Cytomegalovirus infection in early infancy: risk of induction and progression of autoimmunity associated with type 1 diabetes
Aims/hypothesis Type 1 diabetes is an autoimmune disease resulting from a complex interplay between genetic and environmental factors. Cytomegalovirus (CMV) infection is one of the environmental factors implicated in the development of type 1 diabetes, although the association remains unproven. We a...
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| Veröffentlicht in: | Diabetologia 2008-05, Vol.51 (5), p.769-772 |
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| creator | Aarnisalo, J Veijola, R Vainionpää, R Simell, O Knip, M Ilonen, J |
| description | Aims/hypothesis Type 1 diabetes is an autoimmune disease resulting from a complex interplay between genetic and environmental factors. Cytomegalovirus (CMV) infection is one of the environmental factors implicated in the development of type 1 diabetes, although the association remains unproven. We aimed to clarify the possible correlation between CMV infections and type 1 diabetes-associated autoimmunity at the time point of autoantibody appearance in young children with HLA-conferred disease susceptibility. Methods CMV-specific IgG antibodies were analysed from serum samples of 169 children who had developed the first type 1 diabetes-associated autoantibody by the age of 2 years and who turned positive for multiple autoantibodies during later follow-up. We also studied 791 control children matched for sex, age and HLA genotype. The subsequent progression to clinical diabetes was analysed. The serum specimens used were collected at the time of autoantibody seroconversion or within the next 6 months. Results The frequency of CMV antibodies was similar in both study groups at the time of the first autoantibody appearance. Of the index children, 38 (22.5%) were CMV IgG antibody-positive, while the figure for control children was 206 (26.0%; p = 0.38). No association between perinatal CMV infection and progression to type 1 diabetes was observed. Conclusions/interpretation According to these results, perinatal CMV infections are not associated with early serological signs of beta cell autoimmunity or progression to type 1 diabetes in children with diabetes risk-associated HLA genotype. |
| doi_str_mv | 10.1007/s00125-008-0945-8 |
| format | Article |
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Cytomegalovirus (CMV) infection is one of the environmental factors implicated in the development of type 1 diabetes, although the association remains unproven. We aimed to clarify the possible correlation between CMV infections and type 1 diabetes-associated autoimmunity at the time point of autoantibody appearance in young children with HLA-conferred disease susceptibility. Methods CMV-specific IgG antibodies were analysed from serum samples of 169 children who had developed the first type 1 diabetes-associated autoantibody by the age of 2 years and who turned positive for multiple autoantibodies during later follow-up. We also studied 791 control children matched for sex, age and HLA genotype. The subsequent progression to clinical diabetes was analysed. The serum specimens used were collected at the time of autoantibody seroconversion or within the next 6 months. Results The frequency of CMV antibodies was similar in both study groups at the time of the first autoantibody appearance. Of the index children, 38 (22.5%) were CMV IgG antibody-positive, while the figure for control children was 206 (26.0%; p = 0.38). No association between perinatal CMV infection and progression to type 1 diabetes was observed. Conclusions/interpretation According to these results, perinatal CMV infections are not associated with early serological signs of beta cell autoimmunity or progression to type 1 diabetes in children with diabetes risk-associated HLA genotype.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-008-0945-8</identifier><identifier>PMID: 18278478</identifier><language>eng</language><publisher>Berlin/Heidelberg: Berlin/Heidelberg : Springer-Verlag</publisher><subject>Age ; Antibodies ; Antibodies, Viral - blood ; autoantibodies ; Autoimmune Diseases - epidemiology ; Autoimmune Diseases - virology ; Beta cell autoimmunity ; Biological and medical sciences ; Child ; Child, Preschool ; CMV ; Cohort Studies ; Cytomegalovirus ; Cytomegalovirus Infections - complications ; Cytomegalovirus Infections - immunology ; Diabetes ; Diabetes Mellitus, Type 1 - epidemiology ; Diabetes Mellitus, Type 1 - immunology ; Diabetes Mellitus, Type 1 - mortality ; Diabetes Mellitus, Type 1 - virology ; Diabetes risk ; Diabetes. Impaired glucose tolerance ; disease course ; Disease Progression ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Genotype & phenotype ; Health risk assessment ; HLA Antigens - immunology ; HLA genotype ; Human Physiology ; Humans ; Immunoglobulin G - blood ; Infant ; Infections ; Infectious diseases ; insulin-dependent diabetes mellitus ; Internal Medicine ; Medical sciences ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Pediatrics ; Risk Factors ; Short Communication ; Survival Analysis ; Viral diseases</subject><ispartof>Diabetologia, 2008-05, Vol.51 (5), p.769-772</ispartof><rights>Springer-Verlag 2008</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-e9a78d7083ddc2e7b0db6c2a7cdd1cef9f0e77295047cbab14604128286adde73</citedby><cites>FETCH-LOGICAL-c497t-e9a78d7083ddc2e7b0db6c2a7cdd1cef9f0e77295047cbab14604128286adde73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00125-008-0945-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00125-008-0945-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20259224$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18278478$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aarnisalo, J</creatorcontrib><creatorcontrib>Veijola, R</creatorcontrib><creatorcontrib>Vainionpää, R</creatorcontrib><creatorcontrib>Simell, O</creatorcontrib><creatorcontrib>Knip, M</creatorcontrib><creatorcontrib>Ilonen, J</creatorcontrib><title>Cytomegalovirus infection in early infancy: risk of induction and progression of autoimmunity associated with type 1 diabetes</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><addtitle>Diabetologia</addtitle><description>Aims/hypothesis Type 1 diabetes is an autoimmune disease resulting from a complex interplay between genetic and environmental factors. Cytomegalovirus (CMV) infection is one of the environmental factors implicated in the development of type 1 diabetes, although the association remains unproven. We aimed to clarify the possible correlation between CMV infections and type 1 diabetes-associated autoimmunity at the time point of autoantibody appearance in young children with HLA-conferred disease susceptibility. Methods CMV-specific IgG antibodies were analysed from serum samples of 169 children who had developed the first type 1 diabetes-associated autoantibody by the age of 2 years and who turned positive for multiple autoantibodies during later follow-up. We also studied 791 control children matched for sex, age and HLA genotype. The subsequent progression to clinical diabetes was analysed. The serum specimens used were collected at the time of autoantibody seroconversion or within the next 6 months. Results The frequency of CMV antibodies was similar in both study groups at the time of the first autoantibody appearance. Of the index children, 38 (22.5%) were CMV IgG antibody-positive, while the figure for control children was 206 (26.0%; p = 0.38). No association between perinatal CMV infection and progression to type 1 diabetes was observed. Conclusions/interpretation According to these results, perinatal CMV infections are not associated with early serological signs of beta cell autoimmunity or progression to type 1 diabetes in children with diabetes risk-associated HLA genotype.</description><subject>Age</subject><subject>Antibodies</subject><subject>Antibodies, Viral - blood</subject><subject>autoantibodies</subject><subject>Autoimmune Diseases - epidemiology</subject><subject>Autoimmune Diseases - virology</subject><subject>Beta cell autoimmunity</subject><subject>Biological and medical sciences</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>CMV</subject><subject>Cohort Studies</subject><subject>Cytomegalovirus</subject><subject>Cytomegalovirus Infections - complications</subject><subject>Cytomegalovirus Infections - immunology</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 1 - epidemiology</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Diabetes Mellitus, Type 1 - mortality</subject><subject>Diabetes Mellitus, Type 1 - virology</subject><subject>Diabetes risk</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>disease course</subject><subject>Disease Progression</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Genotype & phenotype</subject><subject>Health risk assessment</subject><subject>HLA Antigens - immunology</subject><subject>HLA genotype</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Immunoglobulin G - blood</subject><subject>Infant</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>insulin-dependent diabetes mellitus</subject><subject>Internal Medicine</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Pediatrics</subject><subject>Risk Factors</subject><subject>Short Communication</subject><subject>Survival Analysis</subject><subject>Viral diseases</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkUuL1TAUgIMozp3RH-BGgzDuqiePNuns5OILBlzogLuQJuk1Y9tck1Tpwv9uSi8OuNBVknO-8wgfQk8IvCQA4lUCILSuAGQFLa8reQ_tCGe0Ak7lfbRb0xWRzZczdJ7SLQCwmjcP0RmRVEgu5A792i85jO6gh_DDxzlhP_XOZB-mcsNOx2FZQ3oyyxWOPn3DoS8BO2-Mniw-xnCILqX1XZJ6zsGP4zz5vGCdUjBeZ2fxT5-_4rwcHSbYet257NIj9KDXQ3KPT-cFunn75vP-fXX98d2H_evryvBW5Mq1WkgrQDJrDXWiA9s1hmphrCXG9W0PTgja1sCF6XRHeAOcUEllo611gl2gF1vfsuv32aWsRp-MGwY9uTAnJYDLhjD2X5CC5C2TvIDP_wJvwxyn8glFSQEEb6FAZINMDClF16tj9KOOiyKgVoNqM6iKQbUaVLLUPD01nrvR2buKk7ICXJ4AnYwe-ljc-PSHo0DrltJ1Q7pxqaSmg4t3G_5r-rOtqNdB6UMRrm4-USCsMJIJ2bDf8xa-rw</recordid><startdate>20080501</startdate><enddate>20080501</enddate><creator>Aarnisalo, J</creator><creator>Veijola, R</creator><creator>Vainionpää, R</creator><creator>Simell, O</creator><creator>Knip, M</creator><creator>Ilonen, J</creator><general>Berlin/Heidelberg : Springer-Verlag</general><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</general><scope>FBQ</scope><scope>IQODW</scope><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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7U9</scope><scope>7X8</scope></search><sort><creationdate>20080501</creationdate><title>Cytomegalovirus infection in early infancy: risk of induction and progression of autoimmunity associated with type 1 diabetes</title><author>Aarnisalo, J ; Veijola, R ; Vainionpää, R ; Simell, O ; Knip, M ; Ilonen, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c497t-e9a78d7083ddc2e7b0db6c2a7cdd1cef9f0e77295047cbab14604128286adde73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Age</topic><topic>Antibodies</topic><topic>Antibodies, Viral - blood</topic><topic>autoantibodies</topic><topic>Autoimmune Diseases - epidemiology</topic><topic>Autoimmune Diseases - virology</topic><topic>Beta cell autoimmunity</topic><topic>Biological and medical sciences</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>CMV</topic><topic>Cohort Studies</topic><topic>Cytomegalovirus</topic><topic>Cytomegalovirus Infections - complications</topic><topic>Cytomegalovirus Infections - immunology</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 1 - epidemiology</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Diabetes Mellitus, Type 1 - mortality</topic><topic>Diabetes Mellitus, Type 1 - virology</topic><topic>Diabetes risk</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>disease course</topic><topic>Disease Progression</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Genotype & phenotype</topic><topic>Health risk assessment</topic><topic>HLA Antigens - immunology</topic><topic>HLA genotype</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Immunoglobulin G - blood</topic><topic>Infant</topic><topic>Infections</topic><topic>Infectious diseases</topic><topic>insulin-dependent diabetes mellitus</topic><topic>Internal Medicine</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Pediatrics</topic><topic>Risk Factors</topic><topic>Short Communication</topic><topic>Survival Analysis</topic><topic>Viral diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aarnisalo, J</creatorcontrib><creatorcontrib>Veijola, R</creatorcontrib><creatorcontrib>Vainionpää, R</creatorcontrib><creatorcontrib>Simell, O</creatorcontrib><creatorcontrib>Knip, M</creatorcontrib><creatorcontrib>Ilonen, J</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Virology and AIDS Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aarnisalo, J</au><au>Veijola, R</au><au>Vainionpää, R</au><au>Simell, O</au><au>Knip, M</au><au>Ilonen, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytomegalovirus infection in early infancy: risk of induction and progression of autoimmunity associated with type 1 diabetes</atitle><jtitle>Diabetologia</jtitle><stitle>Diabetologia</stitle><addtitle>Diabetologia</addtitle><date>2008-05-01</date><risdate>2008</risdate><volume>51</volume><issue>5</issue><spage>769</spage><epage>772</epage><pages>769-772</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Aims/hypothesis Type 1 diabetes is an autoimmune disease resulting from a complex interplay between genetic and environmental factors. Cytomegalovirus (CMV) infection is one of the environmental factors implicated in the development of type 1 diabetes, although the association remains unproven. We aimed to clarify the possible correlation between CMV infections and type 1 diabetes-associated autoimmunity at the time point of autoantibody appearance in young children with HLA-conferred disease susceptibility. Methods CMV-specific IgG antibodies were analysed from serum samples of 169 children who had developed the first type 1 diabetes-associated autoantibody by the age of 2 years and who turned positive for multiple autoantibodies during later follow-up. We also studied 791 control children matched for sex, age and HLA genotype. The subsequent progression to clinical diabetes was analysed. The serum specimens used were collected at the time of autoantibody seroconversion or within the next 6 months. Results The frequency of CMV antibodies was similar in both study groups at the time of the first autoantibody appearance. Of the index children, 38 (22.5%) were CMV IgG antibody-positive, while the figure for control children was 206 (26.0%; p = 0.38). No association between perinatal CMV infection and progression to type 1 diabetes was observed. Conclusions/interpretation According to these results, perinatal CMV infections are not associated with early serological signs of beta cell autoimmunity or progression to type 1 diabetes in children with diabetes risk-associated HLA genotype.</abstract><cop>Berlin/Heidelberg</cop><pub>Berlin/Heidelberg : Springer-Verlag</pub><pmid>18278478</pmid><doi>10.1007/s00125-008-0945-8</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Age Antibodies Antibodies, Viral - blood autoantibodies Autoimmune Diseases - epidemiology Autoimmune Diseases - virology Beta cell autoimmunity Biological and medical sciences Child Child, Preschool CMV Cohort Studies Cytomegalovirus Cytomegalovirus Infections - complications Cytomegalovirus Infections - immunology Diabetes Diabetes Mellitus, Type 1 - epidemiology Diabetes Mellitus, Type 1 - immunology Diabetes Mellitus, Type 1 - mortality Diabetes Mellitus, Type 1 - virology Diabetes risk Diabetes. Impaired glucose tolerance disease course Disease Progression Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Genotype & phenotype Health risk assessment HLA Antigens - immunology HLA genotype Human Physiology Humans Immunoglobulin G - blood Infant Infections Infectious diseases insulin-dependent diabetes mellitus Internal Medicine Medical sciences Medicine Medicine & Public Health Metabolic Diseases Pediatrics Risk Factors Short Communication Survival Analysis Viral diseases |
| title | Cytomegalovirus infection in early infancy: risk of induction and progression of autoimmunity associated with type 1 diabetes |
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