Loading…
Gene–environment interactions: Epstein–Barr virus infection and risk of pediatric-onset multiple sclerosis
Background and Objective: Prior Epstein–Barr virus (EBV) infection is associated with an increased risk of pediatric-onset multiple sclerosis (POMS) and adult-onset multiple sclerosis (MS). It has been challenging to elucidate the biological mechanisms underlying this association. We examined the in...
Saved in:
| Published in: | Multiple sclerosis 2024-03, Vol.30 (3), p.308-315 |
|---|---|
| Main Authors: | , , , , , , , , , , , , , , , , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | |
|---|---|
| cites | cdi_FETCH-LOGICAL-c419t-236603b0c5f3614aec112d7249879a1d77ffbe745f3837359ceec9b36b06e5f83 |
| container_end_page | 315 |
| container_issue | 3 |
| container_start_page | 308 |
| container_title | Multiple sclerosis |
| container_volume | 30 |
| creator | Ziaei, Amin Solomon, Olivia Casper, T Charles Waltz, Michael Weinstock-Guttman, Bianca Aaen, Greg Wheeler, Yolanda Graves, Jennifer Benson, Leslie Gorman, Mark Rensel, Mary Mar, Soe Lotze, Tim Greenberg, Benjamin Chitnis, Tanuja Waldman, Amy T Krupp, Lauren James, Judith A Hart, Janace Barcellos, Lisa F Waubant, Emmanuelle |
| description | Background and Objective:
Prior Epstein–Barr virus (EBV) infection is associated with an increased risk of pediatric-onset multiple sclerosis (POMS) and adult-onset multiple sclerosis (MS). It has been challenging to elucidate the biological mechanisms underlying this association. We examined the interactions between candidate human leukocyte antigen (HLA) and non-HLA variants and childhood EBV infection as it may provide mechanistic insights into EBV-associated MS.
Methods:
Cases and controls were enrolled in the Environmental and Genetic Risk Factors for Pediatric MS study of the US Network of Pediatric MS Centers. Participants were categorized as seropositive and seronegative for EBV-viral capsid antigen (VCA). The association between prior EBV infection and having POMS was estimated with logistic regression. Interactions between EBV serostatus, major HLA MS risk factors, and non-HLA POMS risk variants associated with response to EBV infection were also evaluated with logistic regression. Models were adjusted for sex, age, genetic ancestry, and the mother’s education. Additive interactions were calculated using relative risk due to interaction (RERI) and attributable proportions (APs).
Results:
A total of 473 POMS cases and 702 controls contributed to the analyses. Anti-VCA seropositivity was significantly higher in POMS cases compared to controls (94.6% vs 60.7%, p |
| doi_str_mv | 10.1177/13524585231224685 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11093131</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1177_13524585231224685</sage_id><sourcerecordid>2956070431</sourcerecordid><originalsourceid>FETCH-LOGICAL-c419t-236603b0c5f3614aec112d7249879a1d77ffbe745f3837359ceec9b36b06e5f83</originalsourceid><addsrcrecordid>eNp1kc9OFTEUxhsjEbj6AG5IEzdsBvp3OsPGIEE0IXGj66bTOYPFmXZoOyTueAff0Ceh3IsoENNFm3y_851-5yD0lpIDSpU6pFwyIRvJOGVM1I18gXaoUKoirSIvy7vo1R2wjXZTuiSEKMXlK7TNG86ZEmoH-TPw8PvmF_hrF4OfwGfsfIZobHbBpyN8OqcMzhfmg4kRF2xJBRlgDWDjexxd-oHDgGfoncnR2apUQsbTMmY3j4CTHSGG5NJrtDWYMcGb-3uFvn08_XryqTr_cvb55Pi8soK2uWK8rgnviJUDr6kwYCllvWKibVRraK_UMHSgRJEbXiK1FsC2Ha87UoMcGr5C7ze-89JN0NsSK5pRz9FNJv7UwTj9WPHuu74I15pS0nJazgrt3zvEcLVAynpyycI4Gg9hSZq1TJL1EAv67gl6GZboS75CyZooItaGdEPZMokUYXj4DSX6bp362TpLzd6_MR4q_uyvAAcbIJkL-Nv2_463utCrrA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2956070431</pqid></control><display><type>article</type><title>Gene–environment interactions: Epstein–Barr virus infection and risk of pediatric-onset multiple sclerosis</title><source>Sage Journals Online</source><creator>Ziaei, Amin ; Solomon, Olivia ; Casper, T Charles ; Waltz, Michael ; Weinstock-Guttman, Bianca ; Aaen, Greg ; Wheeler, Yolanda ; Graves, Jennifer ; Benson, Leslie ; Gorman, Mark ; Rensel, Mary ; Mar, Soe ; Lotze, Tim ; Greenberg, Benjamin ; Chitnis, Tanuja ; Waldman, Amy T ; Krupp, Lauren ; James, Judith A ; Hart, Janace ; Barcellos, Lisa F ; Waubant, Emmanuelle</creator><creatorcontrib>Ziaei, Amin ; Solomon, Olivia ; Casper, T Charles ; Waltz, Michael ; Weinstock-Guttman, Bianca ; Aaen, Greg ; Wheeler, Yolanda ; Graves, Jennifer ; Benson, Leslie ; Gorman, Mark ; Rensel, Mary ; Mar, Soe ; Lotze, Tim ; Greenberg, Benjamin ; Chitnis, Tanuja ; Waldman, Amy T ; Krupp, Lauren ; James, Judith A ; Hart, Janace ; Barcellos, Lisa F ; Waubant, Emmanuelle</creatorcontrib><description>Background and Objective:
Prior Epstein–Barr virus (EBV) infection is associated with an increased risk of pediatric-onset multiple sclerosis (POMS) and adult-onset multiple sclerosis (MS). It has been challenging to elucidate the biological mechanisms underlying this association. We examined the interactions between candidate human leukocyte antigen (HLA) and non-HLA variants and childhood EBV infection as it may provide mechanistic insights into EBV-associated MS.
Methods:
Cases and controls were enrolled in the Environmental and Genetic Risk Factors for Pediatric MS study of the US Network of Pediatric MS Centers. Participants were categorized as seropositive and seronegative for EBV-viral capsid antigen (VCA). The association between prior EBV infection and having POMS was estimated with logistic regression. Interactions between EBV serostatus, major HLA MS risk factors, and non-HLA POMS risk variants associated with response to EBV infection were also evaluated with logistic regression. Models were adjusted for sex, age, genetic ancestry, and the mother’s education. Additive interactions were calculated using relative risk due to interaction (RERI) and attributable proportions (APs).
Results:
A total of 473 POMS cases and 702 controls contributed to the analyses. Anti-VCA seropositivity was significantly higher in POMS cases compared to controls (94.6% vs 60.7%, p < 0.001). There was evidence for additive interaction between childhood EBV infection and the presence of the HLA-DRB1*15 allele (RERI = 10.25, 95% confidence interval (CI) = 3.78 to 16.72; AP = 0.61, 95% CI = 0.47 to 0.75). There was evidence for multiplicative interaction (p < 0.05) between childhood EBV infection and the presence of DRB1*15 alleles (odds ratio (OR) = 3.43, 95% CI = 1.06 to 11.07). Among the pediatric MS variants also associated with EBV infection, we detected evidence for additive interaction (p = 0.02) between prior EBV infection and the presence of the GG genotype in risk variant (rs2255214) within CD86 (AP = 0.30, 95% CI = 0.03 to 0.58).
Conclusion:
We report evidence for interactions between childhood EBV infection and DRB1*15 and the GG genotype of CD86 POMS risk variant. Our results suggest an important role of antigen-presenting cells (APCs) in EBV-associated POMS risk.</description><identifier>ISSN: 1352-4585</identifier><identifier>EISSN: 1477-0970</identifier><identifier>DOI: 10.1177/13524585231224685</identifier><identifier>PMID: 38332747</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Adult ; Alleles ; Antibodies ; Antigen-presenting cells ; Antigens ; CD86 antigen ; Child ; Children ; Drb1 protein ; Epstein-Barr virus ; Epstein-Barr Virus Infections - complications ; Genotypes ; Herpesvirus 4, Human ; Histocompatibility antigen HLA ; HLA-DRB1 Chains - genetics ; Humans ; Infections ; Multiple Sclerosis ; Pediatrics ; Regression analysis ; Risk Factors</subject><ispartof>Multiple sclerosis, 2024-03, Vol.30 (3), p.308-315</ispartof><rights>The Author(s), 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c419t-236603b0c5f3614aec112d7249879a1d77ffbe745f3837359ceec9b36b06e5f83</cites><orcidid>0000-0001-7003-807X ; 0000-0002-2091-8201 ; 0000-0002-9897-4422 ; 0000-0001-9613-8394 ; 0000-0001-6732-151X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925,79364</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38332747$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ziaei, Amin</creatorcontrib><creatorcontrib>Solomon, Olivia</creatorcontrib><creatorcontrib>Casper, T Charles</creatorcontrib><creatorcontrib>Waltz, Michael</creatorcontrib><creatorcontrib>Weinstock-Guttman, Bianca</creatorcontrib><creatorcontrib>Aaen, Greg</creatorcontrib><creatorcontrib>Wheeler, Yolanda</creatorcontrib><creatorcontrib>Graves, Jennifer</creatorcontrib><creatorcontrib>Benson, Leslie</creatorcontrib><creatorcontrib>Gorman, Mark</creatorcontrib><creatorcontrib>Rensel, Mary</creatorcontrib><creatorcontrib>Mar, Soe</creatorcontrib><creatorcontrib>Lotze, Tim</creatorcontrib><creatorcontrib>Greenberg, Benjamin</creatorcontrib><creatorcontrib>Chitnis, Tanuja</creatorcontrib><creatorcontrib>Waldman, Amy T</creatorcontrib><creatorcontrib>Krupp, Lauren</creatorcontrib><creatorcontrib>James, Judith A</creatorcontrib><creatorcontrib>Hart, Janace</creatorcontrib><creatorcontrib>Barcellos, Lisa F</creatorcontrib><creatorcontrib>Waubant, Emmanuelle</creatorcontrib><title>Gene–environment interactions: Epstein–Barr virus infection and risk of pediatric-onset multiple sclerosis</title><title>Multiple sclerosis</title><addtitle>Mult Scler</addtitle><description>Background and Objective:
Prior Epstein–Barr virus (EBV) infection is associated with an increased risk of pediatric-onset multiple sclerosis (POMS) and adult-onset multiple sclerosis (MS). It has been challenging to elucidate the biological mechanisms underlying this association. We examined the interactions between candidate human leukocyte antigen (HLA) and non-HLA variants and childhood EBV infection as it may provide mechanistic insights into EBV-associated MS.
Methods:
Cases and controls were enrolled in the Environmental and Genetic Risk Factors for Pediatric MS study of the US Network of Pediatric MS Centers. Participants were categorized as seropositive and seronegative for EBV-viral capsid antigen (VCA). The association between prior EBV infection and having POMS was estimated with logistic regression. Interactions between EBV serostatus, major HLA MS risk factors, and non-HLA POMS risk variants associated with response to EBV infection were also evaluated with logistic regression. Models were adjusted for sex, age, genetic ancestry, and the mother’s education. Additive interactions were calculated using relative risk due to interaction (RERI) and attributable proportions (APs).
Results:
A total of 473 POMS cases and 702 controls contributed to the analyses. Anti-VCA seropositivity was significantly higher in POMS cases compared to controls (94.6% vs 60.7%, p < 0.001). There was evidence for additive interaction between childhood EBV infection and the presence of the HLA-DRB1*15 allele (RERI = 10.25, 95% confidence interval (CI) = 3.78 to 16.72; AP = 0.61, 95% CI = 0.47 to 0.75). There was evidence for multiplicative interaction (p < 0.05) between childhood EBV infection and the presence of DRB1*15 alleles (odds ratio (OR) = 3.43, 95% CI = 1.06 to 11.07). Among the pediatric MS variants also associated with EBV infection, we detected evidence for additive interaction (p = 0.02) between prior EBV infection and the presence of the GG genotype in risk variant (rs2255214) within CD86 (AP = 0.30, 95% CI = 0.03 to 0.58).
Conclusion:
We report evidence for interactions between childhood EBV infection and DRB1*15 and the GG genotype of CD86 POMS risk variant. Our results suggest an important role of antigen-presenting cells (APCs) in EBV-associated POMS risk.</description><subject>Adult</subject><subject>Alleles</subject><subject>Antibodies</subject><subject>Antigen-presenting cells</subject><subject>Antigens</subject><subject>CD86 antigen</subject><subject>Child</subject><subject>Children</subject><subject>Drb1 protein</subject><subject>Epstein-Barr virus</subject><subject>Epstein-Barr Virus Infections - complications</subject><subject>Genotypes</subject><subject>Herpesvirus 4, Human</subject><subject>Histocompatibility antigen HLA</subject><subject>HLA-DRB1 Chains - genetics</subject><subject>Humans</subject><subject>Infections</subject><subject>Multiple Sclerosis</subject><subject>Pediatrics</subject><subject>Regression analysis</subject><subject>Risk Factors</subject><issn>1352-4585</issn><issn>1477-0970</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp1kc9OFTEUxhsjEbj6AG5IEzdsBvp3OsPGIEE0IXGj66bTOYPFmXZoOyTueAff0Ceh3IsoENNFm3y_851-5yD0lpIDSpU6pFwyIRvJOGVM1I18gXaoUKoirSIvy7vo1R2wjXZTuiSEKMXlK7TNG86ZEmoH-TPw8PvmF_hrF4OfwGfsfIZobHbBpyN8OqcMzhfmg4kRF2xJBRlgDWDjexxd-oHDgGfoncnR2apUQsbTMmY3j4CTHSGG5NJrtDWYMcGb-3uFvn08_XryqTr_cvb55Pi8soK2uWK8rgnviJUDr6kwYCllvWKibVRraK_UMHSgRJEbXiK1FsC2Ha87UoMcGr5C7ze-89JN0NsSK5pRz9FNJv7UwTj9WPHuu74I15pS0nJazgrt3zvEcLVAynpyycI4Gg9hSZq1TJL1EAv67gl6GZboS75CyZooItaGdEPZMokUYXj4DSX6bp362TpLzd6_MR4q_uyvAAcbIJkL-Nv2_463utCrrA</recordid><startdate>20240301</startdate><enddate>20240301</enddate><creator>Ziaei, Amin</creator><creator>Solomon, Olivia</creator><creator>Casper, T Charles</creator><creator>Waltz, Michael</creator><creator>Weinstock-Guttman, Bianca</creator><creator>Aaen, Greg</creator><creator>Wheeler, Yolanda</creator><creator>Graves, Jennifer</creator><creator>Benson, Leslie</creator><creator>Gorman, Mark</creator><creator>Rensel, Mary</creator><creator>Mar, Soe</creator><creator>Lotze, Tim</creator><creator>Greenberg, Benjamin</creator><creator>Chitnis, Tanuja</creator><creator>Waldman, Amy T</creator><creator>Krupp, Lauren</creator><creator>James, Judith A</creator><creator>Hart, Janace</creator><creator>Barcellos, Lisa F</creator><creator>Waubant, Emmanuelle</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7003-807X</orcidid><orcidid>https://orcid.org/0000-0002-2091-8201</orcidid><orcidid>https://orcid.org/0000-0002-9897-4422</orcidid><orcidid>https://orcid.org/0000-0001-9613-8394</orcidid><orcidid>https://orcid.org/0000-0001-6732-151X</orcidid></search><sort><creationdate>20240301</creationdate><title>Gene–environment interactions: Epstein–Barr virus infection and risk of pediatric-onset multiple sclerosis</title><author>Ziaei, Amin ; Solomon, Olivia ; Casper, T Charles ; Waltz, Michael ; Weinstock-Guttman, Bianca ; Aaen, Greg ; Wheeler, Yolanda ; Graves, Jennifer ; Benson, Leslie ; Gorman, Mark ; Rensel, Mary ; Mar, Soe ; Lotze, Tim ; Greenberg, Benjamin ; Chitnis, Tanuja ; Waldman, Amy T ; Krupp, Lauren ; James, Judith A ; Hart, Janace ; Barcellos, Lisa F ; Waubant, Emmanuelle</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-236603b0c5f3614aec112d7249879a1d77ffbe745f3837359ceec9b36b06e5f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adult</topic><topic>Alleles</topic><topic>Antibodies</topic><topic>Antigen-presenting cells</topic><topic>Antigens</topic><topic>CD86 antigen</topic><topic>Child</topic><topic>Children</topic><topic>Drb1 protein</topic><topic>Epstein-Barr virus</topic><topic>Epstein-Barr Virus Infections - complications</topic><topic>Genotypes</topic><topic>Herpesvirus 4, Human</topic><topic>Histocompatibility antigen HLA</topic><topic>HLA-DRB1 Chains - genetics</topic><topic>Humans</topic><topic>Infections</topic><topic>Multiple Sclerosis</topic><topic>Pediatrics</topic><topic>Regression analysis</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ziaei, Amin</creatorcontrib><creatorcontrib>Solomon, Olivia</creatorcontrib><creatorcontrib>Casper, T Charles</creatorcontrib><creatorcontrib>Waltz, Michael</creatorcontrib><creatorcontrib>Weinstock-Guttman, Bianca</creatorcontrib><creatorcontrib>Aaen, Greg</creatorcontrib><creatorcontrib>Wheeler, Yolanda</creatorcontrib><creatorcontrib>Graves, Jennifer</creatorcontrib><creatorcontrib>Benson, Leslie</creatorcontrib><creatorcontrib>Gorman, Mark</creatorcontrib><creatorcontrib>Rensel, Mary</creatorcontrib><creatorcontrib>Mar, Soe</creatorcontrib><creatorcontrib>Lotze, Tim</creatorcontrib><creatorcontrib>Greenberg, Benjamin</creatorcontrib><creatorcontrib>Chitnis, Tanuja</creatorcontrib><creatorcontrib>Waldman, Amy T</creatorcontrib><creatorcontrib>Krupp, Lauren</creatorcontrib><creatorcontrib>James, Judith A</creatorcontrib><creatorcontrib>Hart, Janace</creatorcontrib><creatorcontrib>Barcellos, Lisa F</creatorcontrib><creatorcontrib>Waubant, Emmanuelle</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Multiple sclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ziaei, Amin</au><au>Solomon, Olivia</au><au>Casper, T Charles</au><au>Waltz, Michael</au><au>Weinstock-Guttman, Bianca</au><au>Aaen, Greg</au><au>Wheeler, Yolanda</au><au>Graves, Jennifer</au><au>Benson, Leslie</au><au>Gorman, Mark</au><au>Rensel, Mary</au><au>Mar, Soe</au><au>Lotze, Tim</au><au>Greenberg, Benjamin</au><au>Chitnis, Tanuja</au><au>Waldman, Amy T</au><au>Krupp, Lauren</au><au>James, Judith A</au><au>Hart, Janace</au><au>Barcellos, Lisa F</au><au>Waubant, Emmanuelle</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gene–environment interactions: Epstein–Barr virus infection and risk of pediatric-onset multiple sclerosis</atitle><jtitle>Multiple sclerosis</jtitle><addtitle>Mult Scler</addtitle><date>2024-03-01</date><risdate>2024</risdate><volume>30</volume><issue>3</issue><spage>308</spage><epage>315</epage><pages>308-315</pages><issn>1352-4585</issn><eissn>1477-0970</eissn><abstract>Background and Objective:
Prior Epstein–Barr virus (EBV) infection is associated with an increased risk of pediatric-onset multiple sclerosis (POMS) and adult-onset multiple sclerosis (MS). It has been challenging to elucidate the biological mechanisms underlying this association. We examined the interactions between candidate human leukocyte antigen (HLA) and non-HLA variants and childhood EBV infection as it may provide mechanistic insights into EBV-associated MS.
Methods:
Cases and controls were enrolled in the Environmental and Genetic Risk Factors for Pediatric MS study of the US Network of Pediatric MS Centers. Participants were categorized as seropositive and seronegative for EBV-viral capsid antigen (VCA). The association between prior EBV infection and having POMS was estimated with logistic regression. Interactions between EBV serostatus, major HLA MS risk factors, and non-HLA POMS risk variants associated with response to EBV infection were also evaluated with logistic regression. Models were adjusted for sex, age, genetic ancestry, and the mother’s education. Additive interactions were calculated using relative risk due to interaction (RERI) and attributable proportions (APs).
Results:
A total of 473 POMS cases and 702 controls contributed to the analyses. Anti-VCA seropositivity was significantly higher in POMS cases compared to controls (94.6% vs 60.7%, p < 0.001). There was evidence for additive interaction between childhood EBV infection and the presence of the HLA-DRB1*15 allele (RERI = 10.25, 95% confidence interval (CI) = 3.78 to 16.72; AP = 0.61, 95% CI = 0.47 to 0.75). There was evidence for multiplicative interaction (p < 0.05) between childhood EBV infection and the presence of DRB1*15 alleles (odds ratio (OR) = 3.43, 95% CI = 1.06 to 11.07). Among the pediatric MS variants also associated with EBV infection, we detected evidence for additive interaction (p = 0.02) between prior EBV infection and the presence of the GG genotype in risk variant (rs2255214) within CD86 (AP = 0.30, 95% CI = 0.03 to 0.58).
Conclusion:
We report evidence for interactions between childhood EBV infection and DRB1*15 and the GG genotype of CD86 POMS risk variant. Our results suggest an important role of antigen-presenting cells (APCs) in EBV-associated POMS risk.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>38332747</pmid><doi>10.1177/13524585231224685</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-7003-807X</orcidid><orcidid>https://orcid.org/0000-0002-2091-8201</orcidid><orcidid>https://orcid.org/0000-0002-9897-4422</orcidid><orcidid>https://orcid.org/0000-0001-9613-8394</orcidid><orcidid>https://orcid.org/0000-0001-6732-151X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1352-4585 |
| ispartof | Multiple sclerosis, 2024-03, Vol.30 (3), p.308-315 |
| issn | 1352-4585 1477-0970 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11093131 |
| source | Sage Journals Online |
| subjects | Adult Alleles Antibodies Antigen-presenting cells Antigens CD86 antigen Child Children Drb1 protein Epstein-Barr virus Epstein-Barr Virus Infections - complications Genotypes Herpesvirus 4, Human Histocompatibility antigen HLA HLA-DRB1 Chains - genetics Humans Infections Multiple Sclerosis Pediatrics Regression analysis Risk Factors |
| title | Gene–environment interactions: Epstein–Barr virus infection and risk of pediatric-onset multiple sclerosis |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-30T20%3A31%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Gene%E2%80%93environment%20interactions:%20Epstein%E2%80%93Barr%20virus%20infection%20and%20risk%20of%20pediatric-onset%20multiple%20sclerosis&rft.jtitle=Multiple%20sclerosis&rft.au=Ziaei,%20Amin&rft.date=2024-03-01&rft.volume=30&rft.issue=3&rft.spage=308&rft.epage=315&rft.pages=308-315&rft.issn=1352-4585&rft.eissn=1477-0970&rft_id=info:doi/10.1177/13524585231224685&rft_dat=%3Cproquest_pubme%3E2956070431%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c419t-236603b0c5f3614aec112d7249879a1d77ffbe745f3837359ceec9b36b06e5f83%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2956070431&rft_id=info:pmid/38332747&rft_sage_id=10.1177_13524585231224685&rfr_iscdi=true |