Association of Epstein-Barr virus antibody titers with a human IL-10 promoter polymorphism in Japanese women
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BioMed Central
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Association of Epstein-Barr virus antibody titers with a human IL-10 promoter polymorphism in Japanese women Yutaka Yasui*1, Nobuyuki Hamajima2, Tsuneya Nakamura3, Noha Sharaf ElDin1, Kazuo Tajima4 and John D Potter5 Address: 1Department of Public Health Sciences, School of Public Health, University of Alberta, Edmonton, AB, Canada, 2Department of Preventive Medicine, Biostatistics, and Medical Decision Making, Nagoya University Graduate School of Medicine, Nagoya, Japan, 3Department of Gastroenterology, Aichi Cancer Center Hospital, Nagoya, Japan, 4Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Nagoya, Japan and 5Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, USA Email: Yutaka Yasui* - [email protected]; Nobuyuki Hamajima - [email protected]; Tsuneya Nakamura - [email protected]; Noha Sharaf El-Din - [email protected]; Kazuo Tajima - [email protected]; John D Potter - [email protected] * Corresponding author
Published: 4 March 2008 Journal of Autoimmune Diseases 2008, 5:2
doi:10.1186/1740-2557-5-2
Received: 6 February 2008 Accepted: 4 March 2008
This article is available from: http://www.jautoimdis.com/content/5/1/2 © 2008 Yasui et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Multiple sclerosis (MS) risk, over 10-fold higher in Western than in Asian countries, is associated with elevated IgG antibody titers against Epstein-Barr viral capcid antigen (anti-EBVCA IgG titers). Given the 84% homology of the open reading frame BCRF1 of Epstein-Barr virus (EBV) to human interleukin 10 (hIL-10) and the remarkable Caucasian-vs.-Asian population differences in hIL-10 gene promoter polymorphisms, this strong association of MS risk with anti-EB-VCA IgG titers may be explained by the genetic variations in the hIL-10 gene. Methods: We evaluated anti-EB-VCA IgG titers in association with a single nucleotide polymorphism (SNP) in the promoter of hIL-10 at position -819 (hIL-10 T-819C) in a crosssectional survey of 241 Japanese. Anti-EB-VCA IgG titer and its elevation (≥ 1:160) were evaluated, stratified by sex and hIL-10 T-819C genotype. Results: The cytosine-allele frequencies at hIL-10 T-819C were 32.9% in women and 30.9% in men. These are consistent with the published reports of Japanese and Chinese, but substantially lower than those of Caucasians (> 70%). In women, the proportion with elevated anti-EB-VCA IgG titers (≥ 1:160) increased appreciably from 53.7% in the T/T genotype group to 66.7% in the T/C group and to 83.3% in the C/C group (P-trend = 0.037). The titers did not differ by the hIL-10 T819C genotype in men. Conclusion: Anti-EB-VCA IgG titers may increase with the number of cytosine alleles at hI
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