s1>
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<fC01 i1="01" l="ENG"><s0>The immunogenicity of HLA-A2-restricted T-cell epitopes in the S protein of the Severe acute respiratory syndrome coronavirus (SARS-CoV) and of human coronavirus strain 229e (HCoV-229e) was analyzed for the elicitation of a T-cell immune response in donors who had fully recovered from SARS-CoV infection. We employed online database analysis to compare the differences in the amino acid sequences of the homologous T epitopes of HCoV-229e and SARS-CoV. The identified T-cell epitope peptides were synthesized, and their binding affinities for HLA-A2 were validated and compared in the T2 cell system. The immunogenicity of all these peptides was assessed by using T cells obtained from donors who had fully recovered from SARS-CoV infection and from healthy donors with no history of SARS-CoV infection. HLA-A2 typing by indirect immunofluorescent antibody staining showed that 51.6% of SARS-CoV-infected patients were HLA-A2 positive. Online database analysis and the T2 cell binding test disclosed that the number of HLA-A2-restricted immunogenic epitopes of the S protein of SARS-CoV was decreased or even lost in comparison with the homologous sequences of the S protein of HCoV-229e. Among the peptides used in the study, the affinity of peptides from HCoV-229e (H77 and H881) and peptides from SARS-CoV (S978 and S1203) for binding to HLA-A2 was higher than that of other sequences. The gamma interferon (IFN-γ) release Elispot assay revealed that only SARS-CoV-specific peptides S1203 and S978 induced a high frequency of IFN-γ-secreting T-cell response in HLA-A2<sup>+</sup>
 donors who had fully recovered from SARS-CoV infection; such a T-cell epitope-specific response was not observed in HLA-A2<sup>+</sup>
 healthy donors or in HLA-A2- donors who had been infected with SARS-CoV after full recovery. Thus, T-cell epitopes S1203 and S978 are immunogenic and elicit an overt specific T-cell response in HLA-A2<sup>+</sup>
 SARS-CoV-infected patients.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A05C10</s0>
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<s2>NW</s2>
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<s2>NM</s2>
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<s2>NM</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Infection</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Infection</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Infección</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0>
<s5>19</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>19</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>19</s5>
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<fC07 i1="07" i2="X" l="FRE"><s0>Poumon pathologie</s0>
<s5>20</s5>
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<s5>20</s5>
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<fC07 i1="07" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>20</s5>
</fC07>
<fN21><s1>187</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
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<fN82><s1>OTO</s1>
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<server><NO>PASCAL 04-0314703 INIST</NO>
<ET>T-cell epitopes in Severe acute respiratory syndrome (SARS) coronavirus spike protein elicit a specific T-cell immune response in patients who recover from SARS</ET>
<AU>WANG (Yue-Dan); SIN (Wan-Yee Fion); XU (Guo-Bing); YANG (Huang-Hua); WONG (Tin-Yau); PANG (Xue-Wen); HE (Xiao-Yan); ZHANG (Hua-Gang); JOICE NA LEE NG; CHENG (Chak-Sum Samuel); JING JU; LI MENG; YANG (Rui-Feng); LAI (Sik-To); GUO (Zhi-Hong); YONG XIE; CHEN (Wei-Feng)</AU>
<AF>Department of Immunology, Peking University Health Science Centre/Beijing/Chine (1 aut., 6 aut., 7 aut., 8 aut., 17 aut.); Department of Biology, Hong Kong University of Science and Technology, Clear Water Bay/Kowloon/Hong-Kong (1 aut., 2 aut., 10 aut., 11 aut., 12 aut., 16 aut.); First Hospital, Peking University/Beijing/Chine (3 aut., 13 aut.); Department of Chemistry, Hong Kong University of Science and Technology, Clear Water Bay/Kowloon/Danemark (4 aut., 15 aut.); Princess Margaret Hospital/Danemark (5 aut., 9 aut., 14 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2004; Vol. 78; No. 11; Pp. 5612-5618; Bibl. 31 ref.</SO>
<LA>Anglais</LA>
<EA>The immunogenicity of HLA-A2-restricted T-cell epitopes in the S protein of the Severe acute respiratory syndrome coronavirus (SARS-CoV) and of human coronavirus strain 229e (HCoV-229e) was analyzed for the elicitation of a T-cell immune response in donors who had fully recovered from SARS-CoV infection. We employed online database analysis to compare the differences in the amino acid sequences of the homologous T epitopes of HCoV-229e and SARS-CoV. The identified T-cell epitope peptides were synthesized, and their binding affinities for HLA-A2 were validated and compared in the T2 cell system. The immunogenicity of all these peptides was assessed by using T cells obtained from donors who had fully recovered from SARS-CoV infection and from healthy donors with no history of SARS-CoV infection. HLA-A2 typing by indirect immunofluorescent antibody staining showed that 51.6% of SARS-CoV-infected patients were HLA-A2 positive. Online database analysis and the T2 cell binding test disclosed that the number of HLA-A2-restricted immunogenic epitopes of the S protein of SARS-CoV was decreased or even lost in comparison with the homologous sequences of the S protein of HCoV-229e. Among the peptides used in the study, the affinity of peptides from HCoV-229e (H77 and H881) and peptides from SARS-CoV (S978 and S1203) for binding to HLA-A2 was higher than that of other sequences. The gamma interferon (IFN-γ) release Elispot assay revealed that only SARS-CoV-specific peptides S1203 and S978 induced a high frequency of IFN-γ-secreting T-cell response in HLA-A2<sup>+</sup>
 donors who had fully recovered from SARS-CoV infection; such a T-cell epitope-specific response was not observed in HLA-A2<sup>+</sup>
 healthy donors or in HLA-A2- donors who had been infected with SARS-CoV after full recovery. Thus, T-cell epitopes S1203 and S978 are immunogenic and elicit an overt specific T-cell response in HLA-A2<sup>+</sup>
 SARS-CoV-infected patients.</EA>
<CC>002A05C10</CC>
<FD>Coronavirus; Homme; Lymphocyte T; Déterminant antigénique; Protéine A; Immunité cellulaire; Microbiologie; Virologie; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Virose; Infection; Appareil respiratoire pathologie; Poumon pathologie</FG>
<ED>Coronavirus; Human; T-Lymphocyte; Antigenic determinant; Protein A; Cellular immunity; Microbiology; Virology; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Viral disease; Infection; Respiratory disease; Lung disease</EG>
<SD>Coronavirus; Hombre; Linfocito T; Determinante antigénico; Proteína A; Inmunidad celular; Microbiología; Virología; Síndrome respiratorio agudo severo</SD>
<LO>INIST-13592.354000111993960090</LO>
<ID>04-0314703</ID>
</server>
</inist>
</record>

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T-cell epitopes in Severe acute respiratory syndrome (SARS) coronavirus spike protein elicit a specific T-cell immune response in patients who recover from SARS

T-cell epitopes in Severe acute respiratory syndrome (SARS) coronavirus spike protein elicit a specific T-cell immune response in patients who recover from SARS

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