Evaluation of HLA polymorphisms in relation to schizophrenia risk and infectious exposure

Mikhil Bamne; Joel Wood; Kodavali Chowdari; Annie M. Watson; Cemil Celik; Hader Mansour; Lambertus Klei; Ruben C. Gur; L. Dianne Bradford; Monica E. Calkins; Alberto Santos; Neil Edwards; Joseph Kwentus; Joseph Patrick McEvoy; Trina B. Allen; Robert M. Savage; Henry A. Nasrallah; Raquel E. Gur; Rodney T. Perry; Rodney C.P. Go; Bernie Devlin; Robert Yolken; Vishwajit L. Nimgaonkar

doi:10.1093/schbul/sbs087

Evaluation of HLA polymorphisms in relation to schizophrenia risk and infectious exposure

Mikhil Bamne, Joel Wood, Kodavali Chowdari, Annie M. Watson, Cemil Celik, Hader Mansour, Lambertus Klei, Ruben C. Gur, L. Dianne Bradford, Monica E. Calkins, Alberto Santos, Neil Edwards, Joseph Kwentus, Joseph Patrick McEvoy, Trina B. Allen, Robert M. Savage, Henry A. Nasrallah, Raquel E. Gur, Rodney T. Perry, Rodney C.P. GoBernie Devlin, Robert Yolken, Vishwajit L. Nimgaonkar

Psychiatry and Health Behavior

Research output: Contribution to journal › Article › peer-review

23 Scopus citations

Abstract

Background: Genome-wide association studies (GWAS) implicate single nucleotide polymorphisms (SNPs) on chromosome 6p21.3-22.1, the human leukocyte antigen (HLA) region, as common risk factors for schizophrenia (SZ). Other studies implicate viral and protozoan exposure. Our study tests chromosome 6p SNPs for effects on SZ risk with and without exposure. Method: GWAS-significant SNPs and ancestry-informative marker SNPs were analyzed among African American patients with SZ (n = 604) and controls (n = 404). Exposure to herpes simplex virus, type 1 (HSV-1), cytomegalovirus (CMV), and Toxoplasma gondii (TOX) was assayed using specific antibody assays. Results: Five SNPs were nominally associated with SZ, adjusted for population admixture (P <. 05, uncorrected for multiple comparisons). These SNPs were next analyzed in relation to infectious exposure. Multivariate analysis indicated significant association between rs3130297 genotype and HSV-1 exposure; the associated allele was different from the SZ risk allele. Conclusions: We propose a model for the genesis of SZ incorporating genomic variation in the HLA region and neurotropic viral exposure for testing in additional, independent African American samples.

Original language	English (US)
Pages (from-to)	1149-1154
Number of pages	6
Journal	Schizophrenia Bulletin
Volume	38
Issue number	6
DOIs	https://doi.org/10.1093/schbul/sbs087
State	Published - Nov 2012

Keywords

African American
HLA
HSV-1
cytomegalovirus
gene
schizophrenia

ASJC Scopus subject areas

Psychiatry and Mental health

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1093/schbul/sbs087

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Bamne, M., Wood, J., Chowdari, K., Watson, A. M., Celik, C., Mansour, H., Klei, L., Gur, R. C., Bradford, L. D., Calkins, M. E., Santos, A., Edwards, N., Kwentus, J., McEvoy, J. P., Allen, T. B., Savage, R. M., Nasrallah, H. A., Gur, R. E., Perry, R. T., ... Nimgaonkar, V. L. (2012). Evaluation of HLA polymorphisms in relation to schizophrenia risk and infectious exposure. Schizophrenia Bulletin, 38(6), 1149-1154. https://doi.org/10.1093/schbul/sbs087

Bamne, M, Wood, J, Chowdari, K, Watson, AM, Celik, C, Mansour, H, Klei, L, Gur, RC, Bradford, LD, Calkins, ME, Santos, A, Edwards, N, Kwentus, J, McEvoy, JP, Allen, TB, Savage, RM, Nasrallah, HA, Gur, RE, Perry, RT, Go, RCP, Devlin, B, Yolken, R & Nimgaonkar, VL 2012, 'Evaluation of HLA polymorphisms in relation to schizophrenia risk and infectious exposure', Schizophrenia Bulletin, vol. 38, no. 6, pp. 1149-1154. https://doi.org/10.1093/schbul/sbs087

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title = "Evaluation of HLA polymorphisms in relation to schizophrenia risk and infectious exposure",

abstract = "Background: Genome-wide association studies (GWAS) implicate single nucleotide polymorphisms (SNPs) on chromosome 6p21.3-22.1, the human leukocyte antigen (HLA) region, as common risk factors for schizophrenia (SZ). Other studies implicate viral and protozoan exposure. Our study tests chromosome 6p SNPs for effects on SZ risk with and without exposure. Method: GWAS-significant SNPs and ancestry-informative marker SNPs were analyzed among African American patients with SZ (n = 604) and controls (n = 404). Exposure to herpes simplex virus, type 1 (HSV-1), cytomegalovirus (CMV), and Toxoplasma gondii (TOX) was assayed using specific antibody assays. Results: Five SNPs were nominally associated with SZ, adjusted for population admixture (P <. 05, uncorrected for multiple comparisons). These SNPs were next analyzed in relation to infectious exposure. Multivariate analysis indicated significant association between rs3130297 genotype and HSV-1 exposure; the associated allele was different from the SZ risk allele. Conclusions: We propose a model for the genesis of SZ incorporating genomic variation in the HLA region and neurotropic viral exposure for testing in additional, independent African American samples.",

keywords = "African American, HLA, HSV-1, cytomegalovirus, gene, schizophrenia",

author = "Mikhil Bamne and Joel Wood and Kodavali Chowdari and Watson, {Annie M.} and Cemil Celik and Hader Mansour and Lambertus Klei and Gur, {Ruben C.} and Bradford, {L. Dianne} and Calkins, {Monica E.} and Alberto Santos and Neil Edwards and Joseph Kwentus and McEvoy, {Joseph Patrick} and Allen, {Trina B.} and Savage, {Robert M.} and Nasrallah, {Henry A.} and Gur, {Raquel E.} and Perry, {Rodney T.} and Go, {Rodney C.P.} and Bernie Devlin and Robert Yolken and Nimgaonkar, {Vishwajit L.}",

year = "2012",

month = nov,

doi = "10.1093/schbul/sbs087",

language = "English (US)",

volume = "38",

pages = "1149--1154",

journal = "Schizophrenia Bulletin",

issn = "0586-7614",

publisher = "Oxford University Press",

number = "6",

}

TY - JOUR

T1 - Evaluation of HLA polymorphisms in relation to schizophrenia risk and infectious exposure

AU - Bamne, Mikhil

AU - Wood, Joel

AU - Chowdari, Kodavali

AU - Watson, Annie M.

AU - Celik, Cemil

AU - Mansour, Hader

AU - Klei, Lambertus

AU - Gur, Ruben C.

AU - Bradford, L. Dianne

AU - Calkins, Monica E.

AU - Santos, Alberto

AU - Edwards, Neil

AU - Kwentus, Joseph

AU - McEvoy, Joseph Patrick

AU - Allen, Trina B.

AU - Savage, Robert M.

AU - Nasrallah, Henry A.

AU - Gur, Raquel E.

AU - Perry, Rodney T.

AU - Go, Rodney C.P.

AU - Devlin, Bernie

AU - Yolken, Robert

AU - Nimgaonkar, Vishwajit L.

PY - 2012/11

Y1 - 2012/11

N2 - Background: Genome-wide association studies (GWAS) implicate single nucleotide polymorphisms (SNPs) on chromosome 6p21.3-22.1, the human leukocyte antigen (HLA) region, as common risk factors for schizophrenia (SZ). Other studies implicate viral and protozoan exposure. Our study tests chromosome 6p SNPs for effects on SZ risk with and without exposure. Method: GWAS-significant SNPs and ancestry-informative marker SNPs were analyzed among African American patients with SZ (n = 604) and controls (n = 404). Exposure to herpes simplex virus, type 1 (HSV-1), cytomegalovirus (CMV), and Toxoplasma gondii (TOX) was assayed using specific antibody assays. Results: Five SNPs were nominally associated with SZ, adjusted for population admixture (P <. 05, uncorrected for multiple comparisons). These SNPs were next analyzed in relation to infectious exposure. Multivariate analysis indicated significant association between rs3130297 genotype and HSV-1 exposure; the associated allele was different from the SZ risk allele. Conclusions: We propose a model for the genesis of SZ incorporating genomic variation in the HLA region and neurotropic viral exposure for testing in additional, independent African American samples.

AB - Background: Genome-wide association studies (GWAS) implicate single nucleotide polymorphisms (SNPs) on chromosome 6p21.3-22.1, the human leukocyte antigen (HLA) region, as common risk factors for schizophrenia (SZ). Other studies implicate viral and protozoan exposure. Our study tests chromosome 6p SNPs for effects on SZ risk with and without exposure. Method: GWAS-significant SNPs and ancestry-informative marker SNPs were analyzed among African American patients with SZ (n = 604) and controls (n = 404). Exposure to herpes simplex virus, type 1 (HSV-1), cytomegalovirus (CMV), and Toxoplasma gondii (TOX) was assayed using specific antibody assays. Results: Five SNPs were nominally associated with SZ, adjusted for population admixture (P <. 05, uncorrected for multiple comparisons). These SNPs were next analyzed in relation to infectious exposure. Multivariate analysis indicated significant association between rs3130297 genotype and HSV-1 exposure; the associated allele was different from the SZ risk allele. Conclusions: We propose a model for the genesis of SZ incorporating genomic variation in the HLA region and neurotropic viral exposure for testing in additional, independent African American samples.

KW - African American

KW - HLA

KW - HSV-1

KW - cytomegalovirus

KW - gene

KW - schizophrenia

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AN - SCOPUS:84869066703

SN - 0586-7614

VL - 38

SP - 1149

EP - 1154

JO - Schizophrenia Bulletin

JF - Schizophrenia Bulletin

IS - 6

ER -

Evaluation of HLA polymorphisms in relation to schizophrenia risk and infectious exposure

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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